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Background <p>Preeclampsia is a multisystem disorder associated with significant maternal and fetal morbidity, yet its underlying mechanisms remain incompletely understood. Oxidative stress is believed to play a central role in its pathophysiology. This study aimed to investigate the relationship between preeclampsia and the expression of inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and transferrin receptor protein 1 (CD71) in placental and umbilical cord tissues, along with serum CD71 levels, which have not been previously examined in this context.</p> Methods <p>This prospective, observational, case–control study was conducted in the Department of Obstetrics and Gynecology at Manisa Celal Bayar University between November 2024 and May 2025. A total of 78 pregnant women were enrolled, including 39 with preeclampsia and 39 normotensive controls. Placental and umbilical cord tissues, as well as cord blood samples, were collected after delivery. Immunohistochemical staining for iNOS, eNOS, and CD71 was performed on tissue samples, and serum CD71 levels were measured using ELISA. Staining intensity and distribution were evaluated using H-scores. Statistical analyses were performed using independent t-tests, with <i>p</i> &lt; 0.05 considered significant.</p> Results <p>Gestational age and birth weight were significantly lower in the preeclampsia group (33.5 ± 2.1 weeks and 1862 ± 412&#xa0;g) than in controls (39.0 ± 1.2 weeks and 3170 ± 395&#xa0;g; <i>p</i> &lt; 0.001). Placental histopathology revealed increased fibrinoid necrosis, syncytial knots, calcifications, and endothelial proliferation in preeclampsia. Placental iNOS expression was significantly decreased, whereas eNOS and CD71 expressions were markedly increased (all <i>p</i> &lt; 0.001). In the umbilical cord, both iNOS and eNOS expressions were higher, while CD71 expression was lower in preeclampsia (all <i>p</i> &lt; 0.001). ELISA results demonstrated significantly higher serum CD71 levels in the preeclampsia group (<i>p</i> &lt; 0.05).</p> Conclusion <p>Alterations in placental and umbilical cord expression of eNOS, iNOS, and CD71 may reflect a complex interplay between oxidative stress, hypoxia, and inflammatory mechanisms in preeclampsia. Increased placental eNOS may represent a compensatory response to hypoxia, while reduced iNOS expression may be associated with chronic inflammatory processes. The elevated iNOS and eNOS expression in the umbilical cord may indicate an adaptive response to impaired uteroplacental perfusion.</p> Trial registration <p>ClinicalTrials.gov NCT06668545. Registered 30 October 2024.</p>

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A study on iNOS, eNOS, and CD71 expression in preeclampsia: findings shedding light on possible gaps in the current understanding of pathogenesis

  • 期刊论文

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  • 发表日期：

    2026年8月5日

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  • Kemal Sarsmaz,
  • Hayrunnisa Yeşil Sarsmaz,
  • Sercan Kantarcı,
  • Seren Gülşen Gürgen

摘要

Background

Preeclampsia is a multisystem disorder associated with significant maternal and fetal morbidity, yet its underlying mechanisms remain incompletely understood. Oxidative stress is believed to play a central role in its pathophysiology. This study aimed to investigate the relationship between preeclampsia and the expression of inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and transferrin receptor protein 1 (CD71) in placental and umbilical cord tissues, along with serum CD71 levels, which have not been previously examined in this context.

Methods

This prospective, observational, case–control study was conducted in the Department of Obstetrics and Gynecology at Manisa Celal Bayar University between November 2024 and May 2025. A total of 78 pregnant women were enrolled, including 39 with preeclampsia and 39 normotensive controls. Placental and umbilical cord tissues, as well as cord blood samples, were collected after delivery. Immunohistochemical staining for iNOS, eNOS, and CD71 was performed on tissue samples, and serum CD71 levels were measured using ELISA. Staining intensity and distribution were evaluated using H-scores. Statistical analyses were performed using independent t-tests, with p < 0.05 considered significant.

Results

Gestational age and birth weight were significantly lower in the preeclampsia group (33.5 ± 2.1 weeks and 1862 ± 412 g) than in controls (39.0 ± 1.2 weeks and 3170 ± 395 g; p < 0.001). Placental histopathology revealed increased fibrinoid necrosis, syncytial knots, calcifications, and endothelial proliferation in preeclampsia. Placental iNOS expression was significantly decreased, whereas eNOS and CD71 expressions were markedly increased (all p < 0.001). In the umbilical cord, both iNOS and eNOS expressions were higher, while CD71 expression was lower in preeclampsia (all p < 0.001). ELISA results demonstrated significantly higher serum CD71 levels in the preeclampsia group (p < 0.05).

Conclusion

Alterations in placental and umbilical cord expression of eNOS, iNOS, and CD71 may reflect a complex interplay between oxidative stress, hypoxia, and inflammatory mechanisms in preeclampsia. Increased placental eNOS may represent a compensatory response to hypoxia, while reduced iNOS expression may be associated with chronic inflammatory processes. The elevated iNOS and eNOS expression in the umbilical cord may indicate an adaptive response to impaired uteroplacental perfusion.

Trial registration

ClinicalTrials.gov NCT06668545. Registered 30 October 2024.