Expression of heat shock protein 70 and endothelial nitric oxide synthase in placental tissue of preeclamptic and intrauterine growth-restricted pregnancies

Abstract

Ischemia, hypoxia, and elevated vascular resistance disturb placental functions by increasing oxidative stress. Heat shock protein 70 (HSP70) is an oxidative stress marker. Endothelial nitric oxide synthase (eNOS) is a nitric oxide enzyme with a key role in pathologic and physiologic angiogenesis and vasculogenesis. This study was performed to investigate the role of oxidative stress in the pathogenesis of preeclampsia and intrauterine growth-restricted (IUGR) pregnancies by comparing the levels of HSP70 and eNOS in placentas from women with these diseases and those with healthy pregnancies. HSP70 and eNOS were examined using the streptavidin-biotin-peroxidase complex technique on formalin-fixed, paraffin-embedded sections from 135 placental villous tissues obtained from normal pregnancies ( n = 45) and pregnancies complicated with preeclampsia ( n = 45) and IUGR ( n = 45). The intensity of labeling in placental tissues with antibodies to HSP70 and eNOS was scored between 0 and 3, using a semiquantitative scale. HSP70 and eNOS levels were increased in the syncytiotrophoblasts, cytotrophoblasts, and extravillous trophoblast cells of preeclamptic and IUGR placentas ( P < 0.001), compared with normal pregnancies. However, their levels were increased only in the villous endothelial cells of IUGR placentas ( P < 0.001). Oxidative stress is thought to play an important role in the pathogenesis of preeclampsia and IUGR pregnancies.