Document Detail


Stress-induced senescence exaggerates postinjury neointimal formation in the old vasculature.
MedLine Citation:
PMID:  19855064     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study aims to demonstrate the role of stress-induced senescence in aged-related neointimal formation. We demonstrated that aging increases senescence-associated beta-galactosidase activity (SA-beta-Gal) after vascular injury and the subsequent neointimal formation (neointima-to-media ratio: 0.8 +/- 0.2 vs. 0.54 +/- 0.15) in rats. We found that senescent cells (SA-beta-Gal(+) p21(+)) were scattered throughout the media and adventitia of the vascular wall at day 7 after injury and reached their maximum number at day 14. However, senescent cells only persisted in the injured arteries of aged animals until day 30. No senescent cells were observed in the noninjured, contralateral artery. Interestingly, vascular senescent cells accumulated genomic 8-oxo-7,8-dihydrodeoxyguanine, indicating that these cells were under intense oxidative stress. To demonstrate whether senescence worsens intimal hyperplasia after injury, we seeded matrigel-embedded senescent and nonsenescent vascular smooth muscle cells around injured vessels. The neointima was thicker in arteries treated with senescent cells with respect to those that received normal cells (neointima-to-media ratio: 0.41 +/- 0.105 vs. 0.26 +/- 0.04). In conclusion, these results demonstrate that vascular senescence is not only a consequence of postinjury oxidative stress but is also a worsening factor for neointimal development in the aging vasculature.
Authors:
Sheik J Khan; Si Pham; Yunteo Wei; Dania Mateo; Melissa St-Pierre; Terace M Fletcher; Roberto I Vazquez-Padron
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-10-23
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  298     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2009-12-18     Completed Date:  2010-01-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H66-74     Citation Subset:  IM    
Affiliation:
Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
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MeSH Terms
Descriptor/Qualifier:
Aging / physiology*
Animals
Arteries / injuries,  physiopathology
Balloon Dilatation
Blood Vessels / cytology,  injuries,  physiology*
Cell Count
Cell Proliferation
Cells, Cultured
Immunohistochemistry
Microscopy, Fluorescence
Muscle, Smooth, Vascular / physiology
Myocytes, Smooth Muscle / physiology
Oxidative Stress / physiology
Rats
Rats, Inbred F344
Rats, Inbred Lew
Reactive Oxygen Species
Stress, Mechanical*
beta-Galactosidase / metabolism
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; EC 3.2.1.23/beta-Galactosidase

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


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