SIRT1 is required for mitochondrial biogenesis reprogramming in hypoxic human pulmonary arteriolar smooth muscle cells
作者： Pengyun Li , Yan Liu , Nana Burns , Ke-Seng Zhao , Rui Song
关键词: Mitochondrial biogenesis 、 SIRT3 、 Gene knockdown 、 Deacetylase activity 、 Sirtuin 1 、 Organelle biogenesis 、 Cell biology 、 TFAM 、 Biology 、 Mitochondrion
摘要: Although recent studies have reported that mitochondria are putative oxygen sensors underlying hypoxic pulmonary vasoconstriction, little is known concerning the sirtuin 1 (SIRT1)-mediated mitochondrial biogenesis regulatory program in arteriolar smooth muscle cells (PASMCs) during hypoxia/reoxygenation (H/R). We investigated epigenetic mechanism of and function human PASMCs H/R. Human were exposed to hypoxia 24-48 h reoxygenation h. The expression SIRT1 was reduced a time-dependent manner. Mitochondrial transcription factor A (TFAM) increased decreased reoxygenation, while release TFAM Lentiviral overexpression preserved SIRT3 deacetylase activity Knockdown PGC-1α suppressed effect on activity. abrogated SIRT1-mediated deacetylation cyclophilin D (CyPD). Notably, knockdown or incremental TFAM, DNA (mtDNA) content cellular ATP levels. Importantly, polydatin restored levels mtDNA In conclusion, by PGC-1α/SIRT3/CyPD mediates protective function. Polydatin improves enhancing PASMCs.
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