15d-Deoxy-Δ12,14-prostaglandin J2 modulates collagen type I synthesis in human hepatic stellate cells by inducing oxidative stress

2005 ◽  
Vol 73 (5) ◽  
pp. 361-367 ◽  
Author(s):  
Kyung-Ah Kim ◽  
Young-Suk Lim ◽  
Kang-Mo Kim ◽  
Jung-Hwan Yoon ◽  
Hyo-Suk Lee
Keyword(s):  
Oxidative Stress ◽  
Hepatic Stellate Cells ◽  
Collagen Type ◽  
Stellate Cells ◽  
Collagen Type I ◽  
Type I ◽  
Prostaglandin J2

scholarly journals CYP2E1-mediated oxidative stress induces collagen type I expression in rat hepatic stellate cells

Hepatology ◽  
1999 ◽  
Vol 30 (4) ◽  
pp. 987-996 ◽  
Author(s):  
Natalia Nieto ◽  
Scott L. Friedman ◽  
Patricia Greenwel ◽  
Arthur I. Cederbaum
Keyword(s):  
Oxidative Stress ◽  
Hepatic Stellate Cells ◽  
Collagen Type ◽  
Stellate Cells ◽  
Collagen Type I ◽  
Type I

scholarly journals Alpha-single chains of collagen type VI inhibit the fibrogenic effects of triple helical collagen VI in hepatic stellate cells

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0254557
Author(s):  
Christian Freise ◽  
Hyunho Lee ◽  
Christopher Chronowski ◽  
Doug Chan ◽  
Jessica Cziomer ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Collagen Type ◽  
Stellate Cell ◽  
Smooth Muscle Actin ◽  
Stellate Cells ◽  
Collagen Type I ◽  
Serum Starvation ◽  
Type I ◽  
Linear Peptide

The interaction of extracellular matrix (ECM) components with hepatic stellate cells (HSCs) is thought to perpetuate fibrosis by stimulating signaling pathways that drive HSC activation, survival and proliferation. Consequently, disrupting the interaction between ECM and HSCs is considered a therapeutical avenue although respective targets and underlying mechanisms remain to be established. Here we have interrogated the interaction between type VI collagen (CVI) and HSCs based on the observation that CVI is 10-fold upregulated during fibrosis, closely associates with HSCs in vivo and promotes cell proliferation and cell survival in cancer cell lines. We exposed primary rat HSCs and a rat hepatic stellate cell line (CFSC) to soluble CVI and determined the rate of proliferation, apoptosis and fibrogenesis in the absence of any additional growth factors. We find that CVI in nanomolar concentrations prevents serum starvation-induced apoptosis. This potent anti-apoptotic effect is accompanied by induction of proliferation and acquisition of a pronounced pro-fibrogenic phenotype characterized by increased α-smooth muscle actin, TGF-β, collagen type I and TIMP-1 expression and diminished proteolytic MMP-13 expression. The CVI-HSC interaction can be disrupted with the monomeric α2(VI) and α3(VI) chains and abrogates the activating CVI effects. Further, functional relevant α3(VI)—derived 30 amino acid peptides lead to near-complete inhibition of the CVI effect. In conclusion, CVI serves as a potent mitogen and activating factor for HSCs. The antagonistic effects of the CVI monomeric chains and peptides point to linear peptide sequences that prevent activation of CVI receptors which may allow a targeted antifibrotic therapy.

scholarly journals Differential effect of somatostatinergic signaling on collagen type i production and the proliferation of cytokine primed rat hepatic stellate cells

Gut ◽  
2011 ◽  
Vol 60 (Suppl 1) ◽  
pp. A242-A242
Author(s):  
S. Klironomos ◽  
G. Notas ◽  
O. Sfakianaki ◽  
I. Drigiannakis ◽  
M. Frangaki ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Differential Effect ◽  
Collagen Type ◽  
Stellate Cells ◽  
Collagen Type I ◽  
Type I

scholarly journals rSJYB1 inhibits collagen type I protein expression in hepatic stellate cells via down‐regulating activity of collagen α1 (I) promoter

2019 ◽  
Vol 23 (5) ◽  
pp. 3676-3682 ◽  
Author(s):  
Liuting Chen ◽  
Zhaodong Ji ◽  
Lian Duan ◽  
Dandan Zhu ◽  
Jinling Chen ◽  
...  
Keyword(s):  
Protein Expression ◽  
Hepatic Stellate Cells ◽  
Collagen Type ◽  
Stellate Cells ◽  
Collagen Type I ◽  
Type I
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