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• W1980032069 abstract "To investigate whether hypoxia-inducible factor (HIF) 1α and cyclosporin A (CsA) can regulate MICA/B expression and affect NK cytotoxicity during ischemia/reperfusion (I/R) injury. We generated an HIF-1αΔODD-expressing adenovirus which can functionally and steadily express HIF-1α during normoxia and transfected human cardiomyocytes (HCMs) to investigate whether HIF-1α, as a single factor, can upregulate MICA/B expression. Alternatively, HCMs were treated with HIF-1α RNAi or CsA, and then cultured under hypoxia/reoxygenation (H/R) condition to simulate I/R injury in vitro. Cells were collected at different time points and used for studies of gene expression and NK cytotoxicity. Expression of MICA/B in HCMs is upregulated through HIF-1α overexpression in normoxia, and inhibited by HIF-1α RNAi treatment during hypoxia-reoxygenation (H/R). NK cytotoxicity towards HCMs shows a positive correlation with HIF-1α expression. Moreover, CsA can inhibit HIF-1α and MICB expression but upregulates MICA expression during H/R. These findings suggest that proper control of HIF-1α expression via CsA dose may be a potential therapeutic approach for avoiding MIC expression, and improving the function and long-term survival of heart allografts." @default.
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• W1980032069 date "2010-07-01" @default.
• W1980032069 modified "2023-09-26" @default.
• W1980032069 title "HIF-1α accumulation upregulates MICA and MICB expression on human cardiomyocytes and enhances NK cell cytotoxicity during hypoxia-reoxygenation" @default.
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• W1980032069 doi "https://doi.org/10.1016/j.lfs.2010.05.012" @default.
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