scholarly journals Sustained Activation of Extracellular Signal-regulated Kinase Stimulated by Hepatocyte Growth Factor Leads to Integrin α2Expression That Is Involved in Cell Scattering

2001 ◽  
Vol 276 (24) ◽  
pp. 21146-21152 ◽  
Author(s):  
Chun-Chi Liang ◽  
Hong-Chen Chen
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Cell Scattering ◽  
Hepatocyte Growth ◽  
Sustained Activation

scholarly journals Hepatocyte Growth Factor Inhibits Apoptosis by the Profibrotic Factor Angiotensin II via Extracellular Signal-regulated Kinase 1/2 in Endothelial Cells and Tissue Explants

2010 ◽  
Vol 21 (23) ◽  
pp. 4240-4250 ◽  
Author(s):  
Young H. Lee ◽  
Ana P. Marquez ◽  
Ognoon Mungunsukh ◽  
Regina M. Day
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Caspase 3 ◽  
Cytoplasmic Localization ◽  
Ang Ii ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Induced Apoptosis ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF), an endogenous tissue repair factor, attenuates apoptosis in many primary cell types, but the mechanism is not completely understood. Our laboratory demonstrated that angiotensin (Ang) II activates the intrinsic apoptotic pathway in primary endothelial cells (ECs) via reduction of the antiapoptotic protein Bcl-xL. Ang II decreased Bcl-xLmRNA half-life by reducing its binding to nucleolin, a protein that normally binds a 3′ AU-rich region and stabilizes Bcl-xLmRNA. We hypothesized HGF may block apoptosis induced by Ang II. We used primary EC and ex vivo cultures of rat lung tissue to investigate HGF inhibition of Ang II-induced apoptosis. Our data indicated HGF abrogated Ang II-induced apoptosis by inhibiting cytochrome c release, caspase-3 activation, and DNA fragmentation. RNA-immunoprecipitation experiments demonstrated that HGF stabilized Bcl-xLmRNA by increasing nucleolin binding to the 3′-untranslated region that was associated with cytoplasmic localization of nucleolin. Cytoplasmic localization of nucleolin and Bcl-xLmRNA stabilization required HGF activation of extracellular signal-regulated kinase (ERK)1/2, but not phosphatidylinositol 3-kinase. HGF also blocked Ang II-induced caspase-3 activation and lactate dehydrogenase release in tissue explants in an ERK-dependent manner.

scholarly journals Activation of NF-κB Is Essential for Hepatocyte Growth Factor-Mediated Proliferation and Tubulogenesis

2002 ◽  
Vol 22 (4) ◽  
pp. 1060-1072 ◽  
Author(s):  
Markus Müller ◽  
Alessandro Morotti ◽  
Carola Ponzetto
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Transcriptional Activation ◽  
Mitogen Activated Protein Kinase ◽  
Phosphatidylinositol 3 Kinase ◽  
Extracellular Signal Regulated Kinase ◽  
Biological Responses ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Hepatocyte Growth

ABSTRACT Hepatocyte growth factor (HGF) and its receptor, Met, regulate a number of biological functions in epithelial and nonepithelial cells, such as survival, motility, proliferation, and tubular morphogenesis. The transcription factor NF-κB is activated in response to a wide variety of stimuli, including growth factors, and is involved in biological responses in part overlapping with those triggered by HGF. In this work we used the liver-derived MLP29 cell line to study the possible involvement of NF-κB in HGF/Met signaling. HGF stimulates NF-κB DNA binding and transcriptional activation via the canonical IκB phosphorylation-degradation cycle and via the extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase cascades. Phosphatidylinositol 3-kinase is not involved in Met-mediated NF-κB activation. Blockage of NF-κB activation in MLP29 cells by forced expression of the NF-κB super-repressor IκBα2A does not interfere with HGF-induced scatter but inhibits proliferation and tubulogenesis. Surprisingly, in the same cells NF-κB appears to be dispensable for the antiapoptotic function of HGF.

scholarly journals Enhancement of Hepatocyte Growth Factor-Induced Cell Scattering in N-Acetylglucosaminyltransferase III-transfected HepG2 Cells

2004 ◽  
Vol 27 (6) ◽  
pp. 781-785 ◽  
Author(s):  
Masashi Hyuga ◽  
Sumiko Hyuga ◽  
Nana Kawasaki ◽  
Miyako Ohta ◽  
Satsuki Itoh ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Cell Scattering ◽  
Hepatocyte Growth
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