TITLE

Characterisation of K+ Channels in Human Fetoplacental Vascular Smooth Muscle Cells

AUTHOR(S)
Brereton, Melissa F.; Wareing, Mark; Jones, Rebecca L.; Greenwood, Susan L.
PUB. DATE
February 2013
SOURCE
PLoS ONE;Feb2013, Vol. 8 Issue 2, p1
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Adequate blood flow through placental chorionic plate resistance arteries (CPAs) is necessary for oxygen and nutrient transfer to the fetus and a successful pregnancy. In non-placental vascular smooth muscle cells (SMCs), K+ channels regulate contraction, vascular tone and blood flow. Previous studies showed that K+ channel modulators alter CPA tone, but did not distinguish between effects on K+ channels in endothelial cells and SMCs. In this study, we developed a preparation of freshly isolated CPASMCs of normal pregnancy and investigated K+ channel expression and function. CPASMCs were isolated from normal human term placentas using enzymatic digestion. Purity and phenotype was confirmed with immunocytochemistry. Whole-cell patch clamp was used to assess K+ channel currents, and mRNA and protein expression was determined in intact CPAs and isolated SMCs with RT-PCR and immunostaining. Isolated SMCs expressed α-actin but not CD31, a marker of endothelial cells. CPASMCs and intact CPAs expressed h-caldesmon and non-muscle myosin heavy chain-2; phenotypic markers of contractile and synthetic SMCs respectively. Whole-cell currents were inhibited by 4-AP, TEA, charybdotoxin and iberiotoxin implicating functional Kv and BKCa channels. 1-EBIO enhanced whole cell currents which were abolished by TRAM-34 and reduced by apamin indicating activation of IKCa and SKCa respectively. BKCa, IKCa and SKCa3 mRNA and/or protein were expressed in CPASMCs and intact CPAs. This study provides the first direct evidence for functional Kv, BKCa, IKCa and SKCa channels in CPASMCs. These cells display a mixed phenotype implicating a dual role for CPASMCs in controlling both fetoplacental vascular resistance and vasculogenesis.
ACCESSION #
87625465

 

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