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AJP - Gastrointestinal and Liver Physiology, Vol 262, Issue 6 945-G953, Copyright © 1992 by American Physiological Society
ARTICLES |
R. K. Wali, C. L. Baum, M. D. Sitrin, M. J. Bolt, P. K. Dudeja and T. A. Brasitus
Department of Medicine, Pritzker School of Medicine, University of Chicago, Illinois 60637.
Recent studies from our laboratory have demonstrated that the in vitro addition of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] rapidly (seconds to minutes) stimulated membrane phosphoinositide turnover, translocated protein kinase C from the cytosolic to particulate fraction, increased cytosolic calcium ([Ca2+]i), and decreased cytoplasmic pH (pHi) via inhibition of Na(+)-H+ exchange in rat colonic epithelium of dietary vitamin D-sufficient rats and in Caco-2 cells. In contrast to these prior findings, in the present experiments, 1,25(OH)2D3 failed to elicit any of these colonic biochemical responses in vitamin D-deficient animals. Bethanechol chloride also failed to alter this signal transduction pathway, [Ca2+]i, or pHi. In vivo administration of this hormone for 5-7 days, moreover, to vitamin D-deficient animals restored the rapid biochemical effects of in vitro 1,25(OH)2D3 and bethanechol chloride. These studies, therefore, indicate that alterations in the vitamin D status of rats modulate the action of 1,25(OH)2D3 and other agents on the colonic phosphoinositide signal transduction system and on [Ca2+]i, which, in turn, may influence important cellular processes in this organ such as Na(+)-H+ exchange.
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S. Khare, M. Bissonnette, B. Scaglione-Sewell, R. K. Wali, M. D. Sitrin, and T. A. Brasitus 1,25-Dihydroxyvitamin D3 and TPA activate phospholipase D in Caco-2 cells: role of PKC-alpha Am J Physiol Gastrointest Liver Physiol, April 1, 1999; 276(4): G993 - G1004. [Abstract] [Full Text] [PDF] |
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