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KLF4 Inhibits the Activation of Human Hepatic Stellate Cell In Vitro.
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- Author(s): Yang XY;Yang XY; Chen Z; Chen Z; Tan J; Tan J; Xue YK; Xue YK; Zheng H; Zheng H
- Source:
Current medical science [Curr Med Sci] 2024 Jun; Vol. 44 (3), pp. 512-518. Date of Electronic Publication: 2024 May 24.- Publication Type:
Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: Huazhong University of Science and Technology Country of Publication: China NLM ID: 101729993 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2523-899X (Electronic) Linking ISSN: 2523899X NLM ISO Abbreviation: Curr Med Sci Subsets: MEDLINE
- Publication Information: Original Publication: Wuhan : Huazhong University of Science and Technology, [2018]-
- Subject Terms: Hepatic Stellate Cells*/metabolism ; Kruppel-Like Factor 4* ; Kruppel-Like Transcription Factors*/genetics ; Kruppel-Like Transcription Factors*/metabolism ; Cell Proliferation*/genetics ; Apoptosis*/genetics; Humans ; Cadherins/metabolism ; Cadherins/genetics ; Cell Line ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Zonula Occludens-1 Protein/metabolism ; Zonula Occludens-1 Protein/genetics ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Cell Cycle/genetics ; Actins/metabolism ; Actins/genetics
- 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 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.
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- Accession Number: 0 (Kruppel-Like Factor 4)
0 (Kruppel-Like Transcription Factors)
0 (KLF4 protein, human)
0 (Cadherins)
0 (Zonula Occludens-1 Protein)
0 (TJP1 protein, human)
0 (RNA, Small Interfering)
0 (Actins) - Publication Date: Date Created: 20240524 Date Completed: 20240627 Latest Revision: 20240719
- Publication Date: 20240719
- Accession Number: 10.1007/s11596-024-2860-8
- Accession Number: 38789819
- Source:
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