Interactions between Estradiol-17β-BSA and Calcitropic Hormones in Ca<SUP>2&#8290;</SUP> Uptake in Renal Proximal Tubule Cells

Interactions between Estradiol-17β-BSA and Calcitropic Hormones in Ca<SUP>2&#8290;</SUP> Uptake in Renal Proximal Tubule Cells

<P> The aim of the present study was to investigate the interaction of estradiol-17β-bovine serum albumin (E<SUB>2</SUB>-BSA) and calcitropic hormones, such as parathyroid hormone, calcitonin, and vitamin D, in regulation of Ca<SUP>2&#8290;</SUP> uptake in primary cultured renal proximal tubule cells. Statistically significant increase in Ca<SUP>2&#8290;</SUP> uptake was found from 2 hours after E<SUB>2</SUB>-BSA (10<SUP>&#8291;9</SUP> M) treatment, while estradiol-17β (10<SUP>&#8291;9</SUP> M) did not affect. Treatment of the cells with E<SUB>2</SUB>-BSA (10<SUP>&#8291;9</SUP> M) together with parathyroid hormone (PTH) (10<SUP>&#8291;8</SUP> M), vitamin D (10<SUP>&#8291;8</SUP> M), or calcitonin (10<SUP>&#8291;8</SUP> M) significantly stimulated Ca<SUP>2&#8290;</SUP> uptake by 32.50%, 29.30%, or 27.75%, respectively, compared with the control. However, calcitropic hormones did not exhibit any synergistic effect on the E<SUB>2</SUB>-BSA-induced stimulation. E<SUB>2</SUB>-BSA significantly increased cAMP generation and PKC activity. The stimulatory effect of cotreatment of E<SUB>2</SUB>-BSA and PTH or vitamin D was blocked by SQ22536 (an adenylate cyclase inhibitor) and staurosporine (a PKC inhibitor), but the effect of cotreatment of E<SUB>2</SUB>-BSA and calcitonin was not blocked. Furthermore, 8-Br-cAMP and TPA (an artificial PKC promoter) increased Ca<SUP>2&#8290;</SUP> uptake by 25.51% and 16.47%, respectively, compared with the control. In conclusion, E<SUB>2</SUB>-BSA combined with calcitropic hormones regulated Ca<SUP>2&#8290;</SUP> uptake partially via cAMP and PKC-dependent mechanisms in renal proximal tubule cells.