Casein kinase 2 inhibition impairs spontaneous and oxytocin-induced contractions in late pregnant mouse uterus

New Findings

• What is the central question of this study?

  Does the inhibition of protein kinase CK2 alter the uterine contractility?

• What is the main finding and its importance?

  Inhibition of protein kinase CK2 impaired the spontaneous and oxytocin-induced contractility in late pregnant mouse uterus. This finding suggests that CK2 is a novel pathway mediating oxytocin-induced contractility in the uterus. And thus opens up the possibility for this class of drugs to be developed as new class of tocolytics

Abstract

Protein kinase CK2 (casein kinase 2) is a ubiquitously expressed serine or threonine kinase known to phosphorylate a bulk of substrates. The aim of this study was to assess the effect of casein kinase-2 inhibition on spontaneous and oxytocin-induced uterine contractions in 19-day pregnant mice. The CK2 inhibitor, CX-4945 elicited a concentration-dependent relaxation in late pregnant mouse uterus. CX-4945 and another selective CK2 inhibitor, apigenin also inhibited the oxytocin-induced contractile response in late pregnant uterine tissue. Apigenin blunted the PGF2α response as well, but CX-4945 did not. CK2 was located in the lipid raft fractions of the cell membrane, and disruption of lipid rafts was found to reverse its effect. The results of the current study suggest that casein kinase 2 located in lipid rafts of the cell membrane, is an active regulator of spontaneous as well as oxytocin-induced uterine contractions in the late pregnant mouse.

This article is protected by copyright. All rights reserved

from Physiology via xlomafota13 on Inoreader http://ift.tt/2tkEWMy
via IFTTT