Premium
Phosphoproteomic profile of differentially phosphorylated proteins in human myocardium before and after cardiac surgery utilizing cardioplegia and cardiopulmonary bypass.
Author(s) -
Clements Richard T,
Ivanov Alexander R,
Smejkal Gary,
Bianchi Cesario,
Sellke Frank W
Publication year - 2010
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.24.1_supplement.601.2
Subject(s) - cardiopulmonary bypass , phosphorylation , heat shock protein , protein phosphorylation , myosin light chain kinase , tropomyosin , troponin , annexin , troponin i , cardiac surgery , medicine , cardiology , chemistry , actin , biochemistry , protein kinase a , pathology , staining , myocardial infarction , gene
Objective Cardiac surgery using cardioplegia and cardiopulmonary bypass(CP/CPB) subjects myocardium to reversible ischemic injury that can impair cardiac function. Changes in myocardial contractile activity are likely regulated in part via acute protein phosphorylation. We performed the following study to determine changes in human myocardial protein phosphorylation following CP/CPB. Methods Right atrial appendage was collected from patients pre and post‐CP/CPB and subjected to two‐dimensional electrophoresis, phospho‐protein staining, image analysis, and tandem mass spectrometry. Results 48 spots were consistently increased in the post CP/CPB group vs pre CP/CPB. There were no consistent changes in the remaining 24 consistently detected proteins post CP/CPB. Some of the identified proteins that changed in phosphorylation included: the cytoskeletal proteins tropomyosin α1, cardiac troponin I, atrial myosin light chain (MLC)‐2, atrial MLC‐4, actin, and heat shock protein 27; the metabolic proteins: ATP‐synthase subunit beta, phosphoglycerate mutase 2, and L‐lactate dehydrogenase B chain; the membrane signaling proteins 14‐3‐3εand annexin A5. Conclusion CP/CPB modifies the phosphorylation of specific cytoskeletal, metabolic, signaling, and serum proteins which may have significant implications for CP/CPB‐induced myocardial stunning. (NIH: HL046716,HL093352)