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ECHDC2, a novel mitochondria protein is abundantly expressed in SS rat hearts: implications for ischemia/reperfusion injury
Author(s) -
Du Jianhai,
Guan Tongju,
Yang Qiuhui,
Xu Hao,
Welak Scott,
Prichard Kirkwood A,
Camara Amadou,
Shi Yang
Publication year - 2011
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.25.1_supplement.639.19
Previously, we reported that SS rats were more susceptible to myocardial ischemia‐reperfusion (I/R) injury than BN rats. To determine potential mechanisms for this differential susceptibility, we used microarray to identify unique genes expressed in the hearts of these rats. Microarray analysis revealed that the mitochondria protein enoyl CoA hydratase containing domain 2 (ECHDC2) is highly expressed in the SS hearts compared with BN hearts. RT‐PCR, western blot analysis and histology revealed that ECHDC2 was expressed ~7 fold higher in SS hearts than in BN hearts. To determine the function of ECHDC2 in the heart, we established HEK cells stably expressing ECHDC2. Induction of ECHDC2 expression by tetracycline increased cell fatty acid‐induced but not glucose‐induced O2 consumption. Under basal conditions, ECHDC2 overexpression did not induce cell death. However, when subjected to simulated ischemia or I/R, cells with ECHDC2 were markedly more susceptible to death. Our data suggest that ECHDC2 increases susceptibility of SS rats to I/R injury in part via modulating mitochondrial bioenergetics. Our findings are the first to suggest that ECHDC2 represents a novel target to prevent ischemic heart injury.