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Alterations in placental TGF‐beta signaling pathways in rats with placental ischemia‐induced hypertension
Author(s) -
Bauer Ashley J,
Banek Christopher T,
Regal Jean F,
Gilbert Jeffrey S
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.907.7
Subject(s) - preeclampsia , medicine , endocrinology , endoglin , ischemia , receptor , transforming growth factor , transforming growth factor beta , placenta , signal transduction , biology , fetus , pregnancy , microbiology and biotechnology , genetics , stem cell , cd34
Preeclampsia is a pregnancy‐specific condition characterized by new‐onset hypertension and decreased signaling by pro‐angiogenic factors such as transforming growth factor beta (TGF‐β). Although previous studies indicate the endogenous TGF‐β inhibitor soluble endoglin (sEng) is increased in preeclampsia and by placental ischemia, little is known about the effects of placental ischemia on other molecules in the TGF‐β signaling cascade such as the TGF‐β receptors, Smad2/3 and heat shock protein (hsp) 90. Therefore, we hypothesized that TGF‐β receptors (TGF‐βR)1, TGF‐βR2, hsp90 would be decreased in the reduced utero‐placental perfusion pressure (RUPP) model of placental ischemia‐induced hypertension in the rat. On day 14 of pregnancy (term=21), silver clips were placed on the inferior abdominal aorta and ovarian arteries to generate RUPP‐hypertension. On day 19, placentas were excised and placental TGF‐βR1, TGF‐βR2, sEng, pSmad2/3 and Hsp90 were measured by Western blot. Placental sEng and HSP 90 were increased (P<0.05) in RUPP compared to NP dams. Placental TGF‐βR2 was decreased (P<0.05) in RUPP compared to NP controls. Placental TGFβ‐R1 and pSmad2/3 were unchanged in RUPP compared to NP controls. These data indicate placental ischemia may decrease TGF‐β signaling via TGFβ‐R2 but not via Smad2 and 3 pathways. Increased HSP 90 expression may be an adaptive response to maintain TGF‐β signaling.