Dr. Canan Hurdag

Demiroglu Bilim University, Histology and Embryology, Istanbul, Turkey

Abstract Title: Exploring the Role of e-NOS and Caveolin-1 Interaction in Endothelium and Syncytiotrophoblast in Vertical Transmission of SARS-CoV-2 within the Human Placenta

Biography:

Professor Hürdağ specializes in reproductive biology, sperm physiology, and oxidative stress. Her research, published in *Acta Histochemica* and *Urology*, explores histological responses, nitric oxide synthase isoforms, and sperm damage. She led Histology and Embryology at Maltepe (2003–2011) and Istanbul Bilim University (2011–2024). An international presenter, she contributed to research on boric acid and nitric oxide in reproductive health. Awarded in 2017, she now teaches and researches at Demiroğlu Bilim University.

Research Interest:

The placenta plays a vital role in fetal protection and maternal-fetal exchange throughout pregnancy. Although vertical transmission of SARS-CoV-2 has not been definitively proven, growing evidence suggests the virus disrupts placental morphology and vascular function, potentially impacting maternal and fetal health. This study investigated whether SARS-CoV-2 can cross the placental barrier and examined the roles of Caveolin-1 and endothelial nitric oxide synthase (eNOS) in this mechanism. Placental tissues were collected from 12 pregnant women (ages 18–35) with and without SARS-CoV-2 infection, all without underlying conditions or pregnancy complications. Histological and immunohistochemical analyses—including H&E, Picrosirius Red staining, and immunofluorescence—revealed significant structural abnormalities in infected placentas. These included villous damage, perivillous fibrin deposition, hypovascularity, and decreased type III collagen. Immunohistochemistry showed significantly reduced Caveolin-1 expression in syncytiotrophoblasts and endothelial cells (p < 0.01), while eNOS expression was elevated in syncytiotrophoblasts but reduced in endothelial cells. In contrast, healthy placentas displayed intact architecture, well-organized collagen, strong Caveolin-1 expression, and typical eNOS localization in vascular endothelium. The low expression of TMPRSS2 in placental tissues may further limit SARS-CoV-2 entry. Caveolin1, a regulator of vesicular transport and eNOS signaling, may restrict viral translocation across the placental barrier. Its downregulation may serve as a defense mechanism. Altered eNOS expression may indicate endothelial dysfunction and impaired vascular integrity. These findings provide insight into the molecular changes in SARS-CoV-2-infected placentas and suggest potential therapeutic targets to protect placental function and fetal health during maternal COVID-19 infection.