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• W2157130211 abstract "Background We reported previously that Brown Norway ( BN ) rats are more resistant to myocardial ischemia/reperfusion (I/R) injury than are Dahl S ( SS ) rats. To identify the unique genes differentially expressed in the hearts of these rats, we used DNA microarray analysis and observed that enoyl coenzyme A hydratase–containing domain 2 ( ECHDC 2) is highly expressed (≈18‐fold) in the SS hearts compared with the BN hearts. Methods and Results RT ‐ PCR , W estern blot, and immunohistochemistry analyses verified that ECHDC 2 was highly expressed in SS hearts compared with the BN hearts. ECHDC 2 gene locates at chromosome 5 of rat and is expressed in mitochondria of the heart, mainly in cardiomyocytes but not in cardiofibroblasts. Overexpression of ECHDC 2 in cells increased susceptibility to I/R injury while knockdown of ECHDC 2 enhanced resistance to I/R injury. Furthermore, we observed that left anterior descending coronary artery ligation–induced myocardial infarction was more severe in the SS hearts than in the BN hearts or SSBN 5 hearts, which was built on SS rats but had the substitution of chromosome 5 from BN rats. We also demonstrated that ECHDC 2 did not alter mitochondrial O 2 consumption, metabolic intermediates and ATP production. By gas chromatography–mass spectrometry, we found that ECHDC 2 overexpression increased the levels of the cellular branched chain amino acids leucine and valine. Conclusion ECHDC 2, a mitochondrial protein, may be involved in regulating cell death and myocardial injury. Its deficiency in BN rats contributes to their increased resistance to myocardial I/R compared with SS rats. ECHDC 2 increases branched chain amino acid metabolism and appears to be a novel regulator linking cell metabolism with cardiovascular disease." @default.
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• W2157130211 date "2013-09-26" @default.
• W2157130211 modified "2023-10-16" @default.
• W2157130211 title "Enoyl Coenzyme A Hydratase Domain–Containing 2, a Potential Novel Regulator of Myocardial Ischemia Injury" @default.
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• W2157130211 doi "https://doi.org/10.1161/jaha.113.000233" @default.
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