Prosaposin regulates coenzyme Q10 levels in HepG2 cells especially those in mitochondria

2014 Fiscal Year Final Research Report

• Project/Area Number: 24500872
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Applied health science
• Research Institution: Tokyo University of Technology
• Principal Investigator: KASHIBA Misato 東京工科大学, 教養学環, 講師 (80338186)
• Co-Investigator(Kenkyū-buntansha): YAMAMOTO Yorihiro 東京工科大学, 応用生物学部, 教授 (60134475)
• Co-Investigator(Renkei-kenkyūsha): KASAHARA Emiko 大阪市立大学, 医学部, 特任講師 (30468269) ; KAGEYAMA Haruaki 桐生大学, 医療保健学部, 准教授 (00433839)
• Research Collaborator: YOSHIMURA Shinichi 東京工科大学, 非常勤講師
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: コエンザイムQ10 / プロサポシン / ミトコンドリア

Outline of Final Research Achievements

Coenzyme Q10 (CoQ10) is a key component of the mitochondrial electron transfer chain and an important antioxidant. We previously reported that saposin B (SapB) binds CoQ10 in human cells. To elucidate the physiological role of this complex, we made stable transfectants (Tf) of HepG2 that express prosaposin (Psap), precursor of saposin B. We also established Psap knockdown strain (KD). CoQ10 contents decreased in the following order: Wt-Tf > parent > KD. CoQ10 contents in mitochondrial fraction also decreased in the same order.Since CoQ10 is a component of the mitochondrial electron transfer chain, rate of oxygen consumption is measured by using clark-type electrode. Rate of oxygen consumption increased in Tf. Reduced form of CoQ10 is a strong antioxidant.　Cellular ROS levels are analyzed by using fluorescence probe DCFH-DA. DCF level was reduced in Tf. These data show that saposin B and/or its precursor Psap regulates cellular CoQ10 level and its effect in HepG2 cells.

Free Research Field

病態生化学