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Dephosphorylation of acyl‐CoAs in the rat ischemic heart (982.4)
Author(s) -
Zhang Guofang,
Li Qingling,
Berthiaume Jessica,
Kemerer Mary
Publication year - 2014
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.28.1_supplement.982.4
Subject(s) - dephosphorylation , ischemia , perfusion , coenzyme a , medicine , phosphorylation , chemistry , pharmacology , endocrinology , biochemistry , enzyme , phosphatase , reductase
Ischemia and reperfusion cause injury to the heart. Metabolomics has been attempted to study the pathological mechanism of ischemia and reperfusion. Coenzyme A and its esters play essential roles in many physiological processes, such as fatty acid oxidation, lipid synthesis/remodeling, ketone body synthesis, xenobiotic metabolism, signaling pathways, and regulation via acylation and deacylation. We investigated how acyl‐CoAs in the rat hearts correspond to the ischemic and reperfusion injuries. Isolated rat (Sprague Dawley rats, 300‐350g) hearts were used for Langendorff perfusion with Krebs‐Ringer bicarbonate buffer. Heart was subjected to various ischemic durations from 5 to 30 minutes after initial 15 minutes equilibrating perfusion. Different reperfusion durations (5 and 45 minutes) after a 30‐minutes ischemia were also conducted. The data showed that: (i) acyl‐CoAs were found to lose 3’‐phosphate to form acyl‐dephospho‐CoAs in the ischemic heart; (ii) acyl‐dephospho‐CoAs constantly went up with the increasing ischemic duration, and returned to baseline after reperfusion; (iii) heart perfusion and in vitro incubation experiment indicated the link between ATP level and acyl‐CoAs dephosphorylation. The dephosphorylation of acyl‐CoA may be due to the energy demanding during the ischemia. Supported by grants from AHA award 12GRNT12050453 and Cleveland Mt. Sinai Health Care Foundation.