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Accumulation of type VI collagen in cardiomyopathic monkey hearts
Author(s) -
Suzuki Osamu,
Ageyama Naohide,
Terao Keiji
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.928.5
Subject(s) - western blot , cardiomyopathy , protein subunit , chemistry , staining , microbiology and biotechnology , biochemistry , biology , heart failure , medicine , pathology , gene
To clarify the etiology of cardiomyopathy, we compared heart protein profiles between normal and cardiomyopathic monkeys, which Ageyama et al. of the Tsukuba Primate Research Center discovered as a monkey model for human cardiomyopathy. Heart proteins from normal and cardiomyopathic monkeys were extracted sequentially from left ventricles into soluble, less soluble, and least soluble fractions according to their solubility using a ReadyPrep sequential extraction kit (Bio‐Rad). These fractions were separated by SDS‐PAGE. On staining the gels with SyproRuby (Invitrogen), the bands were the same for the soluble and less soluble fractions in the two groups of monkey hearts, while one unique band (~200 kDa) was found in the least soluble fraction of the cardiomyopathic hearts. Mass spectrometry and Western blot analyses suggested that the ~200 kDa protein was a collagen type VI α3‐subunit that was produced from an immature ~300 kDa form after C‐terminus cleavage. Western blot analyses confirmed the increase in collagen type VI α1‐ and α2‐subunits as well. These results suggest that the accumulation of type VI collagen is involved in the etiology of cardiomyopathy.