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Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
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Prokineticin1 and pregnancy.

Nadia Alfaidy1

  • 1Institut national de la santé et de la recherche médicale, unité 1036, University Grenoble-Alpes, 38041 Grenoble, France; Commissariat à l'énergie atomique (CEA), BIG-Biology of Cancer and Infection, 38054 Grenoble, France.

Annales D'Endocrinologie
|May 14, 2016
PubMed
Summary

Prokineticin 1 (PROK1) plays a key role in placental development and pregnancy. Dysregulation of PROK1 is linked to preeclampsia and intra-uterine growth restriction.

Keywords:
EG-VEGFIUGRParturitionPlacentaPreeclampsiaProkineticinProkinéticinePré-eclampsieRCIU

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Area of Science:

  • Reproductive biology
  • Endocrinology
  • Developmental biology

Background:

  • Prokineticin 1 (PROK1) is an 86-amino acid peptide functioning through G-protein coupled receptors PROKR1 and PROKR2.
  • PROK1 is significantly expressed in the placenta, suggesting a crucial role in pregnancy.

Purpose of the Study:

  • To investigate the expression and function of PROK1 during normal and pathological pregnancies.
  • To elucidate the role of PROK1 in human placentation, trophoblast behavior, and angiogenesis.

Main Methods:

  • Analysis of PROK1 expression in placental tissue under various conditions (e.g., hypoxia).
  • Assessment of PROK1's effects on trophoblast cell migration, invasion, proliferation, and survival.
  • Measurement of circulating PROK1 levels in pregnant women and correlation with pregnancy complications.
  • In vivo studies in mice to model PROK1-related pregnancy pathologies.

Main Results:

  • PROK1 expression peaks in early pregnancy before feto-maternal circulation establishment.
  • PROK1 inhibits trophoblast migration/invasion but promotes proliferation and survival.
  • PROK1 is a placental pro-angiogenic factor, enhancing endothelial cell activity.
  • Circulating PROK1 levels are elevated in the first trimester and higher in preeclampsia (PE) and isolated intra-uterine growth restriction (IUGR) cases.
  • Elevated PROK1 in mice mimics PE symptoms.

Conclusions:

  • PROK1 is a central factor in human placentation, regulating trophoblast invasion and villous growth.
  • Impaired PROK1 signaling may contribute to the development of PE and IUGR.
  • PROK1 also influences parturition.