MST3 regulated potassium homeostasis through BK channel

• Main Authors: Chen, Yi-Ting, 陳奕廷
• Other Authors: Lu, Te-Jung
• Format: Others
• Language: zh-TW
• Published: 2017
• Online Access: http://ndltd.ncl.edu.tw/handle/32812810970185888389

碩士 === 中華醫事科技大學 === 醫學檢驗生物技術系碩士班 === 105 === BK channels (Big Potassium), also called Maxi-K or slo1, are expressed in the apical membrane of the distal nephron where they could contribute to renal K(+) secretion. High potassium diet increase BK expression to handle K+ secretion, contributing to K+ homeostasis. MST3, a serine/threonine kinase belonging to Ste20 family, also is expressed in the distal nephron to regulate ENaC-mediated Na+ reabsorption. To investigate whether MST3 could regulate K+ balance, the K+ secretion, plasma K+, MST3 and BK expression were compared in WT and MST3-/- mic on high-K+ diet. In addition, the K+ secretion were compared in mice on high-K+ diet with or without BK inhibitor, paxilline administration. We found that MST3-/- mice exhibited higher plasma K+ than that of WT mice on high-K+ diet. The high potassium induced MST3 and BK expression and both the increased MST3 and BK were present on the apical membrane of DCT and CD. In contrast, less MST3 and BK were present on the apical membrane of DCT and CD in MST3-/- mice. The mice with paxilline administration also exhibited similar effect with MST3-/- mice on K+ handling. We concluded that MST3 regulated K+ homeostasis through BK channel.