Premium
Knockout of type VI collagen improves cardiac function and remodeling following myocardial infarction
Author(s) -
Luther Daniel J.,
Thodeti Charles K.,
Weihrauch Dorothee,
Patel Hemal H.,
Niesman Ingrid R.,
Bonaldo Paolo,
Chilian William M.,
Meszaros J. Gary
Publication year - 2012
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.26.1_supplement.1060.13
Subject(s) - medicine , myocardial infarction , ventricular remodeling , chemistry , type i collagen , cardiac function curve , ejection fraction , endocrinology , ultrastructure , cardiology , pathology , heart failure
Cardiac remodeling is a dynamic process that is accelerated following myocardial infarction (MI) injury. We have previously reported that in addition to type I and III collagen, type VI collagen deposition also increases in response to MI. The goal of this project was to determine whether type VI collagen influences post‐MI remodeling using mice lacking this collagen. We induced MI by occluding the LAD in wild type (WT) and collagen VI null mice ( Col6KO ) and studied remodeling 1–8 weeks following MI. Ejection fraction was significantly preserved (43.9 ± 3.3% vs. 29.1 ± 4.3% for WT) and LV chamber dilation was attenuated in the Col6KO MI group (25.8 ± 7.9% increase vs. 62.6 ± 16.5% for WT). Apoptosis was significantly decreased in Col6KO mice at day 14 compared to WT. Isolectin staining indicated baseline blood vessel density in Col6KO mice was greater than WT mice. Interstitial collagen levels were reduced 39.6 ± 9.8% and electron microscopy shows more dramatic mitochondrial and nuclear ultrastructural morphology changes in Col6KO MI mice. We conclude that the absence of type VI collagen preserves cardiac function and limits aberrant remodeling of the myocardium following MI.