| First Author | Li SC | Year | 2016 |
| Journal | Int J Mol Sci | Volume | 17 |
| Issue | 3 | Pages | 324 |
| PubMed ID | 26938532 | Mgi Jnum | J:281775 |
| Mgi Id | MGI:6381193 | Doi | 10.3390/ijms17030324 |
| Citation | Li SC, et al. (2016) Microarray Study of Pathway Analysis Expression Profile Associated with MicroRNA-29a with Regard to Murine Cholestatic Liver Injuries. Int J Mol Sci 17(3):324 |
| abstractText | UNLABELLED: Accumulating evidence demonstrates that microRNA-29 (miR-29) expression is prominently decreased in patients with hepatic fibrosis, which consequently stimulates hepatic stellate cells' (HSCs) activation. We used a cDNA microarray study to gain a more comprehensive understanding of genome-wide gene expressions by adjusting miR-29a expression in a bile duct-ligation (BDL) animal model. METHODS: Using miR-29a transgenic mice and wild-type littermates and applying the BDL mouse model, we characterized the function of miR-29a with regard to cholestatic liver fibrosis. Pathway enrichment analysis and/or specific validation were performed for differentially expressed genes found within the comparisons. RESULTS: Analysis of the microarray data identified a number of differentially expressed genes due to the miR-29a transgene, BDL, or both. Additional pathway enrichment analysis revealed that TGF-beta signaling had a significantly differential activated pathway depending on the occurrence of miR-29a overexpression or the lack thereof. Furthermore, overexpression was found to elicit changes in Wnt/beta-catenin after BDL. CONCLUSION: This study verified that an elevated miR-29a level could alleviate liver fibrosis caused by cholestasis. Furthermore, the protective effects of miR-29a correlate with the downregulation of TGF-beta and associated with Wnt/beta-catenin signal pathway following BDL. |
