Study of PICK1 deficiency-induced OPA1 processing upon uncoupler Carbonyl cyanide m-chlorophenylhydrazone treatment

• Main Authors: Keng-Mao Liao, 廖耿楙
• Other Authors: Wey-Jinq Lin
• Format: Others
• Language: zh-TW
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/72476597504998131200

碩士 === 國立陽明大學 === 生物藥學研究所 === 102 === Protein interacted with C kinase-1 (PICK1) is a scaffold protein involved in a variety of cellular functions.. Our previous study found that PICK1 recruited PKCto mitochondria and stabilized the membrane potential leading to a higher resistance to epotoside-induced apoptosis. Mitochondria are dynamic organelles. Mitochondrial morphology change are associated with functional change. Previous studies of this lab showed that knockdown of PICK1 by RNA interference in NIH cells increased cell death under low glucose conditions. The cell death was associated with an increased LC3II, a known marker for autophagic cell death. In addition, increased mitochondrial fission and OPA1 processing were observed in PICK1-knockdown cell clones. In this study, I found that treatment with mitochondrial uncoupler CCCP also induced mitochondrial fission and OPA1 processing in PICK1-knockdown stable clone S8 cells. Knockdown of PICK1 caused a severe loss of mitochondrial membrane potential. Further investigation is required to elucidate how PICK1 regulates mitochondrial functions.