Apoptosis in Dissociation between DNA Synthesis and Cellular Functions of Activated Hepatic Stellate Cells—A Study with Carbon Tetrachloride-Induced Rat Liver Injury

2001 ◽  
Vol 282 (2) ◽  
pp. 524-528 ◽  
Author(s):  
Nobuaki Osada ◽  
Satoshi Mochida ◽  
Mie Inao ◽  
Yumi Mashimo ◽  
Kenji Fujiwara
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Dna Synthesis ◽  
Rat Liver ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Cellular Functions ◽  
Activated Hepatic Stellate Cells

scholarly journals Differential regulation of TGF-β signal in hepatic stellate cells between acute and chronic rat liver injury

Hepatology ◽  
2002 ◽  
Vol 35 (1) ◽  
pp. 49-61 ◽  
Author(s):  
Yoshiya Tahashi ◽  
Koichi Matsuzaki ◽  
Masataka Date ◽  
Katsunori Yoshida ◽  
Fukiko Furukawa ◽  
...  
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Differential Regulation

Serial changes of apoptosis of hepatic stellate cells in acute carbon tetrachloride induced liver injury

2001 ◽  
Vol 34 ◽  
pp. 90-91
Author(s):  
K.C. Kim ◽  
K.S. Lee ◽  
Y.M. Moon ◽  
S.P. Hong ◽  
S.G. Hwang ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Stellate Cells ◽  
Stellate Cells

scholarly journals IGF-I induces DNA synthesis and apoptosis in rat liver hepatic stellate cells (HSC) but DNA synthesis and proliferation in rat liver myofibroblasts (rMF)

2004 ◽  
Vol 84 (8) ◽  
pp. 1037-1049 ◽  
Author(s):  
Bernhard Saile ◽  
Paola DiRocco ◽  
Joszef Dudas ◽  
Hammudeh El-Armouche ◽  
Holger Sebb ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Rat Liver ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Liver Myofibroblasts ◽  
Igf I

287 Senescence of Activated Hepatic Stellate Cells Limits Liver Fibrosis During Alcoholic Liver Injury

2016 ◽  
Vol 150 (4) ◽  
pp. S1025
Author(s):  
Tianhao Zhou ◽  
Heather L. Francis ◽  
Ying Wan ◽  
Julie Venter ◽  
Nan Wu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Alcoholic Liver Injury ◽  
Activated Hepatic Stellate Cells

scholarly journals Insulin-Like Growth Factor (IGF)-Binding Protein-1 Is Highly Induced during Acute Carbon Tetrachloride Liver Injury and Potentiates the IGF-I-Stimulated Activation of Rat Hepatic Stellate Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3463-3472 ◽  
Author(s):  
Jens-Gerd Scharf ◽  
Frank Dombrowski ◽  
Ruslan Novosyadlyy ◽  
Christoph Eisenbach ◽  
Ilaria Demori ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Stellate Cells ◽  
Binding Protein ◽  
Stellate Cells ◽  
Hepatic Tissue ◽  
Mrna Levels ◽  
Igf I ◽  
Igf Binding ◽  
Igf Binding Protein

Abstract Hepatic stellate cells (HSC) play a pivotal role in hepatic tissue repair and fibrogenesis. IGF-I has been considered a mitogenic signal for activation and proliferation of HSC in vitro. In the present study IGF-I and IGF-binding protein (IGFBP) gene expression was studied in a model of acute liver injury induced by a single intragastric dose of carbon tetrachloride (CCl4) in adult rats. Northern blot analysis revealed a marked increase in IGFBP-1 mRNA levels, with a maximum between 3 and 9 h after CCl4 application, whereas steady state mRNA levels of IGF-I were only moderately altered. In situ hybridization experiments demonstrated that this increase in IGFBP-1 mRNA was due to a strong expression of IGFBP-1 in the perivenous region 6–12 h after CCl4 application, extending to the midzonal region of the acinus within 24–48 h. Consequently, a prominent immunostaining for IGFBP-1 was observed in perivenous areas, with a maximum 24–48 h after intoxication. Preincubation of early cultured HSC with a nonphosphorylated IGFBP-1 from human amniotic fluid resulted in a 3.4-fold increase in IGF-I-induced DNA synthesis. The mitogenic effect of IGF-I was also potentiated when HSC were cocultivated with IGFBP-1-overexpressing BHK-21 cells compared with nontransfected cells. These data suggest that IGFBP-1 released during the early steps of liver tissue damage and repair may interact with HSC and potentiate the sensitivity of IGF-I to mitogenic signals.

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