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Novel expression and modification of the cytoskeletal protein Myozenin during hypertrophic growth
Author(s) -
Paulsson Anna Kristina,
Warburton Sarah,
MitchellJordan Scherise A,
Ren Shuxun,
Wang Yibin,
Vondriska Thomas M
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.lb66
Subject(s) - pressure overload , cytoskeleton , muscle hypertrophy , proteome , phosphatase , microbiology and biotechnology , phosphorylation , biology , cardiac hypertrophy , downregulation and upregulation , medicine , chemistry , endocrinology , bioinformatics , cell , biochemistry , gene
Cardiovascular disease is the leading cause of death in the developed world and includes growth of the heart (hypertrophy) resulting from altered mechanical and neural/hormonal factors. As a major clinical problem resultant from atherosclerosis and heart attacks, novel insights into hypertrophy are needed, in particular regarding changes in the diseased nuclear and cytoskeletal proteomes. To this end, transverse aortic constriction (TAC) was performed to induce pressure overload hypertrophy in mice. Hearts were excised between 1‐8 weeks post‐TAC, nuclei isolated and proteins separated by 2D or 1D PAGE and subjected to LC/MS/MS. Of ~1000 nuclear proteins exhibiting reproducible changes in abundance (p>0.05) after pressure overload, myozenin‐a molecular link between the phosphatase calcineurin and the structural protein α‐actinin‐was found to be upregulated. Further analysis of myozenin via immunoblotting and MS/MS revealed a truncated form that appears during hypertrophy. In addition, novel phosphorylation of residues S106, S116, T107 and T111 on myozenin‐2 was observed. Comparison of apparent mass using electrophoresis, immunoblotting and MS peptide maps revealed regions of modification on myozenin following injury. These studies add a new dimension to the role of myozenin in the heart and provide insights into nuclear‐cytoskeletal communication during cardiac hypertrophy. Support: NIH, AHA