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Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Int+J+Clin+Exp+Pathol 2015 ; 8 (4): 3994-4000 Nephropedia Template TP
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miR-144 regulates transforming growth factor-?1 iduced hepatic stellate cell activation in human fibrotic liver #MMPMID26097586
Liu Z; Yi J; Ye R; Liu J; Duan Q; Xiao J; Liu F
Int J Clin Exp Pathol 2015[]; 8 (4): 3994-4000 PMID26097586show ga
Objectives: Activation of hepatic stellate cells (HSCs) into collagen producing myofibroblasts is critical for pathogenesis of liver fibrosis. Transforming growth factor-?1 (TGF-?1) is one of the main profibrogenic mediators for HSC transdifferentiation. Recent studies have shown effect of microRNAs (miRNAs) on regulating TGF-?1-induced HSC activation during liver fibrosis. Here, we aimed to explore the roles of miR-144 and miR-200c in human liver fibrosis. Methods: Expression of TGF-?1 was detected in 42 fibrotic and 18 normal human liver tissues by quantitative real time polymerase chain reaction (qRT-PCR) and immunohistochemistry, and its correlation with ?-smooth muscle actin (?-SMA) was calculated. miR-144 and miR-200c expression level in fibrotic liver tissues were also detected by qRT-PCR. The correlation of TGF-?1 expression with miR-200c and miR-144 in the fibrotic liver was analyzed. Results: The results showed that TGF-?1 expression was much higher in fibrotic liver than that in normal liver tissues (P<0.05). TGF-?1 protein high expressing liver fibrosis showed ?-SMA positive cells in the liver parenchyma indicating activated HSCs. Expression of TGF-?1 in fibrotic liver was significantly correlated with ?-SMA expression (R=0.633, P<0.001). Furthermore, miR-144 was less expressed in liver fibrosis (P<0.05) and was significantly correlated with expression of TGF-?1 in fibrotic liver tissues (R=-0.442, P<0.01). However, miR-200c did not show significant difference between normal and fibrotic liver (P=0.48) and correlation with TGF-?1 expression (R=0.106, P=0.51). Conclusion: All the results indicate that miR-144 can be a novel regulator of TGF-?1-induced HSC activation during liver fibrosis.