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48 publications mentioning rno-mir-208a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-208a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 145
Other miRNAs from this paper: rno-mir-208b
Over -expression of mir-208a in the sham group without AV shunt significantly increased myocardial endoglin and βMHC protein expression while over -expression of mut-208a in the sham group did not induce myocardial endoglin and βMHC protein expression (Figure 3). [score:9]
Overexpression of mir-208a in cardiac myocytes increases βMHC protein expression and addition of antagomir-208a significantly attenuates the increase of βMHC induced by overexpression of mir-208a [21]. [score:7]
We have previously demonstrated that TGF-β1 can activate mir-208a expression in cardiac myocytes [21] and atorvastatin can inhibit the TGF-β1 expression. [score:7]
Immunohistochemical staining showed that increased myocardial endoglin and βMHC expression after AV shunt and over -expression of mir-208a in the sham group (Figure 5). [score:5]
Over -expression of mir-208a in the sham group without AV shunt significantly increased myocardial endoglin expression. [score:5]
Overexpression of mir-208a in the sham group significantly increased endoglin and MHCβ protein expression. [score:5]
Overexpression of mir-208a did not increase protein expression of thyroid hormone receptor associated protein 1, brain natriuretic peptide and αMHC [21]. [score:5]
Over -expression of mutant mir-208a (mut-208a) did not have the effect on myocardial endoglin and βMHC expression induced by AV shunt. [score:5]
However, the mir-208a level was still higher in the atorvastatin -treated group than in the sham group, indicating that atorvastatin partially but not completely inhibited the increase of mir-208a expression induced by AV shunt. [score:5]
Mir-208 is expressed specifically in the heart with trace expression in the lung [9]. [score:4]
Mir208a may also play a pivotal role in the formation of cardiac fibrosis in congenital heart disease, not just in acquired heart disease. [score:4]
Although mir-208a was upregulated and cardiac hypertrophy was induced in thoracic aortic banding, a pressure overload mo del [8], it is not known whether mir-208a is also induced in volume overload. [score:4]
To investigate the effect of mir-208a on myocardial endoglin expression, over -expression of antogomir208a and mutant type mir-208a (mut-208a) in the left ventricle was performed. [score:3]
Bedsides endoglin, βMHC is also a target of mir-208a. [score:3]
There are significantly increased immunoreactive signals for endoglin and MHCβ after overexpression of mir-208a and AV shunt for 7 days. [score:3]
Aorta-caval shunt increases mir-208a expression in rat myocardium. [score:3]
0084188.g001 Figure 1Pretreatment with atorvastatin significantly attenuated the increase of mir-208a expression induced by AV shunt. [score:3]
Mir-208a is upregulated in pressure overloading with thoracic aortic banding [9] and is activated by mechanical stress [11]. [score:3]
Mutant mir-208a did not change myocardial endoglin and βMHC expression after AV shunt. [score:3]
The constructed plasmid (co -expression mir-208 and green fluorescent protein) was transfected into left ventricular myocardium using a low pressure-accelerated gene gun (Bioware Technologies, Taipei, Taiwan) essentially following the protocol from the manufacturer. [score:3]
As shown in Figure 1, AV shunt significantly increased myocardial mir-208a expression at 3 days after shunting, reached a maximal of 3.1±0.2-fold at 5 days and remained elevated for up to 14 days after shunting. [score:3]
In conclusion, we demonstrate for the first time that mir-208a increases endoglin expression to induce myocardial fibrosis in volume overloaded heart failure. [score:3]
Over -expression of antagomir208a in the AV shunt group significantly decreased myocardial fibrosis area induced by AV shunt, indicating that mir-208a plays a crucial role in the myocardial fibrosis after AV shunt. [score:3]
AV shunt increases myocardial mir-208a expression. [score:3]
Pretreatment with atorvastatin significantly attenuated the increase of mir-208a expression induced by AV shunt. [score:3]
Therapeutic innovation target miR208a to improve cardiac fibrosis may warrant further research. [score:3]
Construction and delivery of mir-208a expression vector. [score:3]
0084188.g005 Figure 5 There are significantly increased immunoreactive signals for endoglin and MHCβ after overexpression of mir-208a and AV shunt for 7 days. [score:3]
The 165 bp amplified product was digested with EcoRI and BamHI restriction enzymes and ligated into pmR-ZsGreen1 plasmid vector (coexpression mir-208 and green fluorescent protein, Clontech Laboratories, Mountain View, CA, USA) digested with the same enzymes. [score:3]
AV shunt and over -expression of mir-208a in the sham group significantly increased myocardial fibrosis area as compared to sham group (Figure 6). [score:2]
Mir-208a mediates the myocardial endoglin expression. [score:2]
Mir-208 expression vector was transfected into left ventricular myocardium by low pressure-accelerated gene gun. [score:2]
Mir-208a can increase endoglin expression in cardiac myoblast [11]. [score:2]
In brief, each 15 µl RT reaction contained purified 10 ng of total RNA, 3 µl miR-208 RT primer (Applied Biosystems®, Life Technologies, Grand Island, NY, USA), 1×RT buffer (Applied Biosystems), 0.25 mM each of dNTPs, 3.33 U/µl MultiScribe™ reverse transcriptase (Applied Biosystems) and 0.25 U/µl RNase inhibitor (Applied Biosystems). [score:2]
Mir-208a is also essential for the expression of the genes involved in cardiac hypertrophic growth. [score:2]
Mir-208a seems to be fundamental for the expression of genes involved in cardiac fibrosis and hypertrophic growth [9], [10]. [score:2]
Mir-208a mediates the myocardial endoglin expression in AV shunt rat. [score:2]
A 71 bp rat-mir-208a precursor construct was generated as follows. [score:1]
Representative microscopic images showing the presence of mir-208a (green color) in the cytoplasm of cardiac myocytes from left ventricular myocardium in AV shunt rats. [score:1]
0084188.g004 Figure 4 detects the presence of mir-208a in the cardiac myocytes. [score:1]
Figure S2 Transfection of mir-208a into myocardium was monitored by a dissecting fluorescence microscope as shown in green color. [score:1]
This finding indicates that mir-208a plays a crucial role in the myocardial fibrosis after AV shunt. [score:1]
The role of mir-208a in volume overload is not known. [score:1]
The sham group or scrambled probe did not detect the presence of mir-208a. [score:1]
Pretreatment with atorvastatin significantly attenuated the increase of mir-208a induced by AV shunt. [score:1]
The prehybridization solution was replaced with 200 µl of hybridization solution containing 10 pmol of the FAM-labeled LNA miR-208a probe (product sequence 5′-3′, CTTTTTGCTCGTCTTAT, Exiqon, Vedbaek, Denmark) and tissues were incubated for 90 minutes at the hybridization temperature and washed twice for 10 minutes in sodium chloride/sodium citrate buffer. [score:1]
The increased endoglin to induce myocardial fibrosis induced by AV shunt was mediated by mir-208a. [score:1]
Therefore, the reason that pretreatment of atorvastatin in volume overload mo del can reduce mir-208a possibly is through the anti-inflammatory or pleiotropic effect of atorvastatin, partially by the anti-TGF-β1 effect. [score:1]
In the present study, we demonstrated for the first time that mir-208a was induced in acute volume overload by AV shunt in rat. [score:1]
The transfection of mir-208a into myocardium was monitored by a dissecting fluorescence microscope as shown in Figure S2. [score:1]
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2
[+] score: 80
In ZDF-M, cardiac miR-208a expression was higher than that in ZL-M, yet lower than ZL-F and ZDF-F. Moreover, in ZDF-M cardiac Agtr2 expression was similar to ZL-M. Conversely, in ZDF-F, cardiac miR-208a expression was increased while Agtr2 expression was reduced. [score:9]
However, Med13 expression was the highest in ZL-F, indicating that cardiac Med13 mRNA expression in healthy ZL-F could be regulated by mechanisms independent of miR-208a. [score:6]
However, reduction in cardiac Agtr2 expression in ZDF-F in the presence of the highest expression of pro-hypertrophic miR-208a may have contributed to the increased myocardial structural damage observed in ZDF-F rat. [score:5]
Notably, though ZL-F has higher cardiac expression of pro-hypertrophic miR-208a, they also have higher expression of cardio-reparative Agtr2 that may counteract miR-208a’s cardio-detrimental effect and keep the heart healthy. [score:5]
Since increased expression of miR-208a is associated with cardiac hypertrophy, the female-specific increase in cardiac miR-208a expression could have contributed to the increased susceptibility to cardiac hypertrophy in ZDF-F. Increases in the circulating levels of miR-29 family miRNAs in children with T1DM and adults with T2DM 42, 43 emphasize the clinical relevance of this biomarker in DM. [score:5]
Our observations underscore the need for clinically expanding existing cardiac assessments in diabetic female patients to detect myocardial deformation, cardiac hypertrophy and capillary density via non-invasive imaging, as well as suggest miR-208a and AT2R as potential therapeutic targets for cardiac disease in females. [score:5]
DM -associated dysregulation of miR-208a-MED13 signaling and increase in miR-29 family miRNAs occur in both male and female ZDF rats, however, only ZDF-F rats exhibited myocardial damage indicating that cardiac repair is impaired in ZDF-F. It is conceivable that the higher expression of cardio-reparative Agtr2 in ZL-F compared to ZL-M (Fig.   9a) could have provided increased protection despite the higher expression of pro-hypertrophic miR-208a in ZL-F heart compared to ZL-M heart. [score:4]
MED13 is a target of miR-208a, a microRNA that promotes cardiac hypertrophy and heart failure 38– 41. [score:3]
TaqMan MicroRNA Assays (Life Technologies) primers for miR-208a, miR-29a, b, c, and U6 snRNA were used for miRNA targets, and Med13 and 18 S rRNA for mRNA targets. [score:3]
Figure 9Expression patterns of cardioprotective Agtr2 and Med13, and cardio- deleterious miR-208a and diabetic marker miR-29 family miRNAs in heart tissues of 5-month old healthy and diabetic, male and female rats. [score:3]
Though reduction in capillary density was a common phenomenon in both ZDF-F and ZDF-M, this effect is likely more deleterious for the hypertrophied myocardium of ZDF-F. It is conceivable that cardiac hypertrophy, capillary rarefaction, and a female-specific loss of cardio-reparative Agtr2 in the setting of a very high expression of pro-hypertrophic miR-208a could have contributed to increased myocardial structural damage in the form of cardiomyocyte loss and scarring as shown in Fig.   8f. [score:3]
Since ZDF-F exhibited cardiac hypertrophy, we examined whether there was a sex bias in the expression of cardiac miR-208a. [score:3]
Female specific increased expression of cardiac miR-208a (as shown in Fig.   9) could render ZDF-F rats more susceptible to hypertrophy. [score:3]
Cardiac expression of AT2R (Agtr2), Med13, miR-208a, and miR-29 family miRNAs were determined using mRNA and miRNA isolated from frozen heart tissues as described previously [44]. [score:3]
Therefore, miR-208a and AT2R can be potential therapeutic targets for CVD in diabetic females. [score:3]
Thus, T2DM caused an imbalance in cardiac miR-208a- Agtr2 expression pattern that would exacerbate cardiac damage. [score:3]
Elevated miR-208a reduces MED13 expression, thus contributing to obesity 38, 39. [score:3]
Elevated levels of cardiac miR-208a expression in ZL-F and ZDF-F compared to ZL-M and ZDF-M could render female rats more susceptible to cardiac hypertrophy. [score:2]
Cardiac miR-208a expression was elevated in both ZDF-F and ZDF-M compared to lean controls, indicating a diabetes -associated elevation of cardiac miR-208a. [score:2]
The miR-208a expression was higher in both ZL-F and ZDF-F compared to their male counterparts. [score:2]
Interestingly, cardiac expression of miR-208a was higher in ZL-F compared to ZL-M and was the highest in ZDF-F (Fig.   9c, p < 0.05). [score:2]
Thus miR-208a exhibits sex bias. [score:1]
MicroRNA miR-208a promotes cardiac hypertrophy and heart failure 40, 41. [score:1]
MED13-miR-208a-axis differs between male and female diabetic animals. [score:1]
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3
[+] score: 43
To confirm the results of the miRNA sequencing data, 4 upregulated miRNAs (rno-miR-122-5p, rno-miR-199a-5p, rno-miR-184 and rno-miR-202-5p) and 4 downregulated miRNAs (rno-miR-208a-3p, rno-miR-208a-5p, rno-miR-6314 and rno-miR-22-3p) were chosen to be further examined using real-time quantitative PCR. [score:7]
Among them, 12 miRNAs (rno-miR-10b-5p, rno-miR-122-5p, rno-miR-184, rno-miR-1843-5p, rno-miR-196c-5p, rno-miR-199a-5p, rno-miR-202-5p, rno-miR-206-3p, rno-miR-208b-5p, rno-miR-224-5p, rno-miR-298-5p and rno-miR-31a-5p) were significantly upregulated(p<0.01, fold-change >1) compared to the control group and only rno-miR-208a-3p were significantly downregulated (p<0.01, fold-change <-1) (Fig 3). [score:6]
It has been reported that miR-208a promotes heart failure progress through modulating cardiac fibrosis through increasing endoglin and collagen I expression[35, 36] and hypertrophy, and could be a biomarker for diagnosis and therapeutic target in treatment of heart failure[9, 37– 39]. [score:5]
Among the top 13 differentially expressed miRNAs, the five most abundantly expressed miRNAs were rno-miR-122-5p, rno-miR-184, rno-miR-31a-5p, rno-miR-199a-5p and rno-miR-208a-3p. [score:5]
We found that in the heart failure group, miR-208b were up regulated, while the miR-208a-3p expression increased in the early stage after myocardial infarction, but decreased in the late stage, indicating that miR-208a-3p and miR-208b play different even opposite roles in heart failure, which needs to be clarified by further research. [score:4]
To further confirm the results of the miRNA sequencing and analyze the dynamic expression pattern of specific miRNAs in HF rats, the dynamic changes of miR-208a-3p (Fig 4B), miR-184 (Fig 4C), miR-122-5p (Fig 4D) and miR-199a-5p (Fig 4E) in the process of post-infarcted heart failure were analyzed. [score:3]
Time-course analysis revealed different expression patterns of 4 miRNAs: rno-miR-122-5p, rno-miR-199a-5p, rno-miR-184 and rno-miR-208a-3p. [score:3]
Furthermore, therapeutic silencing of miR-208a via subcutaneous delivery of antimiR-208a prevents pathological cardiac remo deling, functional deterioration, and lethality during heart disease, which indicated the potential therapeutic roles of modulating cardiac miRNAs during heart failure[9]. [score:3]
MiR-208 family members are highly expressed in cardiomyocytes, and are closely related with ventricular remo deling [34]. [score:2]
In the first miRNA deletion animal mo del in 2007, miR-208, a cardiac-specific miRNA, was found to be required for cardiomyocyte hypertrophy and fibrosis[8]. [score:1]
The miR-208 family includes two subfamilies: miR-208a and miR-208b. [score:1]
Whether or not miR-208 contributes to fibrosis is not fully elucidated. [score:1]
There was a prominent increase of rno-miR-208a-3p in early stage of post-MI, but decreased gradually. [score:1]
Time course analysis of miR-208a-3p (B), miR-184 (C), miR-122-5p (D) and miR-199a-5p (E) were studied. [score:1]
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4
[+] score: 25
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Expression analysis of conserved miRNAs in 14 different tissue types revealed heart-specific expression of miR-499 and miR-208 and liver-specific expression of miR-122. [score:7]
Consistently, miR-208 is specifically and abundantly expressed in the heart, but we found a very weak expression (trace levels) in lungs (Figure 2A). [score:5]
Some miRNAs, including miR-208, miR-101, miR-18a, miR-20 and miR-142-3p, showed a weaker expression than other miRNAs tested by small RNA blot analyses (Figures 2 and 3). [score:3]
These results are in agreement with the expression analysis of miR-208 in rats and humans [48]. [score:3]
Because of their location within the introns of myosin genes and their specific expression in myogenic cells, miR-208 and miR-499 were referred to as MyomiRs [47]. [score:3]
Several miRNAs (miR-1, miR-133, miR-499, miR-208, miR-122, miR-194, miR-18, miR-142-3p, miR-101 and miR-143) have distinct tissue-specific expression patterns. [score:3]
miR-208 is encoded in intron 27 of the human and mouse αMHC gene [48]. [score:1]
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5
[+] score: 23
Our results showed that GS-Rb1 could suppress the expression of mir-208 in mo del group. [score:5]
But there was no enough evidence shown that overexpression or knockdown mir-208 was related to the hypoxia/ischemia injuries and cardiomyocytes apoptosis. [score:4]
Therapeutic inhibition of mir-208a by systemic delivery of antisense oligonucleotide could improve cardiac function and survival during hypertension -induced heart failure [36]. [score:3]
MicroRNAs have been proved to be potential biomarkers for ischemic heart disease, such as mir-1, mir-133, mir-208, and mir-499 [4– 6]. [score:3]
The expression level of mir-1, mir-29a, and mir-208 was increased in the H/I group (5.9-, 3.4-, and 9.3-fold versus control, relatively), while that of mir-21 and mir-320 was significantly decreased (0.35- and 0.41-fold versus control, relatively). [score:3]
Compared with that of the control group, expressions of mir-1, mir-29a, and mir-208 obviously increased in the experimental mo del groups. [score:2]
Plasma mir-208 increased significantly after isoproterenol -induced myocardial injury and showed a similar time course to the concentration of cTnI [35]. [score:1]
A growing number of studies have demonstrated that mir-208 could be selected as a possible biomarker of myocardial injury and myocardial infarction [33, 34]. [score:1]
The relationship of mir-208 and cardiomyocytes injury or cell apoptosis needs to be further studied. [score:1]
[1 to 20 of 9 sentences]
6
[+] score: 22
To be specifically mentioned (fold change >2.5), miR-208, miR-19b, miR-133b and miR-30e were significantly upregulated and miR-99b, miR-100, miR-191a, miR-22 andmiR-181a-1 were significantly downregulated. [score:7]
miR-208a, miR-133b and miR-30e showed more than 2.5-fold upregulation during physiological cardiac hypertrophy, while miR-19b showcased an upregulation of 1.5 fold only. [score:7]
In this study, during physiological cardiac hypertrophy we observed significant upregulation of miR-208a by both small RNA sequencing and qPCR (Figs. 2, 4). [score:4]
Montgomery et al. [30] showed that therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure. [score:3]
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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7
[+] score: 19
MiR-16 inhibited apoptosis of ESCC cells by downregulating RECK and SOX6 [9]; miR-208 [8] and miR-155 [11] promoted ESCC or hepatocellular carcinoma cell proliferation by targeting SOX6. [score:8]
MiR-499 and miR-21 were downregulated in LPS -induced cells in a dose- and time -dependent manner, while there was no significant change to miR-1, miR-133, and miR-208 expression. [score:6]
In the myocardium of rats with acute myocardial infarction, the expression of some miRNAs was altered, including cardiac-abundant miRNAs such as miR-1, miR-133, miR-208, and miR-499 [15– 17]. [score:3]
Cardiac-abundant miRNAs such as miR-1, miR-133, miR-208, and miR-499 regulate diverse aspects of cardiac function, including cardiomyocyte proliferation, differentiation, contractility, and stress responsiveness. [score:2]
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8
[+] score: 19
It is noteworthy that miR-1, miR-133, miR-30, miR-208a, miR-208b, mir-499, miR-23a, miR-9 and miR-199a have previously been shown to be functionally involved in cardiovascular diseases such as heart failure and hypertrophy [40], [41], [42], [43], [44], and have been proposed as therapeutic- or disease-related drug targets [45], [46]. [score:7]
Although the 3 myomiRs miR-208a/miR-208b/miR-499 contain almost identical seed sequences, miR-499 was considerably less potent at inhibiting luc-Csnk2a2 expression than miR-208a/miR-208b, suggesting a functional role for 3′ compensatory interactions between the myomiRs and Csnk2a2 (Figure 7D and H). [score:5]
In particular, several microRNAs that are preferentially expressed in different types of muscles (e. g. miR-1, miR-133, and the myomiRs miR-208, miR-208b and miR-499) play a pivotal role in maintenance of cardiac function [17], [18], and the ablation of microRNAs-RISC machinery can have dramatic effects on cardiac development [19], [20], [21]. [score:4]
Casein kinase 2a2 (Csnk2a2) and miR-208ab have both previously been implicated in cardiovascular pathologies [29], [40], [54] and our data provide further support for cardiac tissue miR208-Csnk2a2 interactions based on their anti-correlated (<−0,8) expression profiles. [score:3]
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9
[+] score: 17
Examples of the expression profiles of miRNAs that change with age and/or sex are shown in Figures  5 and 6. Female-biased miRNA expression is illustrated by miR-421*, miR-499, and miR-208* (Figure  5A-C), all of which showed female-biased expression at 15 and 21 weeks. [score:7]
MiR-208* showed the highest fold change difference between sexes with female expression approximately 16 and 21-fold higher than male expression at 15 and 21 weeks of age, respectively. [score:4]
Those DEMs exhibiting female bias (17 miRNAs, Additional file 3) included miRNAs showing the highest fold-change differences between sexes (miR-208*, with 21-fold change F > M) and most prolonged, sex-biased expression (miR-421*, at 15, 21, 78, and 104 weeks). [score:3]
The miRNA showing the greatest fold-change difference between the sexes was miR-208* which showed approximately 21-fold higher expression in females compared to males at 21 weeks of age (Table  2 and Figure  5). [score:2]
Female-biased miRNAs feature some of the most promising candidates (miR-421*, miR-499, miR-208*) to further investigate the potential impact of sex-biased expression of miRNAs in the kidney. [score:1]
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[+] score: 14
In addition, the roles of miR-208 in heart diseases, such as myocardial hypertrophy [37] and myocardial fibrosis [38], have also been reported. [score:3]
The literatures of miR-208 on cardiovascular diseases were more than miR-146. [score:3]
To better elucidate the mechanism between miR-208 and myocardial I/R injury, we performed the experiments described in this report according to some of the methods reported by Fang et al. [17], who used a miR microarray to analyze an in vivo rat mo del of 4-h myocardial ischemia without reperfusion and found that miR-378 overexpression conveyed a protective role to cardiomyocytes following ischemic injury. [score:3]
In recent years, studies of miR-208 mainly concentrated on plasma biomarkers [33], acute myocardial infarction [34], heart failure [35], and ventricular remo deling [36]. [score:1]
However, there have no reports on the relationship between miR-208 and apoptosis of myocardiocytes following I/R injury. [score:1]
The complicated mechanism between miR-208 and myocardial I/R injury needs to be further explored. [score:1]
Studies have reported that miR-208 is specific to myocardiocytes, at least to some extent [32, 33]. [score:1]
The results of a large-scale clinical trial demonstrated that miR-208 could be detected in the blood of patients after early acute myocardial infarction [33]. [score:1]
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Our data indicate that hsa-/mmu-miR-208b-3p (previously miR-208b) was the main miR-208 isoform expressed in the sheep heart. [score:3]
Two isoforms of miRNA-208-a/b have also been reported in humans, with miRNA-208a exclusively expressed in the heart and miRNA-208b found in both cardiac and skeletal muscle [34]. [score:3]
For the first time we report that not only are the four cardiac-enriched miR-1, miR-133, miR-499 and miR-208 highly expressed in sheep LV, but also provide information on their isomiRs. [score:3]
Four myocardial-enriched miRNAs, miR-1, miR-133, miR-499 and miR-208, were confirmed to be highly expressed in ovine heart tissue. [score:3]
Hsa-/mmu-/rno-miR-208b-3p was the most abundant form of the miR-208 family. [score:1]
MiR-1, miR-133, miR-499 and miR-208 are highly enriched myocardial miRNAs 27, 28 and are highly conserved across multiple species including human [29], mouse [30] rat [31] and porcine [32]. [score:1]
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The direct target of miR-208 has been shown to be p21 [25], and p21 expression in vascular smooth muscle cells has been shown to be crucial in limiting vascular proliferation in vascular remo deling, which is strongly associated with essential hypertension [26]. [score:6]
We found that miR-208 is upregulated in insulin -mediated proliferation of vascular smooth muscle cells and may promote a switch from the G0/G1 phase of the cell cycle to the S phase. [score:4]
In our studies, the most frequently observed and the most promising miRNAs as potential treatment targets are miR-145 [11] and miR-208 [25]. [score:3]
The miRNAs miR-1, miR-155, and miR-208 have significant effects on the RAAS [14]. [score:1]
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[+] score: 9
Other miRNAs from this paper: mmu-mir-208a
We also demonstrated that 12 weeks of Rapamycin treatment in ZO rats resulted in downregulation of cardiac levels of microRNA miR-208a. [score:4]
We have reported previously that Rapamycin treatment suppressed miR-208a that promotes fibrosis in ZO rats [9]. [score:3]
We observed that Rapamycin (750  μg/kg/day; 12 weeks) reduced body weight, body fat, and cardiac microRNA miR-208a (implicated in promoting hypertrophy and fibrosis) and increased cardiac Med13 (that promotes whole body metabolism in Zucker diabetic fatty rats) [9]. [score:1]
miR-208a is a marker for cardiac dysfunction and fibrosis. [score:1]
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[+] score: 7
In line with these results, we found that miR-208a-3p and miR-499-5p -both cardiac specific and highly abundant in the heart [23]- were either undetectable or very lowly expressed in the circulation of mice. [score:3]
In addition to the cardiac specific miR-208a-3p and miR-499-5p, we found that the expression of let-7i-5p, miR-16-5p, miR-27a-3p, miR-199a-3p and miR-223-3p was significantly higher in the heart compared to the kidney, independent of the presence of ischemic heart failure (S4 Fig and S5 Table). [score:2]
Of the cardiac specific miRNAs, miR-208a-3p was not detectable in the plasma of ischemic heart failure mice and miR-499-5p showed the lowest miRNA expression levels in plasma compared to the other miRNAs (Fig 3 and S4 Table). [score:2]
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For example, miR-208 was up-regulated, while miR-1 and miR-133a were down-regulated in MI [14]. [score:7]
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miR-448, let-7b, miR-540, miR-296, miR-880, miR-200a, miR-500, miR-10b, miR-336, miR-30d, miR-208, let-7e, miR-142-5p, miR-874, miR-375, miR-879, miR-501, and miR-188 were upregulated, while miR-301b, miR-134, and miR-652 were downregulated in TMH group (Table 5). [score:7]
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17
[+] score: 5
Other miRNAs from this paper: rno-mir-92a-1, rno-mir-92a-2, rno-mir-320, rno-mir-494, rno-mir-208b
Similarly, Montgomery et al. found that inhibition of miR-208 was also a potent therapeutic target for modulating cardiac function and remo deling [20]. [score:5]
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Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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[+] score: 5
Other miRNAs from this paper: rno-mir-338, rno-mir-346
For example, the heart-specific host gene Myh6 is co-expressed with the intronic miR-208a, the latter of which has the capacity to regulate thyroid hormone associated protein 1 and myostatin, both negative regulators of muscle growth and hypertrophy [31]. [score:5]
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20
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Among these 21 differentially expressed miRNAs, 17 (miR-10b-5p, miR-223-3p, miR-208a-5p, miR-434-3p, miR-190a-5p, miR-30d-5p, miR-347, miR-493-5p, miR-29a-5p, miR-451-5p, miR-190b-5p, miR-466c-5p, miR-883-5p, miR-466b-1-3p, miR-21-3p, miR-3596c, miR3584-3p) were proven significant (P < 0.05) by qRT-PCR, one (miR-487b-3p) had a tendency to be significant (P = 0.06), and three (miR-138-2-3p, miR-1188-3p, miR-665) were not confirmed to be significant (Table  2). [score:3]
To further investigate whether the carnitine -induced increase in the mRNA level of IGF-1, a putative target gene of miR-466b-1-3p but also miR-208a-5p, is also associated with an increase in the protein level of IGF-1, we determined protein levels of IGF-1 in skeletal muscle of the obese Zucker rats. [score:1]
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21
[+] score: 4
The concomitant decrease of miR-208a and Myh6 levels upon DOX treatment (Figure S1A) further support the importance of the regulatory role of myomiRs-myosin interactions in the myosin switch, which is associated with progressive structural changes and pathological cardiac remo deling [40]. [score:2]
MicroRNA-208b, encoded from the intron 28 of rat Myh7, is associated to maintenance of myocardial performance together with 2 other myomirs, i. e. miR-208a/miR-499, which play a pivotal role in the myosin balance [40]. [score:1]
Figure S1 MicroRNA-208a and 208b are regulated similarly to their hosting transcripts (Myh6 and Myh7 respectively) upon DOX treatment (n = 3). [score:1]
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22
[+] score: 4
The results showed that miR-208, miR-124, miR-146a-5p, miR-103, and miR-21 were all expressed abnormally in spinal tissue of ASCI rats (Figure 2). [score:3]
In the ASCI group, the levels of miR-208, miR-124, and miR-146a-5p were decreased, while the levels of miR-103 and miR-21 were increased. [score:1]
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23
[+] score: 4
Reports have shown that miR-208 and miR-140 affect their host genes 25, 26; however, miR-26 suppresses its host gene to regulate neurogenesis [27]. [score:4]
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24
[+] score: 3
Other specifically expressed miRNAs that we verified are mir-208, which is known to be restricted to the heart [47] and mir-122, the most prominent miRNA in liver [48]. [score:3]
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25
[+] score: 3
Other miRNAs from this paper: mmu-mir-208a, rno-mir-499, mmu-mir-499
Transgenic expression of miR-499 also effectively reduced the elevated Sox6 mRNA level in miR-208a [-/-] hearts and reduced the Sox6 mRNA level in skeletal muscles of MCK-miR-499 transgenic mice [19]. [score:3]
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26
[+] score: 3
Circulating miR-208a and miR-126 were found to be significantly and consistently altered in the plasma under different cardiac pathological conditions, like acute myocardial infarction, heart failure and coronary artery disease [13]. [score:3]
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27
[+] score: 3
Interestingly, the miR-133 family, together with miR-1, miR-206 and miR-208, is specifically expressed in muscle; thus, these miRNAs are called myomiRs 42. [score:3]
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28
[+] score: 3
MiR-208a, which is encoded by MHC genes, has been shown to form an intricate regulatory circuit together with their host genes to regulate cardiac hypertrophy [10]. [score:2]
Callis TE MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in miceJ Clin Invest. [score:1]
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Inhibition of miR-208a prevented pathological myosin switching and cardiac remo delling [19]. [score:3]
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30
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It has been observed that many miRNAs regulate cell apoptosis, such as miR-1, miR-133, miR-199, miR-208, miR-320, miR-21, and miR-204, etc [18- 23]. [score:2]
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31
[+] score: 2
Several candidate therapeutic miRNAs have progressed into clinical and preclinical development; for example, antisense miR-122 is being developed as a treatment for hepatitis C virus, miR-208/499 for chronic heart failure, miR-195 for myocardial infarction and miR-34 and let-7 for cancer 10, 11. [score:2]
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32
[+] score: 2
Groups of tissue-specific (e. g., miR-1, miR-206, miR-208) and non-tissue-specific (e. g., miR-29a, miR-23a) microRNAs have been found to control skeletal muscle development in growth and differentiation [13]– [19]. [score:2]
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33
[+] score: 2
Bostjancic E Zidar N Stajer D MicroRNAs miR-1, miR-133a, miR-133b and miR-208 are dysregulated in human myocardial infarctionCardiology. [score:2]
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Recent studies have shown that cardiac muscle-rich miRNAs or myomiRNAs such as mir-208 (mir-208a, b) play crucial roles in CVD [85– 87]. [score:1]
It has also been reported that plasma levels of some miRNAs (mir-1, mir-208, mir-133a, mir-423-5p, mir-499) can be used as biomarkers for myocardial injury [90– 92]. [score:1]
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For instance, miR-208 is a heart-specific miRNA that is released into the blood stream from injured cardiomyocytes [3]. [score:1]
1997.3477 9087178 3. Ji X Plasma miR-208 as a biomarker of myocardial injuryClin Chem. [score:1]
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[+] score: 2
Conversely, miR-206-3p, miR-208-3p, and -499-5p expression was significantly higher in the soleus muscle compared to the EDL (7.4-, 10.7-, and 35.4-fold respectively; Figure 2C). [score:2]
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9 -45.6 mmu-miR-27b -1.8 -71.4 -462.7 mmu-miR-214* -2.6 -5.0 -43.5 mmu-let-7c-1* -73.2 -204.4 -334.1 mmu-miR-34c -9.4 -26.1 -42.7 mmu-miR-542–3p -5.9 -195.6 -319.8 mmu-miR-706 -9.3 -5.0 -38.7 mmu-miR-487b -2.0 -161.5 -263.9 mmu-miR-467b* -10.1 -2.2 -33.6 rno-miR-17–3p -1.6 -152.0 -248.5 mmu-miR-323–3p -3.7 -23.3 -29.8 mmu-miR-10b -2. 4 -136.6 -223.3 mmu-miR-202–3p -6.5 -5.9 -21.4 mmu-miR-29b -3.0 -135.1 -220.9 mmu-miR-339–5p -1.6 -9.6 -19.6 mmu-miR-297a* -2.4 -128.4 -209.8 mmu-miR-181c -2.0 -10.5 -14.6 mmu-miR-692 -41.5 -115.8 -189.2 mmu-miR-203 -4.6 -6.4 -13.8 mmu-miR-208 -40.6 -113.5 -185.5 mmu-miR-467a* -2.6 -3.9 -11.4 mmu-miR-467c -38.9 -108.6 -177. [score:1]
Among other miRNA such as miR-208 is associated with adverse clinical outcomes in human dilated cardiomyopathy [32]. [score:1]
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173 (miR-186-5p, miR-208a-5p, miR-291a-3p, miR-294-3p, miR-295-3p, miR-302a-3p, miR-302b-3p, miR-302c-3p and miR-302d-3p). [score:1]
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39
[+] score: 1
A few miRNAs are found to be enriched in the heart including miR-1, miR-133, miR-208a, miR-208b, and miR-499. [score:1]
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40
[+] score: 1
Other miRNAs from this paper: rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-208b
Only two studies had attempted to identify circulating miR-208 as a marker for DOXO-cardiotoxicity in breast cancer patients and in an animal mo del, but both failed to demonstrate their intention [46, 47]. [score:1]
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41
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Dozens of miRNAs have been identified in myocardial cells, including miR-133a, miR-133b, miR-1d, miR-296, miR-21, miR-208 and miR-195 (4– 18). [score:1]
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42
[+] score: 1
MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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43
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And 2 non-PRmiRs let-7f and miR-208 did so. [score:1]
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44
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Likewise, a combination of miR-1, miR-133, miR-208 and miR-499 is capable of reprogramming fibroblasts into cardiomyocytes [21]. [score:1]
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45
[+] score: 1
J Cell Physiol 8 Callis TE Pandya K Seok HY Tang RH Tatsuguchi M 2009 MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. [score:1]
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46
[+] score: 1
Callis T. E. Pandya K. Seok H. Y. Tang R. H. Tatsuguchi M. Huang Z. P. Chen J. F. Deng Z. Gunn B. Shumate J. MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice J. Clin. [score:1]
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47
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For example, miRNAs involved in cardiac hypertrophy and heart failure such as miR-208, miR-133, miR-195, miR-21, and miR-126 have been reported in several studies [5- 8]. [score:1]
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48
[+] score: 1
Meng LD Meng AC Zhu Q Jia RY Kong QZ Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal ratsAsian Pac. [score:1]
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