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作 者:Xing-yu YANG Zhe CHEN Jun TAN Yin-kai XUE Hai ZHENG
机构地区:[1]Department of Emergency Surgery,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430022,China [2]Department of Thoracic Surgery,The First Affiliated Hospital of Xi’an Jiaotong University,Xi’an,710061,China [3]Department of Thoracic Surgery,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,430022,China
出 处:《Current Medical Science》2024年第3期512-518,共7页当代医学科学(英文)
基 金:supported by the National Natural Science Foundation of China(No.81071541).
摘 要:Objective Hepatic stellate cells(HSCs)play a crucial role in liver fibrosis.Early-stage liver fibrosis is reversible and intimately associated with the state of HSCs.Kruppel-like factor 4(KLF4)plays a pivotal role in a wide array of physiological and pathological processes.This study aimed to investigate the effect of KLF4 on the proliferation,apoptosis and phenotype of quiescent HSCs Methods We designed a KLF4 lentiviral vector and a KLF4 siRNA lentiviral vector,to upregulate and silence KLF4 expression in human HSC LX-2 cells via transfection.Cell proliferation was assessed using the CCK-8 assay.Flow cytometry was used to detect the cell cycle distribution and apoptosis rate.Western blotting was used to determine the levels of some quiescence and activation markers of HSCs Results Overexpression of KLF4 significantly increased the levels of E-cadherin and ZO-1,which are quiescent HSC markers,while significantly decreased the levels of N-cadherin and a-SMA,known activated HSC markers.In contrast,cell proliferation and apoptosis rates were elevated in LX-2 cells in which KLF4 expression was silenced Conclusion KLF4 inhibits the proliferation and activation of human LX-2 HSCs.It might be a key regulatory protein in the maintenance of HSC quiescence and may serve as a target for the inhibition of hepatic fibrosis.
关 键 词:Kruppel-like factor 4 hepatic stellate cells LX-2 cells liver fibrosis
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