CCN6 regulates mitochondrial function.
作者： Milan Patra , Sushil K Mahata , Deepesh K Padhan , Malini Sen , None
DOI: 10.1242/JCS.186247
关键词:
摘要: Despite established links of CCN6, or Wnt induced signaling protein-3 (WISP3), with progressive pseudo rheumatoid dysplasia, functional characterization CCN6 remains incomplete. In light the documented negative correlation between accumulation reactive oxygen species (ROS) and expression, we investigated whether regulates ROS through its influence on mitochondrial function. We found that localizes to mitochondria, depletion in chondrocyte cell line C-28/I2 by using siRNA results altered electron transport respiration. Enhanced chain (ETC) activity CCN6-depleted cells was reflected increased levels association augmented ATP synthesis, membrane potential Ca(2+) Additionally, display ROS-dependent PGC1α (also known as PPARGC1A) induction, which correlates mass volume density, together morphology. Interestingly, transcription factor Nrf2 NFE2L2) repressed expression. Taken together, our suggest acts a molecular brake, is appropriately balanced Nrf2, regulating
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