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Myosin heavy chain expression in emphysema induced hypertrophied right ventricles
Author(s) -
Mattson John P,
Helwig Bryan G
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.776.10
Subject(s) - contractility , myosin , pathogenesis , cardiology , medicine , heart failure , copd , muscle hypertrophy , right ventricular hypertrophy , lung , endocrinology , pulmonary hypertension , biology , microbiology and biotechnology
Development of right ventricular hypertrophy (RVH) is a marker of increased morbidity and mortality in chronic obstructive pulmonary disease (COPD) patients. Cor pulmonale leading to RV failure accounts for 20% of heart failure hospital admissions. To this point, we know surprisingly little about the underlying cell signaling pathways activated in this condition. Myosin heavy chains (MHC) provide structural integrity involved in myocardial contractile and functional properties. Previous reports suggest that changes in either α‐ or β‐MHC lead to alterations in contractility. Furthermore, the proportion of α‐MHC has been demonstrated to decline in heart failure. Given their critical role, a time course of emphysema‐induced alterations in RV MHC expression was measured 4 and 8 months following saline (control) or elastase (emphysema (EMP)) instillation in hamsters. Excised lung volume (>140%) and RV mass (4‐month = 18%; 8‐month = 42%) increased with EMP at both time points. There were no differences in the protein expression of either α‐ or β‐MHC in the RVs of EMP animals at any time point. However, there was a trend for increased expression of both α‐ and β‐MHC in the RVs of 8‐month compared to 4‐month EMP animals. Furthermore, the ratio of β/α ‐ MHC was decreased in the RVs of 8‐month EMP animals. These data suggest α‐ and β‐MHC may have a progressive role in the RV pathogenesis of COPD patients.

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