2004 Fiscal Year Final Research Report Summary
Regulatory mechanism of Na+ reabsorption by hypotonicity through regulatory volume decrease-dependent dephosphorylation of FAK.
| Project/Area Number |
15590189
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
NIISATO Naomi Kyoto Prefectural University of Medicine, Physiology, Assistant Professor, 医学研究科, 講師 (00237645)
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| Co-Investigator(Kenkyū-buntansha) |
MARUNAKA Yoshinori Kyoto Prefectural University of Medicine, Physiology, Professor, 医学研究科, 教授 (00127036)
MIYAZAKI Hiroaki Kyoto Prefectural University of Medicine, Physiology, Research Associate, 医学研究科, 助手 (30360027)
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| Project Period (FY) |
2003 – 2004
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| Keywords | Tyrosine dephophorylation / [Cl^-]_c / NPPB / Regulatory volume decrease / Foacal adhesion kinase / Hypotonic shock |
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| Research Abstract |
Epithelial Na^+ transport in the kidney is important for control of blood pressure and extracellular fluid volume and is regulated by plasma osmolality and hormones. We have already indicated that Na^+ reabsorption is stimulated by extracellular hypotonicity in renal epithelial A6 cell that is a model cell line to study regulatory mechanism of Na^+ reabsorpption. However, the regulatory mechanism behind this is not well understood. Hypotonic shock causes the initial cell swelling followed by regulatory volume decrease(RVD) which is involved in the decrease in cytosolic Cl^- concentration ([Cl^-]_c). Our aim in this study is to clarify the hypothesis that RVD has a crucial role in hyposmotic regulation of Na^+ reabsorption in renal epithelium. We found that 1)hypotonic shock reduced [Cl^-]_c through RVD process by measuring [Cl^-]_c with Cl^- fluorescence dye (N-(6-methoyquinolyl) acetoxy-acetyl-ester, MQAE), 2)hypotonic shock caused dephosphoryaltion of foacal adhesion kinase(FAK) which was abolished by blockade of RVD by NPPB (a Cl^- channel blocker), 3)blockade of RVD caused the sustained tyrosine phosphorylation of FAK, 4)hypotonicity-induced Na^+ reabsorption and epithelial Na^+ channel gene expression were abolished by blocking RVD by NPPB. Taken together these results, it is suggested that hypotonic shock stimulated Na^+ reabsorption RVD-dependent FAK tyrosine dephosphorylation in renal epithelial A6 cells.
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Research Products
(11 results)
