Document Detail


Mir-206 regulates pulmonary artery smooth muscle cell proliferation and differentiation.
MedLine Citation:
PMID:  23071643     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary Arterial Hypertension (PAH) is a progressive devastating disease characterized by excessive proliferation of the Pulmonary Arterial Smooth Muscle Cells (PASMCs). Studies suggest that PAH and cancers share an apoptosis-resistant state featuring excessive cell proliferation. MicroRNA-206 (miR-206) is known to regulate proliferation and is implicated in various types of cancers. However, the role of miR-206 in PAH has not been studied. In this study, it is hypothesized that miR-206 could play a role in the proliferation of PASMCs. In the present study, the expression patterns of miR-206 were investigated in normal and hypertensive mouse PASMCs. The effects of miR-206 in modulating cell proliferation, apoptosis and smooth muscle cell markers in human pulmonary artery smooth muscle cells (hPASMCs) were investigated in vitro. miR-206 expression in mouse PASMCs was correlated with an increase in right ventricular systolic pressure. Reduction of miR-206 levels in hPASMCs causes increased proliferation and reduced apoptosis and these effects were reversed by the overexpression of miR-206. miR-206 over expression also increased the levels of smooth muscle cell differentiation markers α-smooth muscle actin and calponin implicating its importance in the differentiation of SMCs. miR-206 overexpression down regulated Notch-3 expression, which is key a factor in PAH development. These results suggest that miR-206 is a potential regulator of proliferation, apoptosis and differentiation of PASMCs, and that it could be used as a novel treatment strategy in PAH.
Authors:
Samuel Jalali; Gurukumar K Ramanathan; Prasanna Tamarapu Parthasarathy; Salman Aljubran; Lakshmi Galam; Asfiya Yunus; Sara Garcia; Ruan R Cox; Richard F Lockey; Narasaiah Kolliputi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-10-10
Journal Detail:
Title:  PloS one     Volume:  7     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2012  
Date Detail:
Created Date:  2012-10-16     Completed Date:  2013-04-11     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e46808     Citation Subset:  IM    
Affiliation:
Division of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, FL, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia
Apoptosis / genetics
Blotting, Western
Cell Differentiation / genetics*
Cell Movement / genetics
Cell Proliferation*
Cells, Cultured
Down-Regulation
Female
Gene Expression Profiling
Humans
Hypertension, Pulmonary / genetics,  metabolism,  physiopathology
Male
Mice
Mice, Inbred C57BL
MicroRNAs / genetics*
Myocytes, Smooth Muscle / cytology,  metabolism*
Pulmonary Artery / cytology
Receptors, Notch / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Grant Support
ID/Acronym/Agency:
R01 HL105932/HL/NHLBI NIH HHS; R01 HL105932/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/MIRN206 microRNA, human; 0/MicroRNAs; 0/Mirn206 microRNA, mouse; 0/NOTCH3 protein, human; 0/Receptors, Notch
Comments/Corrections

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