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DOI: 10.1055/s-2001-19134
Rapid Effects of Calciotropic Hormones on Female Rat Enterocytes: Combined Actions of 1,25(OH)2-Vitamin D3, PTH and 17β-Estradiol on Intracellular Ca2+ Regulation
Publikationsverlauf
Publikationsdatum:
18. Dezember 2001 (online)
1,25(OH)2-Vitamin D3 [1,25(OH)2D3], PTH and 17β-estradiol increase intracellular Ca2+ levels ([Ca2+]i) in rat enterocytes by stimulating inner Ca2+ store mobilization and voltage-dependent Ca2+ channels through non-genomic activation of second-messenger cascades. The participation of store-operated Ca2+ (SOC) channels in 17β-estradiol regulation of enterocyte [Ca2+]i has also been suggested. The aim of this work was to investigate whether PTH and/or 17β-estradiol exert additive or synergistic effects acting in concert with the classic intestinal calciotropic hormone 1,25(OH)2D3. Fura-2-loaded rat duodenal cells were stimulated using rPTH [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33] [34] (10 nM), 17β-estradiol (0.1 nM) or 1,25(OH)2D3 (0.1 nM). The resulting Ca2+ signal was characterized by an almost immediate rise in [Ca2+]i (within 30 s) rapidly reaching peak levels, followed by a plateau phase that remained sustained as long as the cells were exposed to the stimulus. The addition of PTH at the sustained phase induced by 1,25(OH)2D3 or, conversely, the addition of the secosteroid after the PTH-induced effect, did not induce additional increases in [Ca2+]i. Simultaneous treatment with both hormones resulted in an elevation of [Ca2+]i equivalent to the maximal level caused by either agonist alone, suggesting common components for [Ca2+]i stimulation by PTH and 1,25(OH)2D3. Treatment with 17β-estradiol at the sustained phase induced by 1,25(OH)2D3 or, conversely, treatment with the secosteroid after the 17β-estradiol effect, induced additional increments in [Ca2+]i (58 % and 63 %, respectively). Simultaneous treatment of enterocytes with both steroids potentiated their individual effects to the same extent as when added sequentially, also indicative of additive actions mediated by different sources of calcium signaling cascades. Moreover, 17β-estradiol failed to further increase the 1,25(OH)2D3-induced initial Ca2+ elevation in Ca2+-free medium, thus suggesting that extracellular influx mechanisms rather than intracellular Ca2+ mobilization account for estrogen potentiation of 1,25(OH)2D3 modulation of [Ca2+]i in duodenal cells.
Key words:
Enterocytes - Intestine - Intracellular Calcium - 1,25(OH)2D3 - - 17β-Estradiol - PTH - Non-Genomic Effects - Combined Actions
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Dr. Gabriela Picotto
Dept. Biología, Bioquímica y Farmacia
Universidad Nacional del Sur
San Juan 670
8000 Bahia Blanca
Argentina
Telefon: + 54 (291) 459 51 00, ext. 2430
Fax: + 54 (291) 459 51 30
eMail: gpicotto@criba.edu.ar