PERBANDINGAN EKSPRESI PROTEIN p53 SEL TROPHOBLAS PLASENTA ANTARA PREEKLAMPSIA BERAT DENGAN KEHAMILAN NORMOTENSI

Abstract

Background: The placenta is a central focus and important in the pathogenesis of preeclampsia occurrence. Failure of trophoblast cells do remodeling spiral arteries due to excessive apoptosis causes uteroplacental ischemia and damage the endothelial cells that give rise to the clinical manifestations of preeclampsia. Excessive apoptosis in preeclampsia occurs through the intrinsic pathway of apoptosis mediated intracellular where directly from mitochondria in response to stress such as mitochondrial damage and can be activated by p53, a protein that activates the tumor suppressive action of Bcl-2 proapoptotic. Extrinsic and intrinsic pathways are not independent, because p53 can also enhance the expression of several death receptors. Objective: To compare the expression of p53 protein on pregnancy trophoblast between severe preeclampsia complicated pregnancy and normotension pregnancy. Methods of study: This study is a cross-sectional design of the study population of patients with severe preeclampsia 2011 to March 2012. Placental samples obtained from 43 pregnancies with severe preeclampsia and 38 normotensive placentas from pregnancies. Observation of P53 protein expression by immunohistochemistry technique. Statistical analysis using independent t<0.05)..32 ± 0.18). Results: There were significant differences (p = 0.00) p53 protein expression in the gestational trophoblastic tissue severe preeclampsia (1.99 ± 0.66) compared to the normotensive pregnancies (1 Conclusion: Expression of p53 protein in severe preeclampsia is higher than normotensive pregnancies