» Articles » PMID: 15834620

Parathormone Sensitivity and Responses to Protein Kinases in Subclones of Opossum Kidney Cells

Overview
Journal Pediatr Nephrol
Specialties Nephrology
Pediatrics
Date 2005 Apr 19
PMID 15834620
Citations 1
Authors
Affiliations
Soon will be listed here.
Abstract

Parathyroid hormone (PTH) inhibits sodium-dependent phosphate (Na(+)-Pi) transport in the renal proximal tubule and opossum kidney (OK) cells by mechanisms involving protein kinases (PK) A and C, and 20-hydroxyeicosatetraneoic acid (20-HETE). The magnitude of the effect of PKA and PKC on Na(+)-Pi transport in OK cells varies in different studies, suggesting that OK cell subclones are functionally heterogeneous despite their morphological similarity. We studied the effect of PTH and PK effectors in two separate sets of OK cells at two different time periods. Each group of cells were derived from the same stock, at passages 75-85. In one group of OK cells 20-HETE (10(-7 )M) induced a 24% decrease in Na-(32)Pi transport. Addition of PTH (10(-7) M) inhibited Pi transport by 44%. Addition of TPA (10(-8) M) resulted in a 32% decrease in Na-(32)Pi transport. Exposure of cells to the PKC inhibitor staurosporine (10(-7) M) induced a significant increase in Na-(32)Pi transport. Simultaneous addition of 20-HETE and staurosporine restored baseline Pi transport. Finally, Br-cAMP (10(-7) M) inhibited Na-(32)Pi transport by 32%. In another group of OK cells we reexamined the affect of these substances on Na-(32)Pi transport. 20-HETE (10(-7) M) induced a significant increase (30%) in Na-(32)Pi transport. PTH (10(-7) M) had no effect on Na-(32)Pi transport (P = 0.05). TPA (10(-8) M) induced a 42% increase in Na-(32)Pi transport (P < 0.01). Staurosporine (10(-7) M) induced a slight decrease in Na-(32)Pi transport (P < 0.05). Simultaneous addition of 20-HETE and staurosporine restored Na-(32)Pi transport to baseline levels. Finally, Br-cAMP (10(-7) M) inhibited Na-(32)Pi transport by 23%. We conclude that different groups OK cells have markedly different responses to regulators of Na-Pi cotransport.

Citing Articles

Clinical Implications of 20-Hydroxyeicosatetraenoic Acid in the Kidney, Liver, Lung and Brain: An Emerging Therapeutic Target.

Elshenawy O, Shoieb S, Mohamed A, El-Kadi A Pharmaceutics. 2017; 9(1).

PMID: 28230738 PMC: 5374375. DOI: 10.3390/pharmaceutics9010009.

References
1.
Gomes P, Xu J, Serrao P, Doria S, Jose P, Soares-da-Silva P . Expression and function of sodium transporters in two opossum kidney cell clonal sublines. Am J Physiol Renal Physiol. 2002; 283(1):F73-85. DOI: 10.1152/ajprenal.00340.2001. View

2.
Lederer E, SOHI S, Mathiesen J, Klein J . Regulation of expression of type II sodium-phosphate cotransporters by protein kinases A and C. Am J Physiol. 1998; 275(2):F270-7. DOI: 10.1152/ajprenal.1998.275.2.F270. View

3.
Silverstein D, Spitzer A, Barac-Nieto M . Hormonal regulation of sodium-dependent phosphate transport in opossum kidney cells. Horm Res. 2001; 54(1):38-43. DOI: 10.1159/000063435. View

4.
Satoh T, Cohen H, Katz A . Different mechanisms of renal Na-K-ATPase regulation by protein kinases in proximal and distal nephron. Am J Physiol. 1993; 265(3 Pt 2):F399-405. DOI: 10.1152/ajprenal.1993.265.3.F399. View

5.
Mahon M, Cole J, Lederer E, Segre G . Na+/H+ exchanger-regulatory factor 1 mediates inhibition of phosphate transport by parathyroid hormone and second messengers by acting at multiple sites in opossum kidney cells. Mol Endocrinol. 2003; 17(11):2355-64. DOI: 10.1210/me.2003-0043. View