Blocking Calcium Channel May Delay Premature Birth (IMAGE)
Caption
Coming to terms is shown. As pregnancy advances, the phenotype of the uterine myocyte changes from one that multiplies and enlarges to permit the growth of the fetus to one at term that allows powerful uterine contractions to raise intrauterine pressure and deliver the developed fetus. The contractile myocyte phenotype is characterized by the polymerization of actin molecules to form fibers, the loss of K+ channel activity, the development of gap junctions formed by connexin 43 (Cx43). An additional mechanism proposed by Ying et al. involves an increase in plasma localization of TRPV4 Ca2+ channels as a result of decreased β-arrestins, which facilitates preterm contractions. This material relates to a paper that appeared in the Dec. 23, 2015 issue of Science Translational Medicine, published by AAAS. The paper, by R. Smith at Hunter Medical Research Institute in New Lambton, NSW, Australia, and colleagues was titled, "Reapplying the uterine brake in preterm labor."
Credit
C. Bickel / <i>Science Translational Medicine</i>
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