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

التفاصيل البيبلوغرافية
العنوان: Primary Cilia of inv/inv Mouse Renal Epithelial Cells Sense Physiological Fluid Flow: Bending of Primary Cilia and Ca2+ Influx
المؤلفون: Dai Shiba, Takahiko Yokoyama, Tetsuro Takamatsu
المصدر: Cell Structure and Function. 30:93-100
بيانات النشر: Japan Society for Cell Biology, 2005.
سنة النشر: 2005
مصطلحات موضوعية: medicine.medical_specialty, TRPP Cation Channels, Physiology, Mutant, Tubular fluid, Mice, Transgenic, Biology, Kidney, urologic and male genital diseases, Gene product, Mice, Internal medicine, medicine, Animals, KIF3A, Cilia, Molecular Biology, Cells, Cultured, Microscopy, Video, Tumor Suppressor Proteins, Cilium, Membrane Proteins, Proteins, Epithelial Cells, Extracellular Fluid, Cell Biology, General Medicine, Kidney Diseases, Cystic, biochemical phenomena, metabolism, and nutrition, Mice, Mutant Strains, Cell biology, Endocrinology, medicine.anatomical_structure, Cell culture, Calcium, Intracellular, Transcription Factors
الوصف: 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).
تدمد: 1347-3700
0386-7196
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0b458095fa96f499b7be9f92a9872e3fTest
https://doi.org/10.1247/csf.30.93Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....0b458095fa96f499b7be9f92a9872e3f
قاعدة البيانات: OpenAIRE