Heat shock protein 47 effects on hepatic stellate cell-associated receptors in hepatic fibrosis of Schistosoma japonicum-infected mice

2017 ◽  
Vol 398 (12) ◽  
pp. 1357-1366 ◽  
Author(s):  
Yumin Zhao ◽  
Zhisheng Dang ◽  
Shuo Xu ◽  
Shigui Chong
Keyword(s):  
Heat Shock ◽  
Liver Fibrosis ◽  
Heat Shock Protein ◽  
Schistosoma Japonicum ◽  
Mouse Models ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Endothelin Receptor ◽  
Heat Shock Protein 47

AbstractThe study aimed to explore the regulation of heat shock protein 47 (HSP47) on expressions of receptors associated with hepatic stellate cell (HSC) in liver fibrosis mouse models induced bySchistosoma japonicum(S. japonicum). Mouse fibroblasts (NIH/3T3) were transfected with HSP47 shRNA plasmid by lipofectamine transfection, and experimental fibrosis in HSCs was studied inS. japonicummouse models treated with HSP47 shRNAin vivo. HSP47 expression was assessed using Western blot and real-time PCR. Flow cytometry was adopted to determine the expression of cell membrane receptors. HSP47-shRNA could markedly down-regulate the expression of collagen (Col1a1 and Col3a1). The expressions of HSP47, endothelin receptor A (ETAR) and endothelin receptor B (ETBR) significantly increased in the liver tissue of infected mice. However, the expressions of ETAR and HSP47 and ETBR remarkably decreased after the administration of HSP47 shRNAin vitroandin vivo. ETAR and ETBR levels were found to be positively correlated with HSP47 expression. HSP47 might exert influence on liver fibrosis via the regulation of ETAR and ETBR.

Expression of small heat shock protein αB-crystallin is induced after hepatic stellate cell activation

2000 ◽  
Vol 279 (6) ◽  
pp. G1333-G1342 ◽  
Author(s):  
Alon Lang ◽  
Laura W. Schrum ◽  
Robert Schoonhoven ◽  
Shmuel Tuvia ◽  
Jose A. Solís-Herruzo ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Hepatic Stellate Cell ◽  
Cell Activation ◽  
Stellate Cell ◽  
Small Heat Shock Protein ◽  
Immunocytochemical Staining ◽  
Αb Crystallin ◽  
Quiescent Hscs

Using the differential PCR display method to select cDNA fragments that are differentially expressed after hepatic stellate cell (HSC) activation, we have isolated from activated HSCs a cDNA that corresponds to rat αB-crystallin. Northern blots confirmed expression of αB-crystallin in culture-activated HSCs but not in quiescent HSCs. Western blot analysis and immunocytochemical staining confirmed expression of αB-crystallin protein in activated but not quiescent HSCs. αB-crystallin is induced as early as 6 h after plating HSCs on plastic and continues to be expressed for 14 days in culture. Expression of αB-crystallin was also induced in vivo in activated HSCs from experimental cholestatic liver fibrosis. Confocal microscopy demonstrated a cytoplasmic distribution of αB-crystallin in a cytoskeletal pattern. Heat shock treatment resulted in an immediate perinuclear redistribution that in time returned to a normal cytoskeletal distribution. The expression pattern of αB-crystallin was similar to that of HSP25, another small heat shock protein, but differed from the classic heat shock protein HSP70. Therefore, αB-crystallin represents an early marker for HSC activation.

P635 INVOLVEMENT OF HEAT SHOCK PROTEIN 47 IN SCHISTOSOMA JAPONICUM-INDUCED HEPATIC FIBROSIS IN MICE

2014 ◽  
Vol 60 (1) ◽  
pp. S280
Author(s):  
R. Tao ◽  
J.-Q. Huang ◽  
L. Li ◽  
K. Ma ◽  
X.-X. Fan ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Schistosoma Japonicum ◽  
Hepatic Fibrosis ◽  
Heat Shock Protein 47

Rapamycin inhibits hepatic stellate cell proliferation in vitro and limits fibrogenesis in an in vivo model of liver fibrosis

1999 ◽  
Vol 117 (5) ◽  
pp. 1198-1204 ◽  
Author(s):  
Jianliang Zhu ◽  
Jian Wu ◽  
Edward Frizell ◽  
Shu-Ling Liu ◽  
Reza Bashey ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Fibrosis ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
In Vivo Model ◽  
Proliferation In Vitro

Involvement of heat shock protein 47 in Schistosoma japonicum-induced hepatic fibrosis in mice

2014 ◽  
Vol 44 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Jia-Quan Huang ◽  
Ran Tao ◽  
Lan Li ◽  
Ke Ma ◽  
Lei Xu ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Schistosoma Japonicum ◽  
Hepatic Fibrosis ◽  
Heat Shock Protein 47

Snail1 transcription factor is a critical mediator of hepatic stellate cell activation following hepatic injury

2011 ◽  
Vol 300 (2) ◽  
pp. G316-G326 ◽  
Author(s):  
Melania Scarpa ◽  
Alessia R. Grillo ◽  
Paola Brun ◽  
Veronica Macchi ◽  
Annalisa Stefani ◽  
...  
Keyword(s):  
Wound Healing ◽  
Transcription Factor ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Mrna Expression ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Qrt Pcr

Following liver injury, the wound-healing process is characterized by hepatic stellate cell (HSC) activation from the quiescent fat-storing phenotype to a highly proliferative myofibroblast-like phenotype. Snail1 is a transcription factor best known for its ability to trigger epithelial-mesenchymal transition, to influence mesoderm formation during embryonic development, and to favor cell survival. In this study, we evaluated the expression of Snail1 in experimental and human liver fibrosis and analyzed its role in the HSC transdifferentiation process. Liver samples from patients with liver fibrosis and from mice treated by either carbon tetrachloride (CCl4) or thioacetamide (TAA) were evaluated for mRNA expression of Snail1. The transcription factor expression was investigated by immunostaining and real-time quantitative RT-PCR (qRT-PCR) on in vitro and in vivo activated murine HSC. Snail1 knockdown studies on cultured HSC and on CCl4-treated mice were performed by adenoviral delivery of short-hairpin RNA; activation-related genes were quantitated by real-time qRT-PCR and Western blotting. Snail1 mRNA expression resulted upregulated in murine experimental models of liver injury and in human hepatic fibrosis. In vitro studies showed that Snail1 is expressed by HSC and that its transcription is augmented in in vitro and in vivo activated HSC compared with quiescent HSC. At the protein level, we could observe the nuclear translocation of Snail1 in activated HSC. Snail1 knockdown resulted in the downregulation of activation-related genes both in vitro and in vivo. Our data support a role for Snail1 transcription factor in the hepatic wound-healing response and its involvement in the HSC transdifferentiation process.

965 ACID SPHINGOMYELINASE CONTROLS HEPATIC STELLATE CELL ACTIVATION AND IN VIVO LIVER FIBROSIS

2010 ◽  
Vol 52 ◽  
pp. S373
Author(s):  
A. Moles ◽  
N. Tarrats ◽  
A. Morales ◽  
M. Dominguez ◽  
R. Bataller ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cell ◽  
Cell Activation ◽  
Stellate Cell ◽  
Acid Sphingomyelinase ◽  
Hepatic Stellate Cell Activation

scholarly journals 446. Inhibition of Hepatic Stellate Cell Activation and Liver Fibrosis by Expression of Cytoglobin In Vivo

2006 ◽  
Vol 13 ◽  
pp. S171-S172
Author(s):  
Ruian Xu ◽  
Phillip Harrison ◽  
Xinyan Li ◽  
Miao Chen ◽  
Hua Li ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cell ◽  
Cell Activation ◽  
Stellate Cell ◽  
Hepatic Stellate Cell Activation

Inhibition of hepatic stellate cell proliferation by heat shock protein 90 inhibitors in vitro

2009 ◽  
Vol 330 (1-2) ◽  
pp. 181-185 ◽  
Author(s):  
Xu Sun ◽  
Xiao-Dong Zhang ◽  
Gang Cheng ◽  
You-Hong Hu ◽  
He-Yao Wang
Keyword(s):  
Cell Proliferation ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Heat Shock Protein 90
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