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Aberrant turnover of collagen type VI in the hearts of transgenic mice harboring Galβ1,3GalNAcα2,3‐sialyltranseferase II (ST3Gal II) transgenes
Author(s) -
Suzuki Osamu,
Koura Minako,
Takano Kaoru,
Noguchi Yoko,
UchioYamada Kozue,
Matsuda Junichiro
Publication year - 2007
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.21.6.a868-a
Subject(s) - genetically modified mouse , transgene , wild type , cardiomyopathy , dilated cardiomyopathy , microbiology and biotechnology , biology , heart failure , chemistry , medicine , endocrinology , biochemistry , gene , mutant
At the EB2006 meeting, we reported dilated cardiomyopathy in 100% of homozygous mice of a transgenic mouse line harboring Galβ1,3GalNAcα2,3‐sialyltransferase type II (ST3Gal II) transgenes. To clarify its etiology, we compared heart protein profiles between wild‐type and transgenic (Tg) mice. Heart proteins were extracted sequentially according to their solubility (ReadyPrep Sample Preparation kit, Bio‐Rad) and the three fractions were separated by SDS‐PAGE. Comparing the two mice lines, no different bands were found in the first two fractions, while one different band was found in the third fraction. The protein identified as the collagen type VI α3‐subunit (COL6A3) by mass spectrometry was more abundant in 10‐week‐old Tg mice than in age‐matched wild‐type mice, although the protein disappeared from the Tg mice at the end stage (ca. 6‐month old). The protein content was apparently unchanged in wild‐type mice at these two ages. These results suggest that abnormal sialylation in the heart induces aberrant collagen turnover, which might cause cardiomyopathy. This work was supported in part by a Health and Labor Science Research Grant from MHLW, Japan.