Interactions between Estradiol-17beta-BSA and Calcitropic Hormones in Ca2+ Uptake in Renal Proximal Tubule Cells.
- Author:
Ho Jae HAN
1
;
Yeun Hee LEE
;
Eun Ju SEO
Author Information
1. Department of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University, Gwangju, Korea. hjhan@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
E2-BSA;
Ca2+ uptake;
PTH;
vitamin D;
calcitonin;
cAMP;
PKC
- MeSH:
Adenylyl Cyclases;
Calcitonin;
Estradiol;
Parathyroid Hormone;
Serum Albumin;
Staurosporine;
Vitamin D
- From:The Korean Journal of Physiology and Pharmacology
2002;6(5):261-268
- CountryRepublic of Korea
- Language:English
-
Abstract:
The aim of the present study was to investigate the interaction of estradiol-17beta-bovine serum albumin (E2-BSA) and calcitropic hormones, such as parathyroid hormone, calcitonin, and vitamin D, in regulation of Ca2+ uptake in primary cultured renal proximal tubule cells. Statistically significant increase in Ca2+ uptake was found from 2 hours after E2-BSA (10(-9) M) treatment, while estradiol-17beta (10(-9) M) did not affect. Treatment of the cells with E2-BSA (10(-9) M) together with parathyroid hormone (PTH) (10(-8) M), vitamin D (10(-8) M), or calcitonin (10(-8) M) significantly stimulated Ca2+ 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. E2-BSA significantly increased cAMP generation and PKC activity. The stimulatory effect of cotreatment of E2-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 E2-BSA and calcitonin was not blocked. Furthermore, 8-Br-cAMP and TPA (an artificial PKC promoter) increased Ca2+ uptake by 25.51% and 16.47%, respectively, compared with the control. In conclusion, E2-BSA combined with calcitropic hormones regulated Ca2+ uptake partially via cAMP and PKC-dependent mechanisms in renal proximal tubule cells.
