Maternal nutrient restriction upregulates growth signaling pathways in the cotyledonary artery of cow placentomes

被引:48
作者
Zhu, M. J.
Du, M.
Hess, B. W.
Means, W. J.
Nathanielsz, P. W.
Ford, S. P.
机构
[1] Univ Wyoming, Dept Anim Sci, Laramie, WY 82071 USA
[2] Univ Wyoming, Ctr Study Fetal Programming, Laramie, WY 82071 USA
[3] Univ Texas, Hlth Sci Ctr, Ctr Pregnancy & Newborn Res, San Antonio, TX 78285 USA
关键词
cow; nutrient restriction; placentome vascularity; Akt and ERK1u/2 phosphorylation;
D O I
10.1016/j.placenta.2006.04.005
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
This study evaluated the role of MAPK/ERK1/2 and/or P13-K/Akt signaling pathways in modulating bovine placentomal vascularity in response to maternal nutrient restriction. Beef cows were randomly assigned to control fed (Control, n = 15, 100% of requirements) or nutrient restricted (NR, n = 15, 50% requirements) diets from day 30 to day 125 of gestation. Ten cows from each dietary group were necropsied on day 125 (similar to 45% gestation), and the remaining cows in each diet group were then fed control diets and necropsied on day 250 (similar to 90% gestation). At day 125 of gestation, NR cows exhibited increased (P = 0.06) COT vascularity, improved (P < 0.05) placentome efficiency (fetal weight/placentomal weight), and increased (P < 0.05) phosphorylated Akt and ERK1/2 in COT arteries compared to Control cows. By day 250, however, treatment differences in COT vascularity and phosphorylated Akt and ERK1/2 in COT arteries were lost. On both gestational days, no treatment difference was observed in the levels of phosphorylated Akt or ERK1/2 in CAR arteries. CAR vascularity was similar across treatment on day 125, but tended to be greater (P < 0.10) in NR than Control cows on day 250. These data suggest that conceptuses react to an early gestational nutrient restriction by up-regulating COT growth signaling pathways associated with angiogenesis, and that these compensations do not persist to term. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:361 / 368
页数:8
相关论文
共 41 条
[11]  
FORD SP, 2004, P SOC STUDY REPROD
[12]   Akt mediates cytoprotection of endothelial cells by vascular endothelial growth factor in an anchorage-dependent manner [J].
Fujio, Y ;
Walsh, K .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (23) :16349-16354
[13]   Vascular endothelial growth factor regulates endothelial cell survival through the phosphatidylinositol 3′-kinase Akt signal transduction pathway -: Requirement for Flk-1/KDR activation [J].
Gerber, HP ;
McMurtrey, A ;
Kowalski, J ;
Yan, MH ;
Keyt, BA ;
Dixit, V ;
Ferrara, N .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (46) :30336-30343
[14]   Maternal nutrient restriction and the fetal left ventricle: Decreased angiotensin receptor expression [J].
Gilbert, JS ;
Lang, AL ;
Nijland, MJ .
REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY, 2005, 3 (1)
[15]   Activation of the phosphatidylinositol 3-kinase/protein kinase Akt pathway mediates nitric oxide-induced endothelial cell migration and angiogenesis [J].
Kawasaki, K ;
Smith, RS ;
Hsieh, CM ;
Sun, JX ;
Chao, J ;
Liao, JK .
MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (16) :5726-5737
[16]   Intrauterine growth restriction in humans is associated with abnormalities in placental insulin-like growth factor signaling [J].
Laviola, L ;
Perrini, S ;
Belsanti, G ;
Natalicchio, A ;
Montrone, C ;
Leonardini, A ;
Vimercati, A ;
Scioscia, M ;
Selvaggi, L ;
Giorgino, R ;
Greco, P ;
Giorgino, F .
ENDOCRINOLOGY, 2005, 146 (03) :1498-1505
[17]   Fetal villosity and microvasculature of the bovine placentome in the second half of gestation [J].
Leiser, R ;
Krebs, C ;
Klisch, K ;
Ebert, B ;
Dantzer, V ;
Schuler, G ;
Hoffmann, B .
JOURNAL OF ANATOMY, 1997, 191 :517-527
[18]   Strain-induced vascular endothelial cell proliferation requires PI3K-dependent mTOR-4E-BP1 signal pathway [J].
Li, W ;
Sumpio, BE .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2005, 288 (04) :H1591-H1597
[19]  
Ma L, 2005, CELL, V121, P179, DOI 10.1016/j.cell.2005.02.031
[20]   Activated Ras induces a proangiogenic phenotype in primary endothelial cells [J].
Meadows, KN ;
Bryant, P ;
Vincent, PA ;
Pumiglia, KM .
ONCOGENE, 2004, 23 (01) :192-200