Proteomic analysis reveals virus-specific Hsp25 modulation in cardiac myocytes.

Proteomic analysis reveals virus-specific Hsp25 modulation in cardiac myocytes.
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DOI:
10.1021/pr901151k
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发表时间:
2010-05-07
影响因子:
4.4
通讯作者:
Sherry, Barbara
Sherry, Barbara
中科院分区:
生物学2区
文献类型:
--
作者:
Li, Lianna;Sevinsky, Joel R.;Rowland, Megan D.;Bundy, Jonathan L.;Stephenson, James L.;Sherry, Barbara

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Viruses frequently infect the heart but clinical myocarditis is rare, suggesting that the cardiac antiviral response is uniquely effective. Indeed, the Type I interferon (IFN) response is cardiac cell type-specific and provides one integrated network of protection for the heart. Here, a proteomic approach was used to identify additional proteins that may be involved in the cardiac antiviral response. Reovirus-induced murine myocarditis reflects direct viral damage to cardiac cells, and offers an excellent system for study. Primary cultures of murine cardiac myocytes were infected with myocarditic or non-myocarditic reovirus strains, and whole cell lysates were compared by two-dimensional difference gel electrophoresis (2D-DIGE) and matrix-assisted laser desorption / ionization – time-of-flight (MALDI-TOF/TOF) tandem mass spectrometry. Results were quantitative and reproducible, and demonstrated that whole proteome changes clustered according to viral pathogenic phenotype. Moreover, the data suggest that the heat shock protein Hsp25 is modulated differentially by myocarditic and non-myocarditic reoviruses and may play a role in the cardiac antiviral response. Members of seven virus families modulate Hsp25 or Hsp27 expression in a variety of cell types, suggesting that Hsp25 participation in the antiviral response may be widespread. However, results here provide the first evidence for a virus-induced decrease in Hsp25/27, and suggest that viruses may have evolved a mechanism to subvert this protective response, as they have for IFN.
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