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1 Department of Nutrition and Foodservice Systems, University of North Carolina at Greensboro, Greensboro, North Carolina 27402; and 2 Mineral Bioavailability Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts 02111
Calcium transport in the apical-to-basolateral
(A-to-B) or B-to-A direction was examined in cells treated with 10 nM
1,25-dihydroxyvitamin D3
[1,25(OH)2D3,
calcitriol] for up to 72 h. Net A-to-B calcium transport was
positive at all time points and increased from 0.14 ± 0.06 to 0.50 ± 0.01 nmol · well
1 · min
1
after 72 h of calcitriol treatment. Neither phenol red transport nor
transepithelial electrical resistance was altered by calcitriol treatment, suggesting that the increase in net A-to-B calcium transport
was not due to paracellular movement. Neither 25-hydroxyvitamin D3 nor 24,25-dihydroxyvitamin
D3 (100 nM, 48 h) alters basal or calcitriol-stimulated A-to-B calcium transport. Treatment with the
calmodulin antagonist trifluoperazine (50 µM) reduced
calcitriol-stimulated A-to-B Ca transport by 56%. The transcription
inhibitor actinomycin D inhibited calcitriol-regulated A-to-B calcium
transport as well as calbindin D9k
and 24-hydroxylase mRNA accumulation. These data demonstrate that
calcitriol-mediated A-to-B calcium transport in Caco-2 cells is a
specific, transcellular process that requires transcriptional events
normally mediated through the vitamin D receptor.
trifluoperazine; 24-hydroxylase; calbindin D9k
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