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KLF4 Inhibits Activation of Human Hepatic Stellate Cells LX-2 in vitro


 BackgroundHepatic Stellate Cell (HSC) represents a key factor in liver fibrosis. Early-stage liver fibrosis is still reversible and is intimately associated with the state of HSC. KLF4 has been shown to play a pivotal role in a wide array of physiological and pathological processes. MethodsIn this study, we examined the effect of Kruppel-like factor 4 (KLF4) on the proliferation, apoptosis and phenotype of HSC in resting state in human HSC LX-2 cells, and the role KLF4 plays in the maintenance of the resting state of HSC, with an attempt to provide an experimental basis for the diagnosis, treatment and prognosis evaluation of liver fibrosis. We designed a KLF4 lentiviral vector and a KLF4 shRNA lentiviral vector, to up-regulate and silence KLF4 expression in LX-2 cells by transfection. We examined LX-2 cell proliferation by plate cloning and CCK8 assay, flow cytometrically detected cell cycle distribution and cellular apoptosis rate and determined some quiescence and activation markers of HSC by Western blotting. ResultsOur result showed that E-cadherin and ZO-1, dubbed quiescent HSC markers, were significantly increased. N-cadherin while a-AMA, known as activated HSC marker, was significantly decreased. In contrast, cell proliferation and apoptosis rate were elevated in LX-2 cells whose KLF4 expression had been silenced. Conclusions﻿Our results indicated that KLF4 inhibited the proliferation and activation of human HSC LX-2 and might be a key regulatory protein in the maintenance of quiescence of HSC and might serve as a target for the inhibition of hepatic fibrosis.