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Knockout of type VI collagen preserves mitochondrial structure and function following myocardial infarction
Author(s) -
Luther Daniel J.,
Patel Hemal,
Niesman Ingrid R.,
Kang Patrick T.,
Adapala Ravi K.,
Thoppil Roslin,
Bonaldo Paolo,
Chilian William M.,
Chenn YongRenn,
Thodeti Charles K.,
Meszaros J. Gary
Publication year - 2013
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.27.1_supplement.lb674
Subject(s) - collagen vi , mitochondrion , knockout mouse , mitochondrial fission , myocyte , medicine , chemistry , microbiology and biotechnology , biology , extracellular matrix , receptor
Cardiac remodeling is a dynamic process that is accelerated following myocardial infarction (MI) injury. Previously, fibrillar collagens type I and III have been the focus of the remodeling field however, our lab has uncovered a potentially novel role for non‐fibrillar type VI collagen (Col6) in this process. Mutations in Col6 lead to an age‐related skeletal muscle disorder known as Bethlem's Myopathy due to altered mitochondrial function and myocyte apoptosis. However, recently we were the first to report that Col6 knockout leads to a “paradoxical” improvement in post‐MI cardiac remodeling and function in Col6 −/− mice. To determine the mechanisms by which the absence of Col6 confers protection against ischemic injury, we assessed structural and functional differences of mitochondria between WT and Col6 −/− mice pre‐ and post‐MI. Electron micrographs and western blot analysis revealed differences in mitochondrial fusion/fission protein flux as early as 24 hrs. post‐MI. The basal respiratory control index (RCI) was lower in Col6 −/− mice compared to WT. However, the RCI of Col6 −/− mice did not significantly decline following MI, where as this parameter was attenuated in WT mice. Together, these data indicate that the preservation of mitochondrial morphology and respiration following MI may be an important mechanism underlying cardioprotective effects of col6 knockout in response to MI.