Document Detail


Cardiovascular remodeling in response to long-term exposure to fine particulate matter air pollution.
MedLine Citation:
PMID:  22661498     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Air pollution is a pervasive environmental health hazard that occurs over a lifetime of exposure in individuals from many industrialized societies. However, studies have focused primarily on exposure durations that correspond to only a portion of the lifespan. We therefore tested the hypothesis that exposure over a considerable portion of the lifespan would induce maladaptive cardiovascular responses.
METHODS AND RESULTS: C57BL/6 male mice were exposed to concentrated ambient particles <2.5 µm (particulate matter, PM or PM(2.5)) or filtered air (FA), 6 h/d, 5 d/wk, for 9 months. Assessment of cardiac contractile function, coronary arterial flow reserve, isolated cardiomyocyte function, expression of hypertrophic markers, calcium handling proteins, and cardiac fibrosis were then performed. Mean daily concentrations of PM(2.5) in the exposure chamber versus ambient daily PM(2.5) concentration at the study site were 85.3 versus 10.6 µg/m(3) (7.8-fold concentration), respectively. PM(2.5) exposure resulted in increased hypertrophic markers leading to adverse ventricular remodeling characterized by myosin heavy chain (MHC) isoform switch and fibrosis, decreased fractional shortening (39.8 ± 1.4 FA versus 27.9 ± 1.3 PM, FS%), and mitral inflow patterns consistent with diastolic dysfunction (1.95 ± 0.05 FA versus 1.52 ± 0.07 PM, E/A ratio). Contractile reserve to dobutamine was depressed (62.3 ± 0.9 FA versus 49.2 ± 1.5 PM, FS%) in response to PM(2.5) without significant alterations in maximal vasodilator flow reserve. In vitro cardiomyocyte function revealed depressed peak shortening (8.7 ± 0.6 FA versus 7.0 ± 0.4 PM, %PS) and increased time-to-90% shortening (72.5 ± 3.2 FA versus 82.8 ± 3.2 PM, ms) and re-lengthening (253.1 ± 7.9 FA versus 282.8 ± 9.3 PM, ms), which were associated with upregulation of profibrotic markers and decreased total antioxidant capacity. Whole-heart SERCA2a levels and the ratio of α/β-MHC were both significantly decreased (P<0.05) in PM(2.5)-exposed animals, suggesting a switch to fetal programming.
CONCLUSIONS: Long-term exposure to environmentally relevant concentrations of PM(2.5) resulted in a cardiac phenotype consistent with incipient heart failure.
Authors:
Loren E Wold; Zhekang Ying; Kirk R Hutchinson; Markus Velten; Matthew W Gorr; Christina Velten; Dane J Youtz; Aixia Wang; Pamela A Lucchesi; Qinghua Sun; Sanjay Rajagopalan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-06-01
Journal Detail:
Title:  Circulation. Heart failure     Volume:  5     ISSN:  1941-3297     ISO Abbreviation:  Circ Heart Fail     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-07-19     Completed Date:  2012-09-25     Revised Date:  2013-07-08    
Medline Journal Info:
Nlm Unique ID:  101479941     Medline TA:  Circ Heart Fail     Country:  United States    
Other Details:
Languages:  eng     Pagination:  452-61     Citation Subset:  IM    
Affiliation:
Center for Cardiovascular and Pulmonary Research, The Research Institute at Nationwide Children's Hospital, Department of Pediatrics/Physiology and Cell Biology, The Ohio State University, 700 Children’s Drive, Columbus, OH 43205, USA. Loren.Wold@nationwidechildrens.org
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / metabolism
Blood Pressure
Calcium / metabolism
Cardiomegaly / etiology,  pathology,  physiopathology
Cardiovascular Diseases / etiology*,  metabolism,  pathology,  physiopathology
Collagen / metabolism
Fibrosis
Fractional Flow Reserve, Myocardial
Heart Failure / etiology,  pathology,  physiopathology
Inhalation Exposure
Male
Mice
Mice, Inbred C57BL
Myocardial Contraction
Myocytes, Cardiac / metabolism,  pathology
Myosin Heavy Chains / metabolism
Particulate Matter / toxicity*
Phenotype
Protein Isoforms
Risk Assessment
Sarcoplasmic Reticulum / metabolism,  pathology
Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism
Time Factors
Ventricular Function, Left*
Ventricular Remodeling*
Grant Support
ID/Acronym/Agency:
ES015146/ES/NIEHS NIH HHS; ES016588/ES/NIEHS NIH HHS; ES017290/ES/NIEHS NIH HHS; ES017412/ES/NIEHS NIH HHS; ES018900/ES/NIEHS NIH HHS; ES019616/ES/NIEHS NIH HHS; R01 ES018900/ES/NIEHS NIH HHS; R01 ES019923/ES/NIEHS NIH HHS; R01ES019923/ES/NIEHS NIH HHS; R01HL5604-12/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Myosin Heavy Chains; 0/Particulate Matter; 0/Protein Isoforms; 7440-70-2/Calcium; 9007-34-5/Collagen; EC 3.6.3.8/Atp2a2 protein, mouse; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases
Comments/Corrections

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