Advanced

17 beta-Estradiol induces nongenomic effects in renal intercalated cells through G protein-coupled estrogen receptor 1

Hofmeister, Marlene Vind; Damkier, Helle Hasager; Christensen, Birgitte Monster; Olde, Björn LU ; Leeb-Lundberg, Fredrik LU ; Fenton, Robert A.; Praetorius, Helle A. and Praetorius, Jeppe (2012) In American Journal of Physiology-Renal Physiology 302(3). p.358-368
Abstract
Hofmeister MV, Damkier HH, Christensen BM, Olde B, Leeb-Lundberg LM, Fenton RA, Praetorius HA, Praetorius J. 17 beta-Estradiol induces nongenomic effects in renal intercalated cells through G protein-coupled estrogen receptor 1. Am J Physiol Renal Physiol 302: F358-F368, 2012. First published October 12, 2011; doi: 10.1152/ajprenal.00343.2011.-Steroid hormones such as 17 beta-estradiol (E2) are known to modulate ion transporter expression in the kidney through classic intracellular receptors. Steroid hormones are also known to cause rapid nongenomic responses in a variety of nonrenal tissues. However, little is known about renal short-term effects of steroid hormones. Here, we studied the acute actions of E2 on intracellular Ca2+ signaling... (More)
Hofmeister MV, Damkier HH, Christensen BM, Olde B, Leeb-Lundberg LM, Fenton RA, Praetorius HA, Praetorius J. 17 beta-Estradiol induces nongenomic effects in renal intercalated cells through G protein-coupled estrogen receptor 1. Am J Physiol Renal Physiol 302: F358-F368, 2012. First published October 12, 2011; doi: 10.1152/ajprenal.00343.2011.-Steroid hormones such as 17 beta-estradiol (E2) are known to modulate ion transporter expression in the kidney through classic intracellular receptors. Steroid hormones are also known to cause rapid nongenomic responses in a variety of nonrenal tissues. However, little is known about renal short-term effects of steroid hormones. Here, we studied the acute actions of E2 on intracellular Ca2+ signaling in isolated distal convoluted tubules (DCT2), connecting tubules (CNT), and initial cortical collecting ducts (iCCD) by fluo 4 fluorometry. Physiological concentrations of E2 induced transient increases in intracellular Ca2+ concentration ([Ca2+](i)) in a subpopulation of cells. The [Ca2+](i) increases required extracellular Ca2+ and were inhibited by Gd3+. Strikingly, the classic E2 receptor antagonist ICI 182,780 also increased [Ca2+](i), which is inconsistent with the activation of classic E2 receptors. G proteincoupled estrogen receptor 1 (G.PER1 or GPR30) was detected in microdissected DCT2/CNT/iCCD by RT-PCR. Stimulation with the specific GPER1 agonist G-1 induced similar [Ca2+](i) increases as E2, and in tubules from GPER1 knockout mice, E2, G-1, and ICI 182,780 failed to induce [Ca2+](i) elevations. The intercalated cells showed both E2-induced concanamycin-sensitive H+-ATPase activity by BCECF fluorometry and the E2-mediated [Ca2+](i) increment. We propose that E2 via GPER1 evokes [Ca2+](i) transients and increases H+-ATPase activity in intercalated cells in mouse DCT2/CNT/iCCD. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
distal renal tubules, intracellular calcium signaling, GPER1
in
American Journal of Physiology-Renal Physiology
volume
302
issue
3
pages
358 - 368
publisher
American Physiological Society
external identifiers
  • wos:000300258700008
  • scopus:84856185930
ISSN
1522-1466
DOI
10.1152/ajprenal.00343.2011
language
English
LU publication?
yes
id
346665e1-c86a-42fc-be2e-57bfb6684c82 (old id 2409533)
date added to LUP
2012-04-02 09:30:18
date last changed
2017-06-04 03:26:17
@article{346665e1-c86a-42fc-be2e-57bfb6684c82,
  abstract     = {Hofmeister MV, Damkier HH, Christensen BM, Olde B, Leeb-Lundberg LM, Fenton RA, Praetorius HA, Praetorius J. 17 beta-Estradiol induces nongenomic effects in renal intercalated cells through G protein-coupled estrogen receptor 1. Am J Physiol Renal Physiol 302: F358-F368, 2012. First published October 12, 2011; doi: 10.1152/ajprenal.00343.2011.-Steroid hormones such as 17 beta-estradiol (E2) are known to modulate ion transporter expression in the kidney through classic intracellular receptors. Steroid hormones are also known to cause rapid nongenomic responses in a variety of nonrenal tissues. However, little is known about renal short-term effects of steroid hormones. Here, we studied the acute actions of E2 on intracellular Ca2+ signaling in isolated distal convoluted tubules (DCT2), connecting tubules (CNT), and initial cortical collecting ducts (iCCD) by fluo 4 fluorometry. Physiological concentrations of E2 induced transient increases in intracellular Ca2+ concentration ([Ca2+](i)) in a subpopulation of cells. The [Ca2+](i) increases required extracellular Ca2+ and were inhibited by Gd3+. Strikingly, the classic E2 receptor antagonist ICI 182,780 also increased [Ca2+](i), which is inconsistent with the activation of classic E2 receptors. G proteincoupled estrogen receptor 1 (G.PER1 or GPR30) was detected in microdissected DCT2/CNT/iCCD by RT-PCR. Stimulation with the specific GPER1 agonist G-1 induced similar [Ca2+](i) increases as E2, and in tubules from GPER1 knockout mice, E2, G-1, and ICI 182,780 failed to induce [Ca2+](i) elevations. The intercalated cells showed both E2-induced concanamycin-sensitive H+-ATPase activity by BCECF fluorometry and the E2-mediated [Ca2+](i) increment. We propose that E2 via GPER1 evokes [Ca2+](i) transients and increases H+-ATPase activity in intercalated cells in mouse DCT2/CNT/iCCD.},
  author       = {Hofmeister, Marlene Vind and Damkier, Helle Hasager and Christensen, Birgitte Monster and Olde, Björn and Leeb-Lundberg, Fredrik and Fenton, Robert A. and Praetorius, Helle A. and Praetorius, Jeppe},
  issn         = {1522-1466},
  keyword      = {distal renal tubules,intracellular calcium signaling,GPER1},
  language     = {eng},
  number       = {3},
  pages        = {358--368},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology-Renal Physiology},
  title        = {17 beta-Estradiol induces nongenomic effects in renal intercalated cells through G protein-coupled estrogen receptor 1},
  url          = {http://dx.doi.org/10.1152/ajprenal.00343.2011},
  volume       = {302},
  year         = {2012},
}