scholarly journals Traf2 and NCK Interacting Kinase Is a Critical Regulator of Procollagen I Trafficking and Hepatic Fibrogenesis in Mice

2021 ◽  
Author(s):  
Samuel C. Buchl ◽  
Zachary Hanquier ◽  
Andrew J. Haak ◽  
Yvonne M. Thomason ◽  
Robert C. Huebert ◽  
...  
Keyword(s):  
Hepatic Fibrogenesis

UDCA-LPE modulates different signaling pathways involved in hepatic fibrogenesis

2015 ◽  
Vol 53 (01) ◽  
Author(s):  
J Su ◽  
W Chamulitrat ◽  
W Stremmel ◽  
A Pathil
Keyword(s):  
Signaling Pathways ◽  
Hepatic Fibrogenesis

Inhibiting NOXs with extra-virgin olive oil polyphenols as a strategy to prevent hepatic fibrogenesis

2020 ◽  
Vol 52 ◽  
pp. e65
Author(s):  
D. Gabbia ◽  
S. Carpi ◽  
S. Sarcognato ◽  
S. Munari ◽  
M. Colognesi ◽  
...  
Keyword(s):  
Olive Oil ◽  
Virgin Olive Oil ◽  
Extra Virgin Olive Oil ◽  
Hepatic Fibrogenesis

Hepatotoxicity of Iron Overload: Mechanisms of Iron-Induced Hepatic Fibrogenesis

2005 ◽  
Vol 25 (04) ◽  
pp. 433-449 ◽  
Author(s):  
Grant A Ramm ◽  
Richard G Ruddell
Keyword(s):  
Iron Overload ◽  
Hepatic Fibrogenesis

scholarly journals Circular RNA circPSD3 alleviates hepatic fibrogenesis by regulating the miR-92b-3p/Smad7 axis

2021 ◽  
Vol 23 ◽  
pp. 847-862
Author(s):  
Fang-tian Bu ◽  
Yan Zhu ◽  
Xin Chen ◽  
Ao Wang ◽  
Ya-fei Zhang ◽  
...  
Keyword(s):  
Circular Rna ◽  
Hepatic Fibrogenesis

scholarly journals SAT-174 Loss of CEACAM1 in Endothelial Cells Causes Hepatic Fibrogenesis

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Harrison Muturi ◽  
Saja Khuder ◽  
Hilda Ghadieh ◽  
Raghd Abu Helal ◽  
Hannah Stankus ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Hepatic Fibrogenesis

Hepatic Fibrogenesis

1996 ◽  
Vol 16 (2) ◽  
pp. 361-375 ◽  
Author(s):  
Bernard H. Davis ◽  
Thomas F. Kresina
Keyword(s):  
Hepatic Fibrogenesis

Modulation of hepatic fibrogenesis by antioxidants

1995 ◽  
Vol 31 ◽  
pp. 222
Author(s):  
M. Parola ◽  
G. Leonarduzzi ◽  
A. Scavazza ◽  
S. Camandola ◽  
M. Pinzani ◽  
...  
Keyword(s):  
Hepatic Fibrogenesis

scholarly journals Characterization of the Roles of Vimentin in Regulating the Proliferation and Migration of HSCs during Hepatic Fibrogenesis

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1184 ◽  
Author(s):  
Pei-Wen Wang ◽  
Tung-Ho Wu ◽  
Tung-Yi Lin ◽  
Mu-Hong Chen ◽  
Chau-Ting Yeh ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Messenger Rna ◽  
Rho Gtpase ◽  
Focal Adhesions ◽  
Cytoskeletal Proteins ◽  
Nuclear Antigen ◽  
Dependent Manner ◽  
Hepatic Fibrogenesis ◽  
And Migration ◽  
Proliferation And Migration

The activation of hepatic stellate cells (HSCs) manifested as proliferation and migration is the pivotal event involved in liver fibrogenesis. The vimentin network, an intermediate filament (IF) system, is one of the critical cascades by which the cell morphology, growth, and motility are modulated. However, the vimentin-mediated cytoskeletal cross talk, as well as the signaling transduction, which further coordinates the cellular responses during hepatic fibrogenesis, is poorly understood. In the current study, both messenger RNA (mRNA) and the vimentin protein were significantly increased in a time-dependent manner in the dimethylnitrosamine (DMN)-exposed liver. In particular, vimentin was highly expressed in the activated HSCs. Again, the overexpressed vimentin was observed in the plasma samples derived from patients with hepatic fibrosis/cirrhosis, suggesting that vimentin may be a key factor in regulating the progression of liver fibrosis. Meanwhile, vimentin knockdown suppressed the migratory propensity, provoked morphological changes, and disturbed the focal adhesions in the HSCs due to the breakdown of associated cytoskeletal proteins. Western blotting showed that vimentin deletion inhibited proliferating cell nuclear antigen (PCNA) and arrested the Rho GTPase family, thereby impairing the HSCs’ growth as well as motility. The phosphorylated extracellular-signal regulated kinase (ERK) and AKT signals were also notably reduced in response to the silence of vimentin. Inhibitors of selected signaling pathways suppressed the migration and differentiation of activated HSCs by regulating specific serine phosphorylated sites on vimentin. Taken together, these findings revealed a novel mechanism of vimentin through which various signaling pathways controlled the proliferation, differentiation, and movement of the HSCs via the ERK/AKT and Rho cascades.

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