| pubmed-article:11687880 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11687880 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:11687880 | lifeskim:mentions | umls-concept:C0008778 | lld:lifeskim |
| pubmed-article:11687880 | lifeskim:mentions | umls-concept:C0598829 | lld:lifeskim |
| pubmed-article:11687880 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:11687880 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:11687880 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:11687880 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:11687880 | pubmed:dateCreated | 2001-11-5 | lld:pubmed |
| pubmed-article:11687880 | pubmed:abstractText | 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 Ca2+-influx through mechanically sensitive channels that probably reside in the cilium or its base. The influx is followed by calcium release from IP3-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. | lld:pubmed |
| pubmed-article:11687880 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11687880 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11687880 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11687880 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11687880 | pubmed:issn | 0022-2631 | lld:pubmed |
| pubmed-article:11687880 | pubmed:author | pubmed-author:SpringK RKR | lld:pubmed |
| pubmed-article:11687880 | pubmed:author | pubmed-author:PraetoriusH... | lld:pubmed |
| pubmed-article:11687880 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11687880 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11687880 | pubmed:volume | 184 | lld:pubmed |
| pubmed-article:11687880 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11687880 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11687880 | pubmed:pagination | 71-9 | lld:pubmed |
| pubmed-article:11687880 | pubmed:dateRevised | 2003-11-14 | lld:pubmed |
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| pubmed-article:11687880 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11687880 | pubmed:articleTitle | Bending the MDCK cell primary cilium increases intracellular calcium. | lld:pubmed |
| pubmed-article:11687880 | pubmed:affiliation | NIH, NHLBI, LKEM, 10 Center Drive, Bldg. 10, Bethesda, MD 20892-1603, USA. praetorh@nhlbi.nih.gov | lld:pubmed |
| pubmed-article:11687880 | pubmed:publicationType | Journal Article | lld:pubmed |
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