Document Detail


Pro-inflammatory angiogenesis is mediated by p38 MAP kinase.
MedLine Citation:
PMID:  20803566     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic inflammation is tightly linked to diseases associated with endothelial dysfunction including aberrant angiogenesis. To better understand the endothelial role in pro-inflammatory angiogenesis, we analyzed signaling pathways in continuously activated endothelial cells, which were either chronically exposed to soluble TNF or the reactive oxygen species (ROS) generating H2O2, or express active transmembrane TNF. Testing in an in vitro capillary sprout formation assay, continuous endothelial activation increased angiogenesis dependent on activation of p38 MAP kinase, NADPH oxidase, and matrix metalloproteinases (MMP). p38 MAP kinase- and MMP-9-dependent angiogenesis in our assay system may be part of a positive feed forward autocrine loop because continuously activated endothelial cells displayed up-regulated ROS production and subsequent endothelial TNF expression. The pro-angiogenic role of the p38 MAP kinase in continuously activated endothelial cells was in stark contrast to the anti-angiogenic activity of the p38 MAP kinase in unstimulated control endothelial cells. In vivo, using an experimental prostate tumor, pharmacological inhibition of p38 MAP kinase demonstrated a significant reduction in tumor growth and in vessel density, suggesting a pro-angiogenic role of the p38 MAP kinase in pathological angiogenesis in vivo. In conclusion, our results suggest that continuous activation of endothelial cells can cause a switch of the p38 MAP kinase from anti-angiogenic to pro-angiogenic activities in conditions which link oxidative stress and autocrine TNF production.
Authors:
Gangaraju Rajashekhar; Malgorzata Kamocka; Abby Marin; Mark A Suckow; William R Wolter; Sunil Badve; Aravind Raj Sanjeevaiah; Kevin Pumiglia; Elliot Rosen; Matthias Clauss
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  226     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2010-12-30     Completed Date:  2011-01-27     Revised Date:  2011-09-22    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  800-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Wiley-Liss, Inc.
Affiliation:
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA. rgangara@iupui.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Proliferation / drug effects
Endothelial Cells / drug effects,  enzymology,  pathology
Enzyme Activation / drug effects
Humans
Hydrogen Peroxide / pharmacology
Inflammation / complications*,  enzymology*,  pathology
MAP Kinase Signaling System / drug effects
Matrix Metalloproteinase 9 / metabolism
Mice
Models, Biological
Neoplasms / blood supply,  enzymology,  pathology
Neovascularization, Pathologic / complications*,  enzymology*
Rats
Solubility / drug effects
Tumor Necrosis Factor-alpha / metabolism,  pharmacology
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism*
Grant Support
ID/Acronym/Agency:
R01 CA081419-09/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Tumor Necrosis Factor-alpha; 7722-84-1/Hydrogen Peroxide; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases; EC 3.4.24.35/Matrix Metalloproteinase 9

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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