VEGF and eNOS Expression in Umbilical Cord from Pregnancy Complicated by Hypertensive Disorder with Different Severity

被引:26
作者
Bhavina, K. [1 ]
Radhika, J. [1 ]
Pandian, S. Sundara [1 ]
机构
[1] SRM Med Coll Hosp & Res Ctr, Kanchipuram 603203, Tamil Nadu, India
关键词
NITRIC-OXIDE SYNTHASE; ENDOTHELIAL-CELLS; GENE-EXPRESSION; NO PRODUCTION; GROWTH; PROTEIN; ANGIOGENESIS; MECHANISMS; TROPHOBLAST; INVASION;
D O I
10.1155/2014/982159
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background. Reduced blood flow in hypertensive pregnancy may influence the production vasoconstrictors; subsequently the vessel remains in highly contracted state. NO is a vasodilator; VEGF influences its synthesis by regulating eNOS production. Aim of our study was to evaluate the expression of VEGF and eNOS in different severity of hypertensive pregnancy. Methods. Study was conducted in 4 groups with 40 members: group 1-control, group 2-gestational hypertension, group 3-mild preeclampsia, and group 4-severe preeclampsia. Fetal end of umbilical cord was taken and follows IHC staining protocol for VEGF and eNOS antibody. Staining intensity were measured by semiquantitative scoring method. Mann Whitney U test was used to compare each group. Results. Decreased expression of both VEGF and eNOS was found in hypertensive condition than in normal condition. Among hypertensive group, severe preeclamptic group showed more intensity in staining than gestational hypertension and mild preeclampsia. Conclusion. Reduction of VEGF and eNOS in gestational hypertension may lead to hypoperfusion and subsequent hypoxia of fetus in hypertensive pregnancy. The developed hypoxic state may upregulate the synthesis of VEGF and thereby eNOS. Increased expression of VEGF and eNOS in severe group may be a compensatory mechanism to dilate the blood vessels and to improve blood flow of fetus.
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页数:6
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