Open AccessInteraction between human placental microvascular endothelial cells and a model of human trophoblasts: effects on growth cycle and angiogenic profile
Author(s) -
Troja Weston,
Kil Kicheol,
Klanke Charles,
Jones Helen N.
Publication year - 2014
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.1002/phy2.244
Subject(s) - paracrine signalling , autocrine signalling , trophoblast , andrology , biology , immunocytochemistry , apoptosis , angiogenesis , placental growth factor , cell growth , placenta , fetal membrane , cell culture , microbiology and biotechnology , matrigel , medicine , endocrinology , fetus , cancer research , vascular endothelial growth factor , receptor , biochemistry , pregnancy , vegf receptors , genetics
Intrauterine growth restriction ( IUGR ) is a leading cause of perinatal complications, and is commonly associated with reduced placental vasculature. Recent studies demonstrated over‐expression of IGF ‐1 in IUGR animal models maintains placental vasculature. However, the cellular environment of the placental chorionic villous is unknown. The close proximity of trophoblasts and microvascular endothelial cells in vivo alludes to autocrine/paracrine regulation following Ad‐Hu IGF ‐1 treatment. We investigated the co‐culturing of BeWo Choriocarcinoma and Human Placental Microvascular Endothelial Cells ( HPMVEC s) on the endothelial angiogenic profile and the effect Ad‐Hu IGF ‐1 treatment of one cell has on the other. HPMVECs were isolated from human term placentas and cultured in EGM‐2 at 37°C with 5% CO 2 . BeWo cells were maintained in Ham's F12 nutrient mix with 10% FBS and 1% pen/strep. Co‐cultured HPMVECS+BeWo cells were incubated in serum‐free control media, Ad‐HuIGF‐1, or Ad‐LacZ at MOI 0 and MOI 100:1 for 48 h. Non‐treated cells and mono‐cultured cells were compared to co‐cultured cells. Angiogenic gene expression and proliferative and apoptotic protein expression were analysed by RT‐ qPCR and immunocytochemistry, respectively. Statistical analyses was performed using student's t ‐test with P < 0.05 considered significant. Direct Ad‐Hu IGF ‐1 treatment increased HPMVEC proliferation ( n = 4) and reduced apoptosis ( n = 3). Co‐culturing HPMVEC s+BeWo cells significantly altered RNA expression of the angiogenic profile compared to mono‐cultured HPMVEC s ( n = 8). Direct Ad‐Hu IGF ‐1 treatment significantly increased Ang‐1 ( n = 4) in BeWo cells. Ad‐Hu IGF ‐1 treatment of HPMVEC s did not alter the RNA expression of angiogenic factors. Trophoblastic factors may play a key role in placental vascular development and IGF ‐1 may have an important role in HPMVEC growth.