Abstract

Background: During fetal development, human placenta undergoes both angiogenesis and vasculogenesis. An imbalance in proangiogenic [placental growth factor (PlGF) and vascular endothelial growth factor] and antiangiogenic factors [soluble fms like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng)] seems to play an important role in the pathophysiology of preeclampsia. Heme oxygenase-1 HO-1 is induced by ROS (reactive oxygen species) and NO (nitric oxide) and was recently discovered to be involved in angiogenesis. Methods: Hence, the present study was designed to analyze the proangiogenic and antiangiogenic role of heme oxygenase-1 and endoglin in maternal and cord blood of normotensive and preeclamptic women. Fifty pregnant women were selected and grouped as group 1 (control, n=25) comprising of normotensive women immediately after delivery; group 2 (study group) comprising of age -and sex-matched preeclamptic women. Study samples were drawn (maternal venous blood and umbilical cord blood) and heme oxygenase-1 and endoglin levels were analyzed by competitive enzymelinked immunosorbent assay. Results: Maternal and cord blood heme oxygenase-1 levels were significantly elevated in preeclamptic mothers as compared to normotensive pregnant women (p<0.001). Serum and cord blood endoglin levels were significantly lower in preeclamptic women as compared to normotensive pregnant women (p<0.001). HO-1/Eng ratio was drastically doubled in preeclamptics as compared to normotensive pregnant women. In normotensive [HO]/ [Eng+ IGF] were lower in normotensive pregnant and drastically increased in preeclamptics. Conclusion: The findings of a present study indicating a shift towards antiangiogenic profile in women with preeclampsia confirm their possible role to induce characteristic clinical manifestations of preeclampsia such as proteinuria and hypertension.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.