Membrane progesterone receptor beta (mPRβ/Paqr8) promotes progesterone-dependent neurite outgrowth in PC12 neuronal cells via non-G protein-coupled receptor (GPCR) signaling

• Kasubuchi, Mayu

• Watanabe, Keita

• Hirano, Kanako

• Inoue, Daisuke

• Li, Xuan

• Terasawa, Kazuya

• Konishi, Morichika

• Itoh, Nobuyuki

• Kimura, Ikuo

Abstract

Recently, sex steroid membrane receptors garnered world-wide attention because they may be related to sex hormone-mediated unknown rapid non-genomic action that cannot be currently explained by their genomic action via nuclear receptors. Progesterone affects cell proliferation and survival via non-genomic effects. In this process, membrane progesterone receptors (mPRα, mPRβ, mPRγ, mPRδ, and mPRε) were identified as putative G protein-coupled receptors (GPCRs) for progesterone. However, the structure, intracellular signaling, and physiological functions of these progesterone receptors are still unclear. Here, we identify a molecular mechanism by which progesterone promotes neurite outgrowth through mPRβ (Paqr8) activation. Mouse mPRβ mRNA was specifically expressed in the central nervous system. It has an incomplete GPCR topology, presenting 6 transmembrane domains and did not exhibit typical GPCR signaling. Progesterone-dependent neurite outgrowth was exhibited by the promotion of ERK phosphorylation via mPRβ, but not via other progesterone receptors such as progesterone membrane receptor 1 (PGRMC-1) and nuclear progesterone receptor in nerve growth factor-induced neuronal PC12 cells. These findings provide new insights of regarding the non-genomic action of progesterone in the central nervous system.

Journal

• Scientific Reports

  Scientific Reports 7 2017-07-12

  Springer Nature

Keywords

• Hormone receptors
• Steroid hormones

Details

• CRID: 1050001335851930880
• NII Article ID: 120006364107
• ISSN: 20452322
• HANDLE: 2433/227903
• Text Lang: en
• Article Type: journal article
• Data Source:
  • IRDB
  • CiNii Articles