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2015 ; 8
(4
): 3994-4000
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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
PMID26097586
show 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.