The Korean Journal of Physiology and Pharmacology

The Korean Society of Pharmacology (대한약리학회)
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Interactions between Estradiol-17 ${\beta}-BSA$ and Calcitropic Hormones in $Ca^{2+}$ Uptake in Renal Proximal Tubule Cells

  • Han, Ho-Jae (Department of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University) ;
  • Lee, Yeun-Hee (Department of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University) ;
  • Seo, Eun-Ju (Department of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University)
  • Published : 2002.10.21
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Abstract

The aim of the present study was to investigate the interaction of $estradiol-17{\beta}-bovine$ serum albumin $(E_2-BSA)$ and calcitropic hormones, such as parathyroid hormone, calcitonin, and vitamin D, in regulation of $Ca^{2+}$ uptake in primary cultured renal proximal tubule cells. Statistically significant increase in $Ca^{2+}$ uptake was found from 2 hours after $(E_2-BSA)\;(10^{-9}\;M)$ treatment, while $estradiol-17{\beta}\;(10^{-9}\;M)$ did not affect. Treatment of the cells with $(E_2-BSA)\;(10^{-9}\;M)$ together with parathyroid hormone (PTH) $(10^{-8}\;M),$ vitamin D $(10^{-8}\;M),$ or calcitonin $(10^{-8}\;M)$ significantly stimulated $Ca^{2+}$ 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 E2-BSA-induced stimulation. $E_2-BSA$ significantly increased cAMP generation and PKC activity. The stimulatory effect of cotreatment of $E_2-BSA$ and PTH or vitamin D was blocked by SQ22536 (an adenylate cyclase inhibitor) and staurosporine (a PKC inhibitor), but the effect of cotreatment of $E_2-BSA$ and calcitonin was not blocked. Furthermore, 8-Br-cAMP and TPA (an artificial PKC promoter) increased $Ca^{2+}$ uptake by 25.51% and 16.47%, respectively, compared with the control. In conclusion, $E_2-BSA$ combined with calcitropic hormones regulated $Ca^{2+}$ uptake partially via cAMP and PKC-dependent mechanisms in renal proximal tubule cells.

Keywords

References

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