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18 publications mentioning ssc-mir-199a-2

Open access articles that are associated with the species Sus scrofa and mention the gene name mir-199a-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 183
As shown in Figure 5e, the miR-199a-5p expression increased steadily along with the cell number increased, whereas the expression of the miR-199a-5p target, Cav-1, declined as the cell density increased from 50% to 90% (logarithmic growth phase). [score:7]
Based on the data of the miR-199a-5p expression pattern and target gene validation, we proposed that miR-199a-5p may be a negative regulator of porcine preadipocyte differentiation. [score:6]
As shown in Figure 4b and c, PPARγ, aP2, and FAS expressions were also tested at the protein level, and Western Blotting of these proteins demonstrated a significant decrease upon miR-199a-5p overexpression. [score:5]
Using bioinformatic analyses, we profiled the anti- and pro-adipogenic factors among miR-199a-5p predicted targets, and further experimentation validated that Cav-1 is a bona fide target of miR-199a-5p in porcine adipocytes. [score:5]
Overexpression of miR-199a-5p Attenuated the Lipid Accumulation and Adipogenic Marker Genes Expression in Porcine Adipocytes. [score:5]
However, due to the fact that miRNA-mRNA targeting and the interplay relationship differs among tissue and cell types and physiological/pathological conditions [16], we proposed that in adipose tissue, miR-199a-5p may have a target gene subset different from other tissue types. [score:5]
Additionally, this expression pattern of Cav-1 is generally inverse to miR-199a-5p, the expression of which was sharply decreased at the early stage of differentiation (day 0 to day 4). [score:5]
MiR-199a-5p Is Highly Expressed in SAT and Downregulated in Early Porcine Preadipocyte Differentiation. [score:5]
We also found that overexpression of miR-199a-5p could attenuate the lipid accumulation during porcine preadipocyte differentiation, which is consistent with the anti-adipogenic effect of Cav-1 inhibition [12]. [score:5]
The expression pattern of miR-199a-5p suggests that it may play a role in adipogenesis, and in fact, studies using human bone marrow mesenchymal stem cells (hMSCs) found that miR-199a-5p overexpression can lead to a ~70% decrease in the mRNA level of FABP4 (aP2), an adipogenic marker [11]. [score:5]
In the present study, we established the precise expression pattern of miR-199a-5p during in vitro porcine adipogenesis, which is similar to the expression pattern of miR-199a-5p in the 3T3-L1 adipogenic mo del [9]. [score:5]
org/) and RNAhybrid software to predict the target genes of miR-199a-5p and its interaction schematic with target mRNAs. [score:5]
Rane S. He M. Sayed D. Vashistha H. Malhotra A. Sadoshima J. Vatner D. E. Vatner S. F. Ab dellatif M. Downregulation of miR-199a derepresses hypoxia-inducible factor-1alpha and Sirtuin 1 and recapitulates hypoxia preconditioning in cardiac myocytesCirc. [score:4]
In 2012, Zeng et al. proved that Cav-1 knockdown significantly impaired porcine adipogenesis in vitro [12], which is consistent with our data obtained by miR-199a-5p overexpression. [score:4]
Laine S. K. Alm J. J. Virtanen S. P. Aro H. T. Laitala-Leinonen T. K. MicroRNAs miR-96, miR-124 and miR-199a regulate gene expression in human bone marrow-derived mesenchymal stem cellsJ. [score:4]
MiR-199a-5p is highly expressed in 3T3-L1 preadipocytes, while its expression declines dramatically once adipogenic induction is present and only rebounds at the late stage of differentiation [9]. [score:4]
In cardiomyocytes, miR-199a-5p is confirmed to directly target hypoxia-inducible factor 1α (HIF-1α) and Sirt1 [13, 14], which play important roles upon hypoxia or hypoxia preconditioning of cardiac muscle. [score:4]
In spite of the distinctive expression pattern of miR-199a-5p during preadipocyte differentiation, the possible function of this miRNA in fat development, including porcine adipogenesis, has not been given much attention. [score:4]
Taken together, our study suggests that miR-199a-5p may be a regulator of porcine adipogenesis, functioning at least partially by targeting Cav-1. 2.1. [score:4]
We proposed that such a high expression level of miR-199a-5p in SAT may have a functional consequence. [score:3]
To elucidate the possible function of miR-199a-5p in porcine preadipocyte differentiation, we performed TargetScan 6.2 (http://www. [score:3]
Also, the binding site between miR-199a-5p and Cav-1 mRNA 3′ untranslated region (3′UTR) are conservative among pigs, human, and mice. [score:3]
Cav-1, which is preciously established to be indispensable for adipogenesis in several species, including pigs, was experimentally validated herein to be the target of miR-199a-5p in porcine adipocytes. [score:3]
However, to our understanding, there has not been any research dealing with the specific actions and possible targets of miR-199a-5p in fat cells. [score:3]
Based on an in vitro porcine adipogenesis mo del, we observed that miR-199a-5p expression declines by nearly 70% from day 0 to 4 of adipogenic differentiation (Figure 1c). [score:3]
To elucidate whether miR-199a-5p may also function in proliferating preadipocytes, we used flow cytometry to detect the alterations in the cell cycle caused by miR-199a-5p overexpression. [score:3]
In summary, our data indicated miR-199a-5p to be a facilitator of porcine preadipocyte proliferation whilst being a suppressor of adipogenic differentiation. [score:3]
The temporal expression pattern of miR-199a-5p during porcine preadipocyte differentiation is similar to the previous data obtained in the 3T3-L1 mo del. [score:3]
Apart from Cav-1, many other target genes and sophisticated functions of miR-199a-5p have been intensively studied since miR-199a-5p and-3p were first cloned [8]. [score:3]
By the overexpression of miR-199a-5p, we demonstrated for the first time that miR-199a-5p can affect both porcine preadipocyte proliferation and differentiation. [score:3]
The results showed that agomir transfection led to a ~2500-fold overexpression of miR-199a-5p at 48 h post-transfection, and the enhanced miR-199a-5p level could be maintained for at least 8 days after adipogenic induction (240 h post-transfection) (Figure 3a). [score:3]
The data showed that when miR-199a-5p was overexpressed, the S-phase porcine preadipocytes increased, while the G1-phase cell proportion declined; the change was significant among three independent experiments (Figure 5b). [score:3]
Therefore, Cav-1 showed an opposite expression pattern to miR-199a-5p during the cell number increased. [score:3]
Both the mRNA and protein levels of Cav-1 were significantly decreased by miR-199a-5p overexpression in porcine adipocytes (Figure 2c–e). [score:3]
Overexpression of miR-199a-5p Promoted the Proliferation of Porcine Preadipocytes. [score:3]
However, unlike its role in porcine preadipocyte differentiation, we have not determined whether Cav-1 is also the main target gene of miR-199a-5p during porcine preadipocytes proliferate, as no reports thus far have related Cav-1 to preadipocyte proliferation. [score:3]
Furthermore, we identified Cav-1 as a bona fide target gene of miR-199a-5p in porcine adipocytes. [score:3]
To test this hypothesis, we isolated porcine primary preadipocytes from Guanzhong black piglets and performed miR-199a-5p overexpression using synthetic miRNA agomir. [score:3]
We then performed the Oil Red O staining and extraction assay and observed that miR-199a-5p overexpression attenuated the lipid accumulation in porcine adipocytes (Figure 3b,c). [score:2]
Real-time qPCR measurement showed that on day 8 of differentiation, the mRNA level of adipogenic marker genes, PPARγ, aP2, Perilipin A and LPL were downregulated to different extents by the elevated miR-199a-5p level (Figure 4a). [score:2]
Based on our current observations and preliminary studies on Cav-1’s role in adipogenesis and cell proliferation, we highly proposed that miR-199a-5p may function as a potential controller of cell proliferation and differentiation during porcine adipogenesis, and such a function may at least partially depend on its regulation on Cav-1. These studies were supported by the grants from the National Natural Science Foundation of China: Study of the effects and mechanism of miRNA on commitment and adipogenesis of porcine adipose tissue derived stem cells (ADSCs) (31072014) and the Major Projects for Genetically Modified Organisms Breeding (2014ZX08009-047B). [score:2]
Song X. W. Li Q. Lin L. Wang X. C. Li D. F. Wang G. K. Ren A. J. Wang Y. R. Qin Y. W. Yuan W. J. MicroRNAs are dynamically regulated in hypertrophic hearts, and miR-199a is essential for the maintenance of cell size in cardiomyocytesJ. [score:2]
Hoechst staining of the nuclei demonstrated that miR-199a-5p overexpression led to increased cell number 24 and 48 h post-transfection compared to agomir NC treatment (Figure 5c,d). [score:2]
In human skeletal muscle, miR-199a-5p is capable of regulating the canonical Wnt pathway and affects myoblast proliferation and differentiation [15]. [score:2]
MiR-199a-5p Is Capable of Targeting Cav-1 in Porcine Fat Cells. [score:2]
However, our results showed that miR-199a-5p is even more abundant in SAT than in heart and skeletal muscle. [score:1]
These results suggested that miR-199a-5p may be a facilitator of porcine preadipocyte proliferation, and its function in proliferative porcine preadipocytes may also be mediated by Cav-1. The mature miR-199a-5p sequence possesses high evolutionary conservation among species (Figure 1a). [score:1]
The miR-199a-5p agomir sequence is listed as follows: sense: 5′-CCCAGUGUUAGACUACCUGUUC-3′; antisense: 5′-ACAGGUAGUCUGAACACUGGGUU-3′, and the agomir NC sequences are: sense: 5′-UUCUCCGAACGUGUCACGUTT-3′; antisense: 5′-ACGUGACACGUUCGGAGAATT-3′. [score:1]
The overexpression of miR-199a-5p was measured 48 h post-transfection and on day 8 of adipogenic differentiation, respectively. [score:1]
Our previous work demonstrated that the subcutaneous adipose tissue (SAT) from piglets has a higher level of miR-199-5p relative to SAT from adult pigs [10]. [score:1]
Previous studies of miR-199a-5p were focused on its function in cardiac and skeletal muscle and several types of oncocytes. [score:1]
MiR-199a-5p Agomir Transfection. [score:1]
In this study, we found that the miR-199a-5p level during porcine preadipocyte differentiation shows a similar fluctuation with that in 3T3-L1 adipogenesis. [score:1]
MiR-199a-5p agomir and negative control (NC) are double-strand, designed and synthesized by Genepharm (Shanghai, China). [score:1]
Furthermore, we used flow cytometry and Hoechst staining to show that the elevated miR-199a-5p level could also lead to accelerated proliferation of porcine preadipocytes. [score:1]
The mature miR-199a-5p sequence possesses high evolutionary conservation among species (Figure 1a). [score:1]
We also tested the miR-199a-5p level at different cell densities after the seeding of preadipocytes. [score:1]
24 h later, after seeding, miR-199a-5p agomir and agomir NC were transfected into porcine preadipocytes using Lipofectamine 2000. [score:1]
To determine the tissue distribution profile of miR-199a-5p in pigs, the total RNAs were extracted from several types of tissue and organs of adult Guanzhong black pigs. [score:1]
The luciferase vector was transfected into 293T cells with miR-199a-5p agomir and agomir NC using Lipofectamine 2000 (Invitrogen). [score:1]
These results suggested that miR-199a-5p may be a facilitator of porcine preadipocyte proliferation, and its function in proliferative porcine preadipocytes may also be mediated by Cav-1. Pig has been wi dely accepted to be an apropos research mo del for human obesity as well as the primary meat stock in many countries. [score:1]
Such research will better delineate the mechanisms by which miR-199a-5p affects adipogenesis. [score:1]
Real-time qPCR data showed that SAT has the highest expression level of miR-199a-5p among the seven tissue types or organs measured (Figure 1b). [score:1]
In addition, we observed that miR-199a-5p can promote porcine preadipocyte proliferation; this is the first time evidence about miR-199a-5p’s effect on preadipocyte proliferation. [score:1]
MiR-199a-5p agomir and agomir NC were transfected into cells using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:1]
These results suggested that miR-199a-5p may be a facilitator of porcine preadipocyte proliferation, and its function in proliferative porcine preadipocytes may also be mediated by Cav-1. 2.2. [score:1]
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[+] score: 24
As examples, the liver-specific miR-122 promotes the replication of hepatitis C virus (HCV) [17], [18], while miR-196, miR-199, miR-296, miR-351, miR-431 and miR-448 inhibit HCV genome propagation [19], [20]; miR-32 effectively restricts the accumulation of primate foamy virus type 1 (PFV-1) in human cells [21]; miR-323, miR-491 and miR-654 inhibit the replication of the H1N1 influenza A virus by binding to the viral PB1 gene [22]; miR-28, miR-125b, miR-150, miR-223 and miR-382 target the 3′ end of human immunodeficiency virus (HIV) mRNA, thereby restricting HIV production [23]; miR-199a-3p and miR-210 limit the hepatitis B virus (HBV) surface antigen and polymerase production by degrading and/or inhibiting translation of viral mRNAs encoding these proteins [24]; overexpression of miR-24 and miR-93 suppresses vesicular stomatitis virus (VSV) replication through targeting the viral genes encoding RNA -dependent RNA polymerase (L protein) and phosphoprotein (P protein), respectively [25]; in macrophages, upregulation of miR-155 suppresses VSV replication, while inhibition of miR-155 had the opposite effect. [score:24]
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[+] score: 23
Of the other six differentially expressed miRNAs in the sequencing experiment, mir-199a-5p, which was significantly down regulated in obese subjects in the sequencing data, was also down regulated when assessed by qPCR, but did not reach significance. [score:5]
MicroRNAs miR-96, miR-124, and miR-199a regulate gene expression in human bone marrow-derived mesenchymal stem cells. [score:4]
An exception from this general trend was mir-199-5p which was not significantly differentially expressed in the qPCR study. [score:3]
For the males we found 7 differentially expressed miRNAs, two of which (mir-9-1-3p and mir-199a-5p) overlap with the analysis of the combined dataset. [score:3]
Differential expression in the sequencing data from the lean and obese pigs was calculated using the DESeq2 package in R and revealed six significantly differentially expressed miRNAs between the two groups: mir-9-5p, mir-124a-3p, mir-9-3p, mir-199a-5p, mir-489-3p and mir-34c-3p. [score:3]
Mir-199a-5p has been identified as differentially expressed in subcutaneous adipose tissue from humans, where it was up regulated in obesity [64]. [score:3]
The other mature arm of mir-199a, mir-199a-3p, has been identified as down regulated upon weight loss in morbidly obese human patients [65]. [score:2]
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[+] score: 17
Moreover, 13 miRNAs were differentially expressed: 8 were upregulated (ssc-miR-132, ssc-miR-146b, ssc-miR-215, ssc-miR-371, ssc-miR-27a, ssc-miR-331-3p, ssc-miR-432-5p and ssc-miR-199a/b-3p), while 5 were down-regulated after PRV infection (ssc-mir-10a-5p, ssc-mir-148-3p, ssc-mir-219a, ssc-mir-374b-3p and ssc-miR-532-5p) (Fig 7). [score:9]
miR-199a-3p was recently reported to suppress HBV replication by targeting HBs genes [44]. [score:5]
2009; 183(3): 2150– 8. 44 Zhang GL, Li YX, Zheng SQ, Liu M, Li X, Tang H. Suppression of hepatitis B virus replication by microRNA-199a-3p and microRNA-210. [score:3]
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[+] score: 16
Other miRNAs from this paper: ssc-mir-30d, ssc-mir-27b, ssc-mir-199a-1
Expression of ssc-miR-30d_R-1, ssc-miR-27b, ssc-miR-145_R-1, ssc-miR-23a_R + 1, and ssc-miR-199a-5p mimics and inhibitors in PAM cells (A) and MARC-145 cells (B). [score:5]
We compared the basal expression levels of ssc-miR-30d_R-1, ssc-miR-27b, ssc-miR-145_R-1, ssc-miR-23a_R + 1, and ssc-miR-199a-5p in PAMs by qPCR and found that ssc-miR-30d_R-1 was among the most highly expressed miRNAs examined (data not shown). [score:4]
A panel of 5 miRNA mimics or inhibitors of various miRNAs, including ssc-miR-30d_R-1, ssc-miR-27b, ssc-miR-145_R-1, ssc-miR-23a_R + 1, and ssc-miR-199a-5p, were synthetized to ascertain their impact on PRRSV replication. [score:3]
Cells were infected with PRRSV strain LS-4 (MOI of 1.0), and real-time qRT-PCR analysis of ssc-miR-30d_R-1, ssc-miR-27b, ssc-miR-145_R-1, ssc-miR-23a_R + 1, and ssc-miR-199a-5p expression was carried out in mock-, UV-PRRSV- and PRRSV-infected primary cultured PAMs (A,C) and MAC-145 cells (B,D). [score:3]
However, the changes in other miRNAs—ssc-miR-27b, ssc-miR-145_R-1, ssc-miR-23a_R + 1 and ssc-miR-199a-5p—in PRRSV infection were found to be relatively small in infected PAM (Fig. 1A) and MARC-145 cells (Fig. 1B). [score:1]
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[+] score: 12
Several miRNAs were upregulated during OURT infection, including miR-328, miR-181, miR-1296 and miR-199 (Supplementary Table  S6). [score:4]
Interestingly, another liver -associated miRNA gene, miR-199 was upregulated at 28 days after infection with OURT. [score:4]
RNA-Seq revealed only a limited number of miRNA genes upregulated during ASFV infection, including miR-122, miR-138, miR-181A, miR-199A-2, and miR-1296 (Tables  2 and 3, Supplementary Table  S6). [score:4]
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[+] score: 9
Other miRNAs from this paper: ssc-mir-122, ssc-mir-125b-2, ssc-mir-181b-2, ssc-mir-20a, ssc-mir-23a, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-107, ssc-mir-21, ssc-mir-29c, ssc-mir-30c-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-20a, bta-mir-21, bta-mir-26b, bta-mir-30d, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-199a-1, bta-mir-30b, bta-mir-107, bta-mir-10a, bta-mir-127, bta-mir-142, bta-mir-181b-2, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-132, bta-mir-138-2, bta-mir-17, bta-mir-181c, bta-mir-192, bta-mir-199b, bta-mir-200a, bta-mir-200c, bta-mir-214, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-455, bta-let-7g, bta-mir-10b, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-mir-30c, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-99b, ssc-mir-99b, ssc-mir-17, ssc-mir-30b, ssc-mir-199b, bta-mir-1-2, bta-mir-1-1, bta-mir-129-1, bta-mir-129-2, bta-mir-133a-2, bta-mir-133a-1, bta-mir-133b, bta-mir-135b, bta-mir-138-1, bta-mir-143, bta-mir-144, bta-mir-146b, bta-mir-146a, bta-mir-181d, bta-mir-190a, bta-mir-199a-2, bta-mir-202, bta-mir-206, bta-mir-211, bta-mir-212, bta-mir-223, bta-mir-26a-1, bta-mir-29d, bta-mir-30f, bta-mir-338, bta-mir-33a, bta-mir-33b, bta-mir-375, bta-mir-429, bta-mir-451, bta-mir-92a-1, bta-mir-92b, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-133a-1, ssc-mir-1, ssc-mir-146b, ssc-mir-181a-1, ssc-mir-30a, bta-mir-199c, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-133b, ssc-mir-29a, ssc-mir-30d, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-10b, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-99a, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-192, ssc-mir-142, ssc-mir-127, ssc-mir-202, ssc-mir-129a, ssc-mir-455, ssc-mir-125b-1, ssc-mir-338, ssc-mir-133a-2, ssc-mir-146a, bta-mir-26c, ssc-mir-30c-1, ssc-mir-126, ssc-mir-199a-1, ssc-mir-451, ssc-let-7a-2, ssc-mir-129b, ssc-mir-429, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-132, ssc-mir-138, ssc-mir-144, ssc-mir-190a, ssc-mir-212, bta-mir-133c, ssc-mir-26b, ssc-mir-200b, ssc-mir-223, ssc-mir-375, ssc-mir-33b
Paula et al. (2017) showed that a short period of food restriction significantly increased the expression of miR-1, miR-206, miR-199, and miR-23a in fast muscle and significantly decreased the expression of miR-1 and miR-206 in slow muscle, while their targets (IGF-1 for miR-1, miR-206, and miR-199; mTOR for miR-199; and MFbx and PGC1a for miR-23a) exhibited negatively correlated expression profiles. [score:9]
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[+] score: 9
In contrast, miR-199a is a potential regulator of myogenesis through suppression of WNT-signaling factors and regulation of muscle growth and homeostasis (Alexander et al., 2013); its expression was higher in the E90, 0-d, and 30-d stages than in the 180-d and 7-y stages, which indicates that miR-199a is an important myogenic regulatory factor in early fetal and newborn muscle development. [score:9]
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[+] score: 8
Ssc-miR-21, ssc-miR-30d, ssc-miR-181, ssc-miR-199*, and ssc-miR-378 were all expressed at higher levels at the prenatal compared with the neonatal stage, and their distinct expression patterns during muscle development clearly reflected the relationship between miRNA and myogenesis. [score:5]
Nine differentially expressed miRNAs (ssc-miR-7a, ssc-miR-10b, ssc-miR-21, ssc-miR-30d, ssc-miR-127, ssc-miR-148a, ssc-miR-181, ssc-miR-199*, and ssc-miR-378) were chosen for the validation of the Solexa sequencing data via RT-qPCR. [score:3]
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[+] score: 8
For example, hsa-miR-133a, hsa-miR-200b, hsa-miR-206, and hsa-miR-218 were considered as tooth tissue-specific miRNAs [4]; eight differentially expressed miRNAs were expressed during morphogenesis and seven were expressed in the incisor cervical loop containing the stem cell niche [1]; the three most highly expressed microRNAs in dental epithelium were identified as mmu-miR-24, mmu-miR-200c, and mmu-miR-205, while mmu-miR-199a-3p and mmu-miR-705 were found in dental mesenchyme [2]; and miR-200 was suggested to play an important role in the formation of incisor cervical loop during stem cell–fueled incisor growth [5]. [score:8]
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[+] score: 8
In total, 92, 107, 95, 77 and 111 miRNAs were identified as being differentially expressed in PCMV-infected lung, liver, spleen, kidney and thymus samples, compared with their levels in the uninfected controls (p < 0.0001) ssc-miR-24-3p (172% increase), ssc-miR-199a-5p (1000% increase), ssc-miR-214 (3012% increase), ssc-miR-425-5p (1750% increase) and ssc-miR-199a-5p (2270% increase) were the most upregulated in PCMV-infected lung, liver, spleen, kidney and thymus samples, respectively, compared with their levels in the uninfected samples. [score:4]
In total, 92, 107, 95, 77 and 111 miRNAs were identified as being differentially expressed in PCMV-infected lung, liver, spleen, kidney and thymus samples, compared with their levels in the uninfected controls (p < 0.0001) ssc-miR-24-3p (172% increase), ssc-miR-199a-5p (1000% increase), ssc-miR-214 (3012% increase), ssc-miR-425-5p (1750% increase) and ssc-miR-199a-5p (2270% increase) were the most upregulated in PCMV-infected lung, liver, spleen, kidney and thymus samples, respectively, compared with their levels in the uninfected samples. [score:4]
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[+] score: 6
Additionally, looking at normalised counts for each breed (Table S6), there were some miRNAs with low frequency which their expression was higher in some breed, such as Hsa-miR-193b-5p, Hsa-miR-140-5p, Ssc-miR-19b, Ssc-miR-423-5p and Ssc-miR-24 in Iberian breed, Ssc-miR-151-5p, Hsa-miR-4454, Ssc-miR-199a-3p and Ssc-miR-374b-5p in Landrace breed, Ssc-miR-486 in Piétrain breed and Ssc-let-7f and Hsa-let-7i-5p in Meishan breed. [score:3]
There are also few cases where the most expressed isomiR is different in almost each breed, such as in Ssc-miR-199a* and Ssc-miR-423-5p. [score:3]
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[+] score: 5
Similarly, miR-199a, miR-195, miR-10 and miR-23 expression were correlated with TG and haematological traits. [score:3]
For example, serum TG was correlated with miR-744, miR-199, miR-10, miR-23, miR-195 and miR-155, which were also correlated with erythrocyte-related traits (RBC, MCHC, HGB and MCV). [score:1]
Some of these miRNA are known biomarkers for hepatocellular carcinoma, including miR-199a [29] and miR-195 [30]. [score:1]
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[+] score: 4
For example, miR-199a was reported to regulate cell proliferation by targeting Dyrk1a through the Calcineurin/NFAT pathway [28]. [score:4]
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[+] score: 4
Moreover, several hypoxia-regulated miRNAs play roles in cell survival in hypoxic environments and have been implicated in the regulation of both upstream and downstream HIF signaling pathways, e. g., miR-20b and miR-17-92 clusters, while miR-199a regulates HIF-1α under hypoxic conditions [8– 10], and miR-107, miR-210, miR-373, miR-23, miR-24, and miR-26 are induced by HIFs [7, 11, 12]. [score:4]
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[+] score: 4
Seven key miRNAs including let-7f, miR-125b, miR-133a, miR-199a, miR-200b, miR-200c and miR-455 are highly expressed in the mesenchyme or epithelium of different tooth development stages, but their functions have not been elucidated [6], [8]. [score:4]
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[+] score: 2
MiR-1285 and miR-199a-5p were also up regulated with fold changes of > 1.5 and p values < 0.05. [score:2]
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[+] score: 1
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-17, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-148a, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-206, hsa-mir-1-1, hsa-mir-128-2, hsa-mir-29c, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-133b, hsa-mir-424, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-128-1, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-503, hsa-mir-411, hsa-mir-378d-2, hsa-mir-208b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-17, ssc-mir-221, ssc-mir-133a-1, ssc-mir-1, ssc-mir-503, ssc-mir-181a-1, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-29a, ssc-mir-128-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-486-1, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-23b, ssc-mir-148b, ssc-mir-208b, ssc-mir-424, ssc-mir-127, ssc-mir-125b-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-411, ssc-mir-133a-2, ssc-mir-126, ssc-mir-199a-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-378j, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, hsa-mir-486-2, ssc-mir-378b
In addition to the best-studied myomiRs (miR-1, -206 and miR-133 families), 11 other DE muscle-related miRNAs (miR-378 [24], miR-148a [27], miR-26a [28, 29], miR-27a/b [30, 31], miR-23a [32, 33], miR-125b [34], miR-24 [35], miR-128 [36], miR-199a [37] and miR-424 [38]) with high abundance (average RPM >1,000) and another 14 (miR-181a/b/c/d-5p [26], miR-499-5p [11], miR-503 [38], miR-486 [39], miR-214 [40], miR-29a/b/c [41– 43], miR-221/222 [44] and miR-208 [11] with low abundance (average RPM <1,000) were detected in myogenesis of pig. [score:1]
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