miR-133a mediates TGF-β-dependent derepression of collagen synthesis in hepatic stellate cells during liver fibrosis

MicroRNAs in the Communication between Cancer Associated Fibroblasts (CAF) and Cancer Cells

“…[32] In HSCs another cluster member, miR-133a, is downregulated by TGF-β with subsequent stimulated expression of collagens. [34] The expression levels of fibrosis related genes (TIMP-1, MMP13, α1-procollagen) in HSCs were increased by overexpression of other members of the miR-214 cluster (miR-199a, 199a*). [36] Moreover, miR-200b appears to enhance expression of matrix metalloproteinase-2 (MMP-2), which may increase the migration of HSCs during liver fibrosis progression.…”

“…Upregulation was also identified for miR-199a-5p/199a-3p and miR-221/222 in hepatitis C induced liver fibrosis in a fibrosis progression-dependent manner. [31] Members of the miR-17-92 cluster (19a, 19b, 92a) [32], miR-29, miR-133, miR-193 and miR-30c [33,34] were observed to be specifically downregulated in human liver fibrosis and HSC, while they showed a reciprocal expression pattern after recovery from liver fibrosis. Reduced expression of miR-144 was correlated with elevated HSC-specific expression of transforming growth factor-β1 (TGF-β1) and expression of α-SMA in fibrotic liver tissues.…”

“…In addition, miR-133a serum levels were increased in patients with chronic liver disease and indicative for the presence and progression of liver cirrhosis. [34] Overall, the body of evidence for clinically useful miR expression patterns in CAFs as prognostic or predictive markers is not yet sufficient for any recommendation into clinical applications. In addition, a systematic approach for identification of the relevant miR expression profiles has not been done thoroughly and, therefore an overall picture for patients is not available yet.…”

Long non-coding RNA APTR promotes the activation of hepatic stellate cells and the progression of liver fibrosis

“…TGF-β 1 can mediate the expression of many non-coding genes, such as the miR-29 family and miR-133a [18,19]. Here we examined whether TGF-β 1 could mediate the expression of APTR in HSCs.…”

MicroRNAs in Human Microbial Infections and Disease Outcomes

“…Regarding antifibrotic miRNAs, overexpression of miR-122 in HSC leads to decreased extracellular matrix production by suppressing P4HA1 expression -a key enzyme in collagen maturation [99]. Overexpression of miR-27a and miR-27b causes the reversion of activated HSCs to a quiescent phenotype by regulating the retinoid X receptor [100], and both miR-29 [101] and miR-133 [102] cause a reduction in collagen expression. Furthermore, overexpression of miR-150 and miR-194 targets c-MYB and RAC1 genes [103], miR-146a negatively regulates TGF-β signaling by decreasing the expression of SMAD4 [104], and miR-19b negatively regulates TGF-β signaling by decreasing TGF-β receptor II, SMAD3, and procollagen expression [105], in all cases leading to inhibition of HSC activation.…”