sort by

5 publications mentioning ocu-mir-21

Open access articles that are associated with the species Oryctolagus cuniculus and mention the gene name mir-21. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 503
Other miRNAs from this paper: rno-mir-21
The major findings of this study include the following: (1) our real-time PCR and quantitative analyses revealed that RAP -induced AF significantly down-regulated Smad7 expression, which was associated with an increase in TGF-β [1] and collagen I/III; (2) the AF -induced up-regulation of miR-21 was negatively correlated with Smad7 expression; (3) in isolated adult rat cardiac fibroblasts, treatment with TGF-β [1] caused the down-regulation of Smad7 expression and increased the levels of miR-21 and collagen I/III; (4) the luciferase reporter assays suggested that Smad7 is a validated miR-21 target in CFs; and (5) in the presence of TGF-β [1], inhibiting or upregulating miR-21 could increase and decrease Smad7 expression, respectively, indicating that the TGF-β [1] -induced decrease in Smad7 expression might be mediated by miR-21. [score:26]
T, unpaired t test; n = 10 independent samples for each group) Over -expression of TGF-β [1] induces Smad7 down-regulation through miRNA-21Our results indicated that TGF-β [1] -induced collagen I/III expression might occur through the up-regulation of miR-21, meanwhile we found in our previous studies that the over -expression of TGF-β [1] induced the degradation of Smad7 which may decrease the inhibitory feedback regulation of TGF-β [1]/Smad signaling pathway, so we sought to determine the relationship between miR-21 and Smad7 in TGF-β [1] -induced collagen expression. [score:18]
More interestingly, the molecular mechanism underlying this phenomenon is as follows: the expression of TGF-β [1] leads to miR-21 up-regulation, and miR-21 over -expression directly down-regulates Smad7 expression, which leads to amplification of TGF-β [1] signaling and ultimately results in RAP -induced fibrosis. [score:14]
T, unpaired t test; n = 10 independent samples for each group) Our results indicated that TGF-β [1] -induced collagen I/III expression might occur through the up-regulation of miR-21, meanwhile we found in our previous studies that the over -expression of TGF-β [1] induced the degradation of Smad7 which may decrease the inhibitory feedback regulation of TGF-β [1]/Smad signaling pathway, so we sought to determine the relationship between miR-21 and Smad7 in TGF-β [1] -induced collagen expression. [score:13]
Thus, we speculate that miR-21 over -expression significantly enhances TGF-β [1] -induced collagen expression and that Smad7 can directly inhibit collagen expression in RAP -induced myocardial fibrosis. [score:10]
Interesting, inhibiting miR-21 expression weakened the TGF-β [1] -mediated down-regulation of Smad7 expression. [score:10]
At the end of the experiment, we found that miR-21 expression was significantly lower in the hearts of treated animals (Fig.   2a–c, p < 0.05), suggesting that miR-21 inhibitor lentiviral vectors can inhibit miR-21 expression in the heart. [score:9]
Taken together, our data show that miR-21 over -expression directly down-regulates Smad7 expression. [score:9]
The expression of the wild-type luciferase-Smad7-3′UTR reporter was remarkably lower than the mutant luciferase-Smad7-3′UTR reporter and control plasmid (Fig.   5a, b), suggesting that Smad7 is a validated miR-21 target in CFs and that miR-21 can inhibit Smad7 expression, leading to the further amplification of TGF-β [1] signaling. [score:9]
In vitro, we found that miR-21 over -expression increased collagen I/III expression and that miR-21 over -expression after treatment with TGF-β [1] further increased collagen I/III expression. [score:9]
Interestingly, we found that miR-21 inhibition significantly weakened TGF-β [1] -induced Smad7 mRNA down-regulation in the CFs that treated with TGF-β [1] plus the miR-21 inhibitor (Fig.   5d). [score:8]
These data show that the miR-21 inhibitor could inhibit myocardial fibrosis by up -regulating Smad7 expression in vivo. [score:8]
Interestingly, we found that miR-21 inhibition significantly weakened TGF-β [1] -induced collagen I/III mRNA expression in the CFs that were treated with TGF-β [1] plus the miR-21 inhibitor. [score:7]
Next, CFs were transfected with miR-control and miR-21 over -expression lentiviral vectors before being transfected with TGF-β [1] (10 ng/ml) for 48 h. TGF-β [1] plus miR-21 overexpression enhanced collagen I/III mRNA expression more significantly than TGF-β [1] treatment alone (Fig.   4h, i). [score:7]
The miR-21 inhibitor decreased miR-21 expression in the heart of experimental rabbits (rabbits were treated with the miR-21 inhibitor and RAP for 4 weeks). [score:7]
In summary, our data demonstrate that TGF-β [1] -induced miR-21 over -expression enhances TGF-β [1] -induced collagens expression by directly down -regulating Smad7. [score:7]
In this study, the cells were divided into the following groups: cells without transfection (blank control group, Group CR), cells transfected with the miR-control lentiviral vector (30 μM) (miR-control group, Group M), cells transfected with the pre-miR-21 (miR-21 over -expression) (30 μM) lentiviral vector (pre-miR-21 group, Group PM), cells treated with 10 ng/ml TGF-β [1] (TGF-β [1] group, Group T), cells treated with 10 ng/ml TGF-β [1] plus the pre-miR-21 vector (30 μM) (TGF-β [1] + pre-miR-21 group, Group TP), and cells treated with 10 ng/ml TGF-β [1] plus the miR-21 inhibitor (30 μM) (TGF-β [1] + miR-21 inhibitor group, Group TI). [score:7]
f Northern blot verifying the down-regulation of miR-21 in rat fibroblasts after transfection with the miR-21 inhibitor. [score:6]
Adam recently confirmed miR-21 levels were significantly higher in patients with atrial fibrillation, and the up-regulation of miR-21 target genes can increase fibrin deposition [19]. [score:6]
The expression of endogenous miR-21 in the heart and the up-regulation of miR-21 were verified with Northern blot analysis (Fig.   1b, c). [score:6]
Over -expression of TGF-β [1] induces Smad7 down-regulation through miRNA-21. [score:6]
In the present study, our aim was to determine if miR-21 up-regulation could enhance TGF-β [1] -induced myocardial fibrosis by inhibiting Smad7. [score:6]
Next, we tested the effect of miR-21 overexpression on TGF-β [1] -induced Smad7 down-regulation. [score:6]
Furthermore, miR-21 over -expression significantly enhanced TGF-β [1] -induced Smad7 down-regulation. [score:6]
Thus, our study further suggested that miR-21 may be involved in the regulation of RAP -induced myocardial fibrosis, and we speculate that miR-21 over -expression significantly enhances TGF-β [1] -induced collagen expression. [score:6]
MicroRNA-21 (miR-21) is consistently reported to be upregulated in both cancer and various forms of cardiovascular disease [13, 14]. [score:6]
In addition, blocking miR-21 expression reverses the TGF-β [1-]induced up-regulation of collagen I/III. [score:6]
In vivo, we found that RAP induced TGF-β [1] and miR-21 up-regulation with the increased expression of collagen. [score:6]
Male New Zealand rabbits (2.0–2.5 kg) were randomly divided into 4 groups (n = 10 for each group): normal control (CR), sham control (SH), rapid atrial pacing (RAP) and RAP + miR-21 inhibitor(the miR-21 inhibitor was administered to this group through a lentiviral vector, Genechem, Shanghai, China). [score:5]
Fig.  3Effect of the miR-21 inhibitor on RAP -induced Smad7 and collagen I/III expression in vivo. [score:5]
Furthermore, through the computational prediction of target genes, we identified Smad7 as a potential target for miR-21. [score:5]
Taken together, our results demonstrate that TGF-β [1] -induced collagen I/III expression might result from the expression of miR-21 in vitro. [score:5]
It reported that miR-21 is expressed much higher in cardiac fibroblasts and accompanied by the increased expression of collagen in pathological states of heart failure [42]. [score:5]
Next, we found that the incidence of atrial fibrillation after transfection with the miR-21 inhibitor lentiviral vector decreased from 89 % in the RAP group to 50 % in the lentiviral group (8 of 9 in the RAP group, 5 of 10 in the RAP+miR-21 inhibitor group). [score:5]
c Mean miR-21 expression levels in the CR group and the RAP+miR-21 inhibitor group. [score:5]
The inhibition of miR-21 by synthetic miRNA antagonists improved heart function in a cardiac disease mo del [16– 19]. [score:5]
More importantly, Smad7 expression increased after transfection with miR-21 inhibitor, whereas collagen I/III decreased (Fig.   3, p < 0.05). [score:5]
We found that miR-21 over -expression decreases Smad7 expression, which was similar to the change that occurred with TGF-β [1] treatment. [score:5]
miR-21 overexpression enhances the TGF-β [1] -induced epithelial-to-mesenchymal transition by targeting Smad7 and aggravates renal damage in diabetic nephropathy. [score:5]
These results strongly suggest that the miR-21 -mediated degradation of Smad7 might decrease the inhibitory feedback regulation of TGF-β1/Smad signaling and serves as a new insight into the development of atrial fibrosis due to atrial fibrillation. [score:5]
a qRT-PCR demonstrating that TGF-β1 (10 ng/ml) and TGF-β1 inhibitor(10 μg/ml) induces and decrease miR-21 expression at 48 h. b Representative Northern blot showing miR-21. [score:5]
miR-21 has therefore emerged as an interesting candidate for the development of therapeutic strategies against many forms of heart disease. [score:4]
Animal experiments found that miR-21 expression affected the TGF-β [1] -induced renal tubular epithelial-to-mesenchymal transition in diabetic nephropathy by regulating Smad7 [25]. [score:4]
In a rat mo del of myocardial infarction, the down-regulation of miR-21 can reduce the degree of atrial fibrosis and the incidence of AF [43]. [score:4]
It has been reported that TGF-β [1] can increase miR-21 expression in cardiac fibroblasts and may be involved in the regulation of myocardial fibrosis [22, 24]. [score:4]
d Northern blot verifying the upregulation of miR-21 in rats fibroblast after transfection with pre-miR-21. [score:4]
Fig.  5Effect of miR-21 on the TGF-β [1] -mediated down-regulation of Smad7. [score:4]
The same beneficial effects were observed in miR-21 knockout mice subjected to pressure-overload of the left ventricle, underlining the potential of miR-21 as a therapeutic target [20]. [score:4]
TGF-β1 induces myocardial fibrosis by upregulating miR-21. [score:4]
The results of this assay demonstrated that miR-21 over -expression significantly enhanced TGF-β [1] -induced Smad7 down-regulation compared with the TGF-β [1] group and the miR-control group (Fig.   5d). [score:4]
The GFP reporter gene was inserted at the 3′ end of the miR-21 inhibitor gene. [score:3]
Next, TGF-β [1] -treated CFs were transfected with the miR-control and miR-21 over -expression lentiviral vectors. [score:3]
Cardiac fibroblasts were treated with TGF-β [1] in the presence or absence of miR-21 for 48 h. d Quantitative analysis of Smad7 expression by qRT-PCR. [score:3]
Transfection with the miR-21 inhibitor caused a significant decrease in hydroxyproline content, collagen I and collagen III deposition, left atrial weight, and left atrial mass index and attenuated the progression of RAP -induced atrial fibrosis. [score:3]
Next, we investigated whether miR-21 over -expression promoted the TGF-β [1] -induced expression of collagen I/III, which were detected by qRT-PCR and. [score:3]
The miR-21 inhibitor, but not pre-miR-21, increased the accumulation of Smad7 (Fig.   5c). [score:3]
First, miR-21 expression in the presence of TGF-β [1] (10 ng/ml) was examined by qRT-PCR and Northern blot. [score:3]
Before treating the cells with TGF-β [1], CFs were transfected with miR-control and miR-21 over -expression lentiviral vectors. [score:3]
c Mean Smad7 protein levels in the CR, RAP and RAP + miR-21 inhibitor groups. [score:3]
CFs were co -transfected with the GV306 vector containing the Smad7 3′-UTR and the miR-21 overexpression plasmid using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:3]
However, whether miR-21 over -expression enhanced TGF-β [1] -induced myocardial fibrosis in AF remained elusive. [score:3]
g qRT-PCR demonstrating that miR-21 levels deceased in rat fibroblasts after transfection with the miR-21 inhibitor. [score:3]
MiR-control lentivirus vectors (109 TU/ml, 4 μl/day) and miR-21 inhibitor lentivirus vectors (109 TU/ml, 4 μl/day) were injected 2 times/per week for 4 weeks. [score:3]
h Mean collagen I and III protein levels in the CR, RAP and RAP + miR-21 inhibitor groups. [score:3]
Down -expression of miR-21 ameliorates myocardial fibrosis in vivo. [score:3]
Fig.  2The effect of a miR-21 inhibitor in RAP -induced myocardial fibrosis in vivo. [score:3]
These findings prompted us to focus on exploring the role of miR-21 in AF and the association with Smad7 expression. [score:3]
CR, unpaired t test; n ≥ 9 independent samples for each group) On the basis of the above findings, we decided to examine whether reduced expression of miR-21 ameliorates myocardial fibrosis in AF. [score:3]
Effect of TGF-β [1] on miR-21 expression in vitro. [score:3]
RAP caused significant collagen deposition in the left atria that was attenuated by the miR-21 inhibitor (* p < 0.05 vs. [score:3]
c Values of miR-21 expression are the mean ± SE. [score:3]
The transcript for the miR-21 inhibitor was PCR purified and inserted into the lentiviral vector under the control of the CMV promoter. [score:3]
c Mean miR-21 expression levels in the control group (CR), sham group (SH), and rapid atrial pacing group (RAP) groups. [score:3]
In recent years, additional roles of miR-21 in cardiovascular and pulmonary diseases have been described, including cardiac and pulmonary fibrosis as well as myocardial infarction [21– 23]. [score:3]
Fig.  4Effect of miR-21 on TGF-β [1] -induced collagen I/III expression. [score:3]
k Mean collagen I and III levels in the control (CR), miR-control (M), pre-miR-21 (PM), TGF-β [1] (T), TGF-β [1] + pre-miR-21 (TP) and TGF-β [1] + miR-21 inhibitor (TI) groups (* p < 0.05 vs. [score:3]
f Mean Smad7 protein levels in the control (CR), miR-control (M), pre-miR-21 (PM), TGF-β [1] (T), TGF-β [1] + pre-miR-21 (TP) and TGF-β [1] + miR-21 inhibitor (TI) groups (* p < 0.05 vs. [score:3]
a Alignment of hsa-miR-21 and mmu-miR-21 with human Smad7 3′-UTR and mouse Smad7 3′-UTR based on TargetScan and Pictar software (http://www. [score:3]
In contrast to the RAP group (89 % incidence of AF), treatment with the miR-21 inhibitor decreased the incidence of AF to 50 % (* p < 0.05). [score:3]
First, miR-21 inhibitor lentiviral vectors were injected into the jugular vein of rabbits 2 times per week for 4 weeks. [score:3]
Before treatment with TGF-β [1], CFs were transfected with the miR-control and miR-21 over -expression lentiviral vectors. [score:3]
We found that TGF-β [1] can enhance miR-21 expression (Fig.   4a–c, p < 0.05). [score:3]
e Masson trichrome staining of rabbit atrial samples from the CR, RAP, and RAP+miR-21 inhibitor groups. [score:3]
To examine whether Smad7 is a valid target of miR-21, a single copy of the putative miR-21-recognition element from the 3′-UTR of the Smad7 gene was cloned into the GV306 plasmid vector downstream of the dual luciferase reporter gene (Genechem, Shanghai, China). [score:3]
Increasing evidence indicates that targeting TGF-β [1]/Smad-specific miRNAs related to fibrosis may be a better approach for combating heart disease [38– 40], with miR-21 being the best characterized miRNA associated with TGF-β [1] -mediated fibrosis [41]. [score:3]
miR-21 over -expression increased collagen I/III mRNA and protein levels. [score:3]
Transfection with the miR-21 inhibitor, we found it reduce the incidence of AF and ameliorated RAP -induced atrial fibrosis. [score:3]
b Representative Northern blot depicts the expression of miR-21 mRNA. [score:3]
RAP caused a significant increase in miR-21 expression. [score:3]
de/) and previous experiments, Smad7 is a validated target of miR-21 [25, 33]. [score:3]
After treatment with the miR-21 inhibitor, the level of collagen I and III decreased significantly compared with the CR and RAP group (* p < 0.05 vs. [score:2]
TaqMan MicroRNA Reverse transcription reactions and TaqMan MicroRNA quantitative polymerase chain reactions (qPCR) were performed to detect miR-21 and an endogenous control, RNA U6 small nuclear (RNU6B) expression using the MicroRNA TaqMan Reverse Transcription Kit and the TaqMan MicroRNA Assays (Applied BioSystems, Carlsbad, CA, USA) according to manufacturer’s instructions. [score:2]
RAP, n ≥ 9 independent protein samples for each group) Effect of TGF-β [1] on miR-21 expression in vitroEarlier reports have shown that miR-21 is extensively involved in myocardial fibrosis, and miR-21 is considered to be associated with TGF-β [1] -induced myocardial fibrosis [22, 32]. [score:2]
However, the regulation mechanism linking miR-21 and Smad7 in RAP -induced myocardial fibrosis was unclear. [score:2]
In this assay, we found that miR-21 over -expression decreased Smad7 mRNA levels. [score:2]
Moreover, bioinformatics and the luciferase reporter assays showed that Smad7 is a validated target of miR-21. [score:2]
Fibroblasts in the cardiovascular system are enriched in miR-21, which contributes to the development of fibrosis and heart failure [15]. [score:2]
Therefore, to further confirm that Smad7 is a validated miR-21 target in CFs, we performed luciferase reporter assays. [score:2]
MiRNA-21 expression profile in atrial tachypacing -induced rabbit mo del of AF. [score:2]
After treatment with the miR-21 inhibitor, the level of Smad7 increased significantly compared with the CR group and the RAP group. [score:2]
For example, miR-21 and Smad7 are critical regulators of TGF-β [1] signaling during the induction of carcinoma -associated fibroblast formation [33, 45, 46]. [score:2]
When the cells reached 70–80 % confluency, they were transfected with pre-miR-21 or control pre-miR (Ambion, Austin, TX, USA) using the TransIT T KO transfection reagent (Mirus Bio, Madison, WI, USA). [score:1]
These data suggest that RAP -induced atrial fibrosis may be ameliorated by blocking miR-21 in the heart. [score:1]
T, unpaired t test; n = 10 independent samples for each group) In this study, we examined the relationship between miR-21 and TGF-β [1]/Smad7 signaling in AF -induced atrial fibrosis. [score:1]
To investigate the role of miR-21 in TGF-β [1] -induced collagen expression, we performed miR-21 transfection experiments in CFs. [score:1]
The miRNA expression levels were calculated as the cycle threshold (- delta CT) of miR-21 and normalized with an endogenous control. [score:1]
b Representative Northern blot showing miR-21. [score:1]
However, mechanistic data on the relationship between miR-21 and the TGF-β [1]/Smad7 signaling pathway in AF are still missing. [score:1]
These findings prompted us to focus on exploring the role of miR-21 in AF and the associated atrial remo deling. [score:1]
In this study, we explored the relationship between miR-21 and TGF-β [1] in cardiac fibroblasts. [score:1]
Next, we investigated the effect of miR-21 over -expression on Smad7 mRNA and protein, which were detected by RT-PCR and western blot. [score:1]
e qRT-PCR demonstrating that miR-21 levels increased in rat fibroblasts after transfection with pre-miR-21. [score:1]
Several nucleotides in the 50-region of miR-21 (human and mouse) contain a perfect match with the 3′-UTR sequences of the human and mouse Smad7 genes. [score:1]
As shown in Fig.   1a, qRT-PCR analysis confirmed that miR-21 was elevated by 4.5 times in RAP samples over control samples (Fig.   1a). [score:1]
a miR-21 mRNA levels were examined by qRT-PCR. [score:1]
T, unpaired t test; n = 10 independent samples for each group) As shown in Fig.   1a, qRT-PCR analysis confirmed that miR-21 was elevated by 4.5 times in RAP samples over control samples (Fig.   1a). [score:1]
However, there are few reports about the role of miR-21 in AF. [score:1]
[1 to 20 of 117 sentences]
2
[+] score: 20
miR-21 regulates the tumor suppressor genes PTEN and tropomyosin [23, 24] and promotes cellular transformation by mediating the downregulation of the programmed cell death 4 gene [25, 26]. [score:7]
Zhu S. Si M. L. Wu H. Mo Y. Y. MicroRNA-21 targets the tumor suppressor gene tropomyosin 1 (TPM1) J. Biol. [score:4]
Frankel L. B. Christoffersen N. R. Jacobsen A. Lindow M. Krogh A. Lund A. H. Programmed cell death 4 (PDCD4) is an important functional target of the microRNA miR-21 in breast cancer cells J. Biol. [score:3]
In this study, the highest expression level was obtained for miR-21 (Figure 2). [score:3]
Knockdown of miR-21 was found to disrupt cancer growth in the brain [27]. [score:2]
Corsten M. F. Miranda R. Kasmieh R. Krichevsky A. M. Weissleder R. Shah K. MicroRNA-21 knockdown disrupts glioma growth in vivo and displays synergistic cytotoxicity with neural precursor cell delivered S-trail in human gliomas Cancer Res. [score:1]
[1 to 20 of 6 sentences]
3
[+] score: 3
Other miRNAs from this paper: hsa-mir-21
MicroRNA-21 regulates vascular smooth muscle cell function via targeting tropomyosin 1 in arteriosclerosis obliterans of lower extremities. [score:3]
[1 to 20 of 1 sentences]
4
[+] score: 1
Other miRNAs from this paper: hsa-mir-21, mmu-mir-21a, mmu-mir-21b, mmu-mir-21c
Li X-GEnabling [[18]F]-bicyclo[6.1.0]nonyne for oligonucleotide conjugation for positron emission tomography applications: [[18]F]-anti-microRNA-21 as an exampleChem. [score:1]
[1 to 20 of 1 sentences]
5
[+] score: 1
For example, serum miR-21, miR-122 and miR-223 are elevated in patients with hepatocellular carcinoma and chronic hepatitis and thus, have the potential to serve as novel biomarkers for liver injury [18]. [score:1]
[1 to 20 of 1 sentences]