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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #140000
Title: DIFFERENTIAL EFFECTS OF 17-BETA-ESTRADIOL AND 1,25-DIHYDROXYVITAMIN D ON CAT1 AND CALBINDIN D GENE EXPRESSION AND TRANSEPITHELIAL CALCIUM TRANSPORT IN CACO2 CELLS

Author
item WOOD, RICHARD - HNRCA
item TAPARIA, SHVETA - HNRCA
item TCHACK, LAURIE - HNRCA

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/1/2002
Publication Date: 4/1/2002
Citation: WOOD, R.J., TAPARIA, S., TCHACK, L. DIFFERENTIAL EFFECTS OF 17-BETA-ESTRADIOL AND 1,25-DIHYDROXYVITAMIN D ON CAT1 AND CALBINDIN D GENE EXPRESSION AND TRANSEPITHELIAL CALCIUM TRANSPORT IN CACO2 CELLS. JOURNAL OF FEDERATION OF AMERICAN SOCIETIES FOR EXPERIMENTAL BIOLOGY. 16: A462, 2002.

Interpretive Summary:

Technical Abstract: Estrogen deficiency has been associated with low intestinal calcium (Ca) absorption and increased bone loss. Studies in experimental animals and humans have shown that estrogen treatment has a positive effect on calcium absorption. However, it is unclear whether estrogen has a direct effect on calcium transport at the level of the enterocyte. Since enterocytes have a nuclear receptor for estrogen, the objective of this study was to determine if 17-b-estradiol (E2) treatment increases Ca transport across a monolayer of Caco-2 cells, a human intestinal cell line, grown on permeable filter supports and if E2 affects the expression of CaT1 and calbindin D9K mRNA, two genes whose products are believed to be important in regulating intestinal Ca absorption. The presence of the estrogen receptor in Caco-2 cells was first confirmed by Western blotting. Then, in a 2 x 2 factorial design study, cells were treated for 48h on day 15 in culture with 100nM 17-b estradiol, or 100nM 1,25-dihydroxyvitamin D3, or with both hormones, or vehicle alone as a control in phenol red-free DMEM. Transepithelial Ca transport was significantly increased by 1,25-dihydroxyvitamin D treatment. In addition, vitamin D treatment significantly increased the expression of CaT1 and calbindin D, consistent with a putative role of these proteins in regulating cellular Ca transport. In contrast, estrogen had no effect on any of these parameters. We conclude that E2 does not directly modulate Ca transport in Caco-2 cells presumably due to an inability to up regulate the expression of CaT1 and calbindin D.