Cellular and Molecular Life Sciences

, Volume 67, Issue 16, pp 2815–2824

Depletion of calcium stores contributes to progesterone-induced attenuation of calcium signaling of G protein-coupled receptors

Authors

    • Institute of Pharmaceutics and BiochemistryUniversity of Mainz
  • Jirina Slaninova
    • Institute of Organic Chemistry and Biochemistry (IOCB)Academy of Sciences of the Czech Republic (ASCR)
  • Gerald Gimpl
    • Institute of Pharmaceutics and BiochemistryUniversity of Mainz
Research Article

DOI: 10.1007/s00018-010-0360-4

Cite this article as:
Gehrig-Burger, K., Slaninova, J. & Gimpl, G. Cell. Mol. Life Sci. (2010) 67: 2815. doi:10.1007/s00018-010-0360-4

Abstract

Progesterone non-genomically attenuates the calcium signaling of the human oxytocin receptor and several other Gαq protein-coupled receptors. High progesterone concentrations are found in the endometrium during pregnancy opposing the responsiveness of the underlying myometrium to labor-inducing hormones. Here, we demonstrate that within minutes, progesterone inhibits oxytocin- and bradykinin-induced contractions of rat uteri, calcium responses induced by platelet-activating factor in the human endometrial cell line MFE-280, and oxytocin-induced calcium signals in PHM1-31 immortalized pregnant human myometrial cells. Using human embryonic kidney (HEK293) cells as model system, we analyzed the molecular mechanisms underlying these effects. Our data indicate that progesterone rapidly depletes intracellular calcium stores. The resulting desensitization of the cells might contribute to the quiescence of the uterus during pregnancy.

Keywords

Non-genomic effectOxytocinBradykininProgesteroneUterusEndoplasmic reticulumCalciumG protein-coupled receptor (GPCR)

Copyright information

© Springer Basel AG 2010