miR-181b promotes hepatic stellate cells proliferation by targeting p27 and is elevated in the serum of cirrhosis patients
Autor: | Baocan Wang, Yuqin Wang, Wenxi Li, Yongtao Xiao, Jiangao Fan, Kun Guo |
---|---|
Rok vydání: | 2012 |
Předmět: |
Liver Cirrhosis
medicine.medical_specialty Cirrhosis Cell Biophysics Regulator Biology Biochemistry Cell Line Transforming Growth Factor beta Internal medicine microRNA medicine Hepatic Stellate Cells Humans Molecular Biology Cell Proliferation Cell growth Cell Biology Cell cycle medicine.disease MicroRNAs medicine.anatomical_structure Endocrinology Cell culture Hepatic stellate cell Cancer research Cyclin-Dependent Kinase Inhibitor p27 |
Zdroj: | Biochemical and biophysical research communications. 421(1) |
ISSN: | 1090-2104 |
Popis: | MicroRNAs, as a kind of negative gene regulators, were demonstrated to be involved in many types of diseases. In this study, we found that transforming growth factor-beta 1 could induce the expression of miR-181a and miR-181b, and miR-181b increased in the much higher folds than miR-181a. Because of the important role of transforming growth factor-beta 1 in HSC activation and liver cirrhosis, we investigate the effect of miR-181a and miR-181b on HSC proliferation. The results showed that miR-181b could promote HSC-T6 cell proliferation by regulating cell cycle. Further study showed p27, the cell cycle regulator, was the direct target of miR-181b in HSC-T6 cell. But miR-181a had no effects on HSC-T6 cell proliferation and cell cycle, and did not target p27. Interestingly, miR-181b is elevated significantly in serum of liver cirrhosis cases comparing to that of normal persons, whereas miR-181a expression was in the similar level with that of normal persons. These results suggested that miR-181b could be induced by TGF-β1 and promote the growth of HSCs by directly targeting p27. The elevation of miR-181b in serum suggested that it may be potential diagnostic biomarkers for cirrhosis. As for miR-181a, it may work in TGF-β1 pathway by a currently unknown mechanism. |
Databáze: | OpenAIRE |
Externí odkaz: |