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Obstetrics & Gynecology 2000;96:271-276
© 2000 by The American College of Obstetricians and Gynecologists
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ORIGINAL RESEARCH

Placental Apoptosis in Preeclampsia

ALEXANDER D. ALLAIRE, MD, MSPH, KELLY A. BALLENGER, MD, STEVEN R. WELLS, MD, MICHAEL J. MCMAHON, MD, MPH and BRUCE A. LESSEY, MD, PhD

From the Divisions of Maternal-Fetal Medicine and Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.

Address reprint requests to: Alexander D. Allaire, MD, MSPH Department of Obstetrics and Gynecology University of North Carolina, Chapel Hill 214 MacNider Campus Box #7570 Chapel Hill, NC 27599-7570 E-mail: allaire{at}med.unc.edu

Objective: To determine whether preeclampsia is associated with an increase in placental apoptosis and differential expression of mediators of apoptosis.

Methods: Placental samples from 31 preeclamptic women and 31 normotensive controls were analyzed using terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling staining. Expression of Fas, Fas ligand, Bcl-2, and Bax was assessed using immunohistochemistry.

Results: The median percent apoptotic nuclei was significantly higher for the study group than for the controls (0.49 versus 0.19; P = .001), as was the median percent apoptotic nuclei in the trophoblast nuclei (0.33 versus 0.09; P < .01). Fas ligand expression was significantly less and Fas expression significantly greater in the villus trophoblast among the study subjects compared with controls. There was no difference in the expression of Bax or Bcl-2 between groups.

Conclusion: Placental apoptosis and altered expression of Fas and Fas ligand in trophoblast might influence pathogenesis or sequelae of preeclampsia.




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