Document Detail


PDGF-BB enhances monocyte chemoattractant protein-1 mRNA stability in smooth muscle cells by downregulating ribonuclease activity.
MedLine Citation:
PMID:  16720030     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Platelet-derived growth factor (PDGF) has protean manifestations, including the regulation of growth and migration, in many cell types. We have previously reported that PDGF-BB induces the accumulation of monocyte chemoattractant protein (MCP)-1 mRNA in smooth muscle cells (SMC), in large part due to an increase in mRNA stability. To elucidate the mechanism by which PDGF-BB stabilizes MCP-1 mRNA, we have employed in vitro RNA gel mobility shift and decay assays. Cytoplasmic extracts from PDGF-BB-treated SMC increased the half-life of in vitro transcribed MCP-1 mRNA from approximately 45 min to >2 h. PDGF-BB-inhibitable degradation was not dependent on specific regions of the MCP-1 mRNA and was equally effective on a variety of in vitro transcribed mRNAs. Angiotensin II had a similar effect on MCP-1 mRNA stability, whereas tumor necrosis factor-alpha and basic fibroblast growth factor did not. The PDGF-BB-inhibitable RNAse activity was active at pH 6.6 and heat stable, but was sensitive to proteinase K. Extracts from PDGF-BB- or angiotensin II-treated cells inhibited the RNAse activity of control extracts, suggesting that the effect of PDGF-BB and angiotensin II are due to activation of a soluble inhibitor of the RNAse. The effect of PDGF-BB was blocked by inhibitors of tyrosine phosphorylation, but not by inhibitors of phosphatidylinositol 3-kinase or mitogen-activated protein kinases. These studies provide new insights into the mechanisms by which PDGF-BB enhances mRNA accumulation.
Authors:
Bin Liu; Michael Poon; Mark B Taubman
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-05-23
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  41     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-07-03     Completed Date:  2006-10-27     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  160-9     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Rochester, Box 679, 601 Elmwood Avenue, Rochester, NY 14642, USA.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / metabolism
Angiotensin II / pharmacology
Animals
Cells, Cultured
Chemokine CCL2 / drug effects,  genetics*
Down-Regulation
Enzyme Inhibitors / pharmacology
Half-Life
Isoenzymes / metabolism
Male
Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism
Muscle, Smooth, Vascular / drug effects*,  metabolism
Platelet-Derived Growth Factor / metabolism,  pharmacology*
Protein Kinase C / antagonists & inhibitors,  metabolism
RNA Stability / drug effects*
RNA, Messenger / drug effects,  metabolism
Rats
Rats, Sprague-Dawley
Receptors, Platelet-Derived Growth Factor / metabolism
Ribonucleases / drug effects,  metabolism*
src-Family Kinases / antagonists & inhibitors,  metabolism
Grant Support
ID/Acronym/Agency:
P01 77789//PHS HHS; R01 HL73364/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Chemokine CCL2; 0/Enzyme Inhibitors; 0/Isoenzymes; 0/Platelet-Derived Growth Factor; 0/RNA, Messenger; 0/platelet-derived growth factor BB; 11128-99-7/Angiotensin II; EC 2.7.1.-/PDGF receptor tyrosine kinase; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.1.137/phosphatidylinositol 3-kinase gamma; EC 2.7.10.1/Receptors, Platelet-Derived Growth Factor; EC 2.7.10.2/src-Family Kinases; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.1.-/Ribonucleases

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


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