Estrogen responsiveness of renal calbindin-D28k gene expression in rat kidney

Criddle, R.A.; Zheng, Minghao; Dick, Ian M.; Callus, Bernard A.; Prince, Richard

doi:10.1002/(sici)1097-4644(19970601)65:3<340::aid-jcb4>3.0.co;2-s

Cited by 22 publications

(8 citation statements)

References 33 publications

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“…Among postmenopausal women, however, estrogen replacement therapy resulted in unchanged or increased renal 1␣-OHase activity (30,34 (20,29,36,37). In contrast, some studies suggested a direct effect of 17␤-E 2 on Ca 2ϩ reabsorption, independent of vitamin D (3,28).…”

Section: Discussionsupporting

confidence: 87%

1,25-Dihydroxyvitamin D3-Independent Stimulatory Effect of Estrogen on the Expression of ECaC1 in the Kidney

Abel¹,

Hoenderop²,

Dardenne

et al. 2002

Journal of the American Society of Nephrology

136

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Abstract. Estrogen deficiency results in a negative Ca 2ϩ balance and bone loss in postmenopausal women. In addition to bone, the intestine and kidney are potential sites for estrogen action and are involved in Ca 2ϩ handling and regulation. The epithelial Ca 2ϩ channel ECaC1 (or TRPV5) is the entry channel involved in active Ca 2ϩ transport. Ca 2ϩ entry is followed by cytosolic diffusion, facilitated by calbindin-D 28K and/or calbindin-D 9k , and active extrusion across the basolateral membrane by the Na ϩ /Ca 2ϩ -exchanger (NCX1) and plasma membrane Ca 2ϩ -ATPase (PMCA1b). In this transcellular Ca 2ϩ transport, ECaC1 probably represents the final regulatory target for hormonal control. The aim of this study was to determine whether 17␤-estradiol (17␤-E 2 ) is involved in Ca 2ϩ reabsorption via regulation of the expression of ECaC1. The ovariectomized rat model was used to investigate the regulation of ECaC1, at the mRNA and protein levels, by 17␤-E 2 replacement therapy. Using real-time quantitative PCR and immunohistochemical analyses, this study demonstrated that 17␤-E 2 treatment at pharmacologic doses increased renal mRNA levels of ECaC1, calbindin-D 28K , NCX1, and PMCA1b and increased the protein abundance of ECaC1. Furthermore, the involvement of 1,25-dihydroxyvitamin D 3 in the effects of 17␤-E 2 was examined in 25-hydroxyvitamin D 3 -1␣-hydroxylase-knockout mice. Renal mRNA expression of calbindin-D 9K , calbindin-D 28K , NCX1, and PMCA1b was not significantly altered after 17␤-E 2 treatment. In contrast, ECaC1 mRNA and protein levels were both significantly upregulated. Moreover, 17␤-E 2 treatment partially restored serum Ca 2ϩ levels, from 1.63 Ϯ 0.06 to 2.03 Ϯ 0.12 mM. In conclusion, this study suggests that 17␤-E 2 is positively involved in renal Ca 2ϩ reabsorption via the upregulation of ECaC1, an effect independent of 1,25-dihydroxyvitamin D 3 .

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Section: Discussionsupporting

confidence: 87%

1,25-Dihydroxyvitamin D3-Independent Stimulatory Effect of Estrogen on the Expression of ECaC1 in the Kidney

Abel¹,

Hoenderop²,

Dardenne

et al. 2002

Journal of the American Society of Nephrology

136

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“…In keeping with these findings, another study in rats found that estradiol's ability to increase intestinal calcium absorption was independent of 1,25(OH) 2 D 3 [201]. A study by Criddle et al [202] suggests the decrease in renal calcium excretion associated with estrogen replacement is independent of 1,25(OH) 2 D 3 and may be dependent on increased expression of calbindin D28k protein, located in the distal renal tubule. Furthermore, Liel et al [203] found that the administration of estrogen to ovariectomized rats was found to increase intestinal calcium absorption by increasing the activity of duodenal vitamin D receptors (VDRs), rather than increasing levels of 1,25(OH) 2 D 3 .…”

Section: Estradiolsupporting

confidence: 76%

Drug and Hormone Effects on Vitamin D Metabolism

Weinstein¹,

Epstein²

2011

Vitamin D

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“…Only 18% of this increase in basal output can be accounted for by the increase in the serum (ultrafiltrable) calcium concentration; the rest is associated with the reduced tubular reabsorption of calcium that we have previously reported [14,15] and that is compatible with the in vitro effect of estrogen on calcium transport in the kidney [28]. This fall in TmCa is not due to a fall in serum PTH (which tends to rise) and suggests the loss of a direct effect of estrogen on renal tubular calcium transport, presumably mediated by the estrogen receptors in the kidney [29].…”

Section: Discussionmentioning

confidence: 99%

Biochemical Variables in Pre- and Postmenopausal Women: Reconciling the Calcium and Estrogen Hypotheses

Nordin

Need

Morris

et al. 1999

Osteoporosis International

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There is controversy as to whether the rise in urinary calcium at the menopause is the cause or the result of the rise in bone resorption at that time. In an attempt to resolve this issue, we have compared the relevant biochemical variables in 102 premenopausal volunteers (mean age 37 years; range 21-52) and 86 apparently normal postmenopausal women (mean age 55 years; range 40-60). We measured the fasting serum calcium, creatinine, proteins, electrolytes and intact parathyroid hormone (PTH), and the urinary calcium and creatinine both after an overnight fast and in a 24-h collection. We calculated serum calcium fractions, creatinine clearance and the notional tubular maximum reabsorptive capacity for calcium. Creatinine excretion and clearance were lower in the post- than in the premenopausal women after correction for surface area and age. Total serum calcium was higher in the post- than in the premenopausal women but this was accounted for by the higher ligand concentrations in the former. Fasting and 24-h urinary calcium were also higher in the post- than in the premenopausal women due in part to the former's higher filtered load of calcium (due to their higher serum complexed calcium) but mainly to their reduced tubular reabsorption of calcium despite their slightly raised serum PTH. Our analysis resolves the rise in urinary calcium at the menopause into its two components: increased filtered load and reduced tubular reabsorption. The changes in these two variables, neither of which can be attributed to increased bone resorption, produce an increase in calcium requirement that is sufficient to account for postmenopausal bone loss. However, the translation of this menopausal increase in calcium requirement into an increase in bone resorption at near-normal serum PTH levels requires some menopause-dependent change in the responsiveness of the bone to calcium demand. We suggest that this change may occur at the level of the osteoclasts and that estrogen may modify the calcium feedback setpoint in these cells in a manner analogous to calcitonin. This model resolves the apparent conflict between the estrogen and calcium hypotheses and explains the synergism between these two treatment modalities.

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Estrogen responsiveness of renal calbindin-D28k gene expression in rat kidney

Cited by 22 publications

References 33 publications

1,25-Dihydroxyvitamin D3-Independent Stimulatory Effect of Estrogen on the Expression of ECaC1 in the Kidney

1,25-Dihydroxyvitamin D3-Independent Stimulatory Effect of Estrogen on the Expression of ECaC1 in the Kidney

Drug and Hormone Effects on Vitamin D Metabolism

Biochemical Variables in Pre- and Postmenopausal Women: Reconciling the Calcium and Estrogen Hypotheses

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