| Co-Investigator(Kenkyū-buntansha) |
TAKEMURA Haruo Sapporo Medical University, Lecturer, 医学部, 講師 (20106462)
HATTA Sinnnichi Sapporo Medical University, Asso. Professor, 医学部, 助教授 (60094223)
ATSUSHI Miyamoto Sapporo Medical University, Asso. Professor, 医学部, 助教授 (50166196)
TANEMOTO Masayuki Osaka Univ. Medical School, Assis. Professor, 大学院・医学系研究科, 助手 (40303945)
INANOBE Atsushi Osaka Univ. Medical School, Assis. Professor, 大学院・医学系研究科, 助手 (00270851)
|
|---|
| Research Abstract |
(3) Kir4.1 was expressed in satellite cells of cochlea ganglia. Because Kir4.1 prominently localized in myelin sheaths of satellite cells, Kir4.1 may participate in KィイD1+ィエD1 spatial buffering action of cochlea ganglia.
We found that inwardly rectifying potassium channel, Kir4.1/KィイD2abィエD2-2, was expressed in glial cell. To investigate further the distribution and function of Kir4.1, we examined various tissues and obtained following results.
(1) Using immunoelectron microscopic technique, we found that Kir4.1 co-localized with water channel, AQP4, in the membranes of retinal Muller glial cells adjacent to basal membranes. Previously, water transport has been considered to couple KィイD1+ィエD1 transport. Thus, Kir401 and AQP4 may regulate water content of neural tissues.
(2) Kir4.1 was found in retinal pigment epithelial cells, suggesting Kir4.1 participates in extracellular KィイD1+ィエD1 homeostasis of rod outer segments.
(4) Kir4.1 was expressed in gastric parietal cells. BaィイD12+aィエD1, an inhibitor of inwardly rectifying KィイD1+ィエD1 channel, suppressed acid secretion of isolated rat parietal cells, but inhibitors of voltage sensitive and CaィイD12+ィエD1-activated KィイD1+ィエD1 channels did not. Immunoelectron microscopic examination indicated that Kir4.1 localized in apical membranes but not in tubulovesicles and basolateral membranes of parietal cells. These results indicated that Kir4.1 may participate in acid secretion of stomach. Kir4.1 may export KィイD1+ィエD1 ions into gastric lumen which are imported into parietal cells by HィイD1+ィエD1. KィイD1+ィエD1-ATPase.
|
