KLF4 Inhibits the Activation of Human Hepatic Stellate Cell In Vitro.
Curr Med Sci
; 44(3): 512-518, 2024 Jun.
Article
in En
| MEDLINE
| ID: mdl-38789819
ABSTRACT
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 HSCsMETHODS:
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 HSCsRESULTS:
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 silencedCONCLUSION:
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.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Apoptosis
/
Cell Proliferation
/
Kruppel-Like Transcription Factors
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Hepatic Stellate Cells
/
Kruppel-Like Factor 4
Limits:
Humans
Language:
En
Journal:
Curr Med Sci
Year:
2024
Document type:
Article