Primary Cilia of inv/inv Mouse Renal Epithelial Cells Sense Physiological Fluid Flow: Bending of Primary Cilia and Ca2+ Influx

Cell Structure and Function

Tetsuro Takamatsu¹  Takahiko Yokoyama²  Dai Shiba² 

[1] Department of Pathology and Cell Regulation, Graduate School of Medical Science, Kyoto Prefectural University of Medicine;Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine

关键词: primary cilia;    kidney;    Ca2+;    inv;    fluid stress;    inversin;   

DOI  :  10.1247/csf.30.93

学科分类：分子生物学，细胞生物学和基因

来源: Japan Society for Cell Biology

【 摘 要 】

References(33)Cited-By(18)Supplementary materials(3)Primary cilia are hypothesized to act as a mechanical sensor to detect renal tubular fluid flow. Anomalous structure of primary cilia and/or impairment of increases in intracellular Ca2+ concentration in response to fluid flow are thought to result in renal cyst formation in conditional kif3a knockout, Tg737 and pkd1/pkd2 mutant mice. The mutant inv/inv mouse develops multiple renal cysts like kif3a, Tg737 and pkd1/pkd2 mutants. Inv proteins have been shown to be localized in the renal primary cilia, but response of inv/inv cilia to fluid stress has not been examined. In the present study, we examined the mechanical response of primary cilia to physiological fluid flow using a video microscope, as well as intracellular Ca2+ increases in renal epithelial cells from normal and inv/inv mice in response to flow stress. Percentages of ciliated cells and the length of primary cilia were not significantly different between primary renal cell cultures from normal and inv/inv mutant mice. Localization of inv protein was restricted to the base of primary cilia even under flow stress. Inv/inv mutant cells had similar bending mechanics of primary cilia in response to physiological fluid flow compared to normal cells. Furthermore, no difference was found in intracellular Ca2+ increases in response to physiological fluid flow between normal and inv/inv mutant cells. Our present study suggests that the function of the inv protein is distinct from polaris (the Tg737 gene product), polycystins (pkd1 and pkd2 gene products).

【 授权许可】

Unknown