Progesterone (P4) is a steroid hormone synthesized in the ovary, placenta and adrenal gland, and required for ovulation and pregnancy. It controls the neural signal for ovulation, prepares the uterus for implantation and maintenance of pregnancy, regulates ovarian granulosa cell function, alters fallopian tube cilia, and plays a role in breast development. More recently, P4 has been shown to also regulate a wide range of non-reproductive functions including neurogenesis, neuroprotection, mood alteration, lymphocyte production, oxidative metabolism, glucose tolerance and cancer progression.
The classical mechanism of P4 action involves binding to the progestin receptor (PgR) and activation of gene transcription. However, P4 also acts through the PgR to trigger rapid non-genomic effects through such signaling systems as the mitogen-activated protein kinase and c-Src pathways. Additionally, P4 exerts effects in the absence of PgR. At least some of these effects are mediated by novel progestin signaling molecules including membrane progesterone receptor-alpha (mPRa), mPRß, mPR?, progesterone receptor membrane component-1 (PGRMC1), PGRMC2, plasminogen activator inhibitor 1 (PAIRBP1) and neudesin.
This Research Topic will provide a comprehensive overview of the non-classical P4 signaling mechanisms. We encourage mini-reviews on any of the topics described above.
Progesterone (P4) is a steroid hormone synthesized in the ovary, placenta and adrenal gland, and required for ovulation and pregnancy. It controls the neural signal for ovulation, prepares the uterus for implantation and maintenance of pregnancy, regulates ovarian granulosa cell function, alters fallopian tube cilia, and plays a role in breast development. More recently, P4 has been shown to also regulate a wide range of non-reproductive functions including neurogenesis, neuroprotection, mood alteration, lymphocyte production, oxidative metabolism, glucose tolerance and cancer progression.
The classical mechanism of P4 action involves binding to the progestin receptor (PgR) and activation of gene transcription. However, P4 also acts through the PgR to trigger rapid non-genomic effects through such signaling systems as the mitogen-activated protein kinase and c-Src pathways. Additionally, P4 exerts effects in the absence of PgR. At least some of these effects are mediated by novel progestin signaling molecules including membrane progesterone receptor-alpha (mPRa), mPRß, mPR?, progesterone receptor membrane component-1 (PGRMC1), PGRMC2, plasminogen activator inhibitor 1 (PAIRBP1) and neudesin.
This Research Topic will provide a comprehensive overview of the non-classical P4 signaling mechanisms. We encourage mini-reviews on any of the topics described above.
