Roles of claudins in kidney water and electrolyte transport

2016 Fiscal Year Final Research Report

• Project/Area Number: 25461253
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: Jichi Medical University
• Principal Investigator: MUTO SHIGEAKI 自治医科大学, 医学部, 教授 (40190855)
• Co-Investigator(Renkei-kenkyūsha): FURUSE MIKIO 自然科学研究機構生理学研究所, 脳形態解析研究部門, 教授 (90281089)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: claudin / タイトジャンクション / 細胞間短絡路 / 近位尿細管 / 集合管 / 腎臓血管内皮細胞

Outline of Final Research Achievements

In mice lacking claudin-2, which is expressed mainly at the proximal tubule tight junction, a reduction in proximal tubule paracellular Na reabsorption may completely compensate by increasing Na reabsorption from the furosemide-, thiazide-, and amiloride-sensitive distal nephron segments. Mice lacking claudin-8, which is expressed at the collecting duct tight junction, exhibited elevated fractional Ca excretion without reduced serum Ca concentrations. Mice lacking claudin-15, which is expressed only at the kidney vascular endothelial cell tight junction, showed hypercalcemia with relatively reduced fractional Ca excretion and hypomagnesemia due to elevated fractional Mg excretion. Future studies will be required to clarify the mechanisms responsible for the observed urine electrolyte disorders in mice lacking claudin-15.

Free Research Field

医歯薬学