期刊
JOURNAL OF MEMBRANE BIOLOGY
卷 184, 期 1, 页码 71-79出版社
SPRINGER
DOI: 10.1007/s00232-001-0075-4
关键词
flow; calcium-induced calcium release; mechanical sensitivity; IP(3); gap junction; gadolinium
We tested the hypothesis that the primary cilium of renal epithelia is mechanically sensitive and serves as a flow sensor in MDCK cells using differential interference contrast and fluorescence microscopy. Bending the cilium, either by suction with a micropipette or by increasing the flow rate of perfusate, causes intracellular calcium to substantially increase as indicated by the fluorescent indicator, Fluo-4. This calcium signal is initiated by Ca(2+)-influx through mechanically sensitive channels that probably reside in the cilium or its base. The influx is followed by calcium release from IP(3)-sensitive stores. The calcium signal then spreads as a wave from the perturbed cell to its neighbors by diffusion of a second messenger through gap junctions. This spreading of the calcium wave points to flow sensing as a coordinated event within the tissue, rather than an isolated phenomenon in a single cell. Measurement of the membrane potential difference by microelectrode during perfusate flow reveals a profound hyperpolarization during the period of elevated intracellular calcium. We conclude that the primary cilium in MDCK cells is mechanically sensitive and responds to flow by greatly increasing intracellular calcium.
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