Differential Expression of HtrA1 and ADAM12 in Placentas from Preeclamptic and Normotensive Pregnancies
- Corresponding Author:
- Daniel A. Enquobahrie, MD
PhD, Center for Perinatal Studies
Swedish Medical Center, 1124 Columbia Street
Suite 750, Seattle, WA 98104, USA
Tel: 206 215 2595
Fax: 206 215 6995
E-mail: [email protected]
Received Date: February 23, 2012; Accepted Date: July 25, 2012; Published Date: July 27, 2012
Citation: Enquobahrie DA, Hevner K, Qiu C, Abetew DF, Sorensen TK, et al. (2012) Differential Expression of HrtA1 and ADAM12 in Placentas from Preeclamptic and Normotensive Pregnancies. Reprod Sys Sexual Disorders 1:110. doi: 10.4172/2161-038X.1000110
Copyright: © 2012 Enquobahrie DA, et al.. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: High temperature requirement factor A 1 (HtrA1) and A Disintegrin And Metalloproteinase 12 (ADAM12), which play roles in placental implantation and placental growth, have been implicated in the pathogenesis of preeclampsia.
Methods: We investigated relative mRNA expression of both genes in placental tissues from women with preeclampsia (N = 18) (average gestational age 36 weeks) and an equal number of women with normotensive pregnancies (average gestational age 39 weeks). Real-time polymerase chain reaction was used to measure mRNA extracted from term placental biopsies. Differential gene expression was evaluated using Student’s T-test and fold change analyses.
Results: Statistically significant increases in placental HtrA1 (1.69-fold, p = 0.030) and ADAM12 (1.48-fold, p =0.010) mRNA expression were observed among preeclamptic cases as compared with normotensive controls. HtrA1expression was correlated with maternal age (p-value< 0.01) among preeclampsia cases.
Conclusion: Increases in HtRA1 and ADAM12 placental gene expression in placentas from preeclamptic
pregnancies are consistent with some earlier reports of altered serum protein concentrations in preeclampticpregnancies. This adds to the literature suggesting that defects in placentation (e.g. involving trophoblast invasion) are of etiologic importance in preeclampsia.