The placental syncytium and the pathophysiology of preeclampsia and intrauterine growth restriction: A novel assay to assess syncytial protein expression

Annals of the New York Academy of Sciences

Volumn 1127, Issue , 2008, Pages 129-133

  Guller, Seth ^a   Ma, Yula Y ^a   Fu, Han Hsuan ^a   Krikun, Graciela ^a   Abrahams, Vikki M ^a   Mor, Gil ^a  

^a YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Apoptosis; Fas ligand; IUGR; Laser capture microdissection; Pathophysiology of preeclampsia; Placenta; Reactive oxygen species; Syncytiotrophoblast

Indexed keywords

PLASMINOGEN ACTIVATOR INHIBITOR 1; REACTIVE OXYGEN METABOLITE;

APOPTOSIS; CELL INTERACTION; CELL STRUCTURE; CONFERENCE PAPER; FEMALE; GROWTH RETARDATION; HUMAN; HUMAN TISSUE; HYPOXIA; INTRAUTERINE GROWTH RESTRICTION; MICRODISSECTION; PATHOPHYSIOLOGY; PLACENTA; PLACENTAL SYNCYTIUM; PREECLAMPSIA; PREGNANCY COMPLICATION; REPERFUSION INJURY; WESTERN BLOTTING;

EID: 42449130107     PISSN: 00778923     EISSN: 17496632     Source Type: Book Series    
DOI: 10.1196/annals.1434.015     Document Type: Conference Paper

References (32)

1. Redman, C.W. & I.L. Sargent. 2005. Latest advances in understanding preeclampsia. Science 308 : 1592 1594.
2. Kaufmann, P. et al. 2003. Endovascular trophoblast invasion: implications for the pathogenesis of intrauterine growth retardation and preeclampsia. Biol. Reprod. 69 : 1 7.
3. Stepan, H. et al. 2006. New insights into the biology of preeclampsia. Biol. Reprod. 74 : 772 776.
4. Benirschke, K. 1998. Remarkable placenta. Clin. Anat. 11 : 194 205.
5. Benyo, D.F. et al. 2001. Expression of inflammatory cytokines in placentas from women with preeclampsia. J. Clin. Endocrinol. Metab. 86 : 2505 2512.
6. Conrad, K.P. et al. 1998. Circulating levels of immunoreactive cytokines in women with preeclampsia. Am. J. Reprod. Immunol. 40 : 102 111.
7. Walsh, S.W. et al. 2000. Placental isoprostane is significantly increased in preeclampsia. Faseb. J. 14 : 1289 1296.
8. Myatt, L. & X. Cui. 2004. Oxidative stress in the placenta. Histochem. Cell. Biol. 122 : 369 382.
9. Sikkema, J.M. et al. 2001. Placental superoxide is increased in pre-eclampsia. Placenta 22 : 304 308.
10. Maynard, S.E. et al. 2003. Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. J. Clin. Invest. 111 : 649 658.
11. Venkatesha, S. et al. 2006. Soluble endoglin contributes to the pathogenesis of preeclampsia. Nat. Med. 12 : 642 649.
12. Goswami, D. et al. 2006. Excess syncytiotrophoblast microparticle shedding is a feature of early-onset pre-eclampsia, but not normotensive intrauterine growth restriction. Placenta 27 : 56 61.
13. Knight, M. et al. 1998. Shedding of syncytiotrophoblast microvilli into the maternal circulation in pre-eclamptic pregnancies. Br. J. Obstet. Gynaecol. 105 : 632 640.
14. Poston, L. & M.T. Raijmakers. 2004. Trophoblast oxidative stress, antioxidants and pregnancy outcome - a review. Placenta 25 (Suppl A S72 78.
15. Many, A. et al. 2000. Invasive cytotrophoblasts manifest evidence of oxidative stress in preeclampsia. Am. J. Pathol. 156 : 321 331.
16. Myatt, L. et al. 1996. Nitrotyrosine residues in placenta. Evidence of peroxynitrite formation and action. Hypertension 28 : 488 493.
17. Ishihara, N. et al. 2002. Increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or intrauterine growth retardation. Am. J. Obstet. Gynecol. 186 : 158 166.
18. Levy, R. et al. 2002. Trophoblast apoptosis from pregnancies complicated by fetal growth restriction is associated with enhanced p53 expression. Am. J. Obstet. Gynecol. 186 : 1056 1061.
19. Hung, T.H. et al. 2002. Hypoxia-reoxygenation: a potent inducer of apoptotic changes in the human placenta and possible etiological factor in preeclampsia. Circ. Res. 90 : 1274 1281.
20. Abrahams, V.M. et al. 2004. First trimester trophoblast cells secrete Fas ligand which induces immune cell apoptosis. Mol. Hum. Reprod. 10 : 55 63.
21. Runic, R. et al. 1998. Apoptosis and Fas expression in human fetal membranes. J. Clin. Endocrinol. Metab. 83 : 660 666.
22. Runic, R. et al. 1996. Expression of Fas ligand by human cytotrophoblasts: implications in placentation and fetal survival. J. Clin. Endocrinol. Metab. 81 : 3119 3122.
23. Neale, D.M. & G. Mor. 2005. The role of Fas mediated apoptosis in preeclampsia. J. Perinat. Med. 33 : 471 477.
24. Humphrey, R.G. et al. 2005. Fibrin enhances differentiation, but not apoptosis, and limits hypoxic injury of cultured term human trophoblasts. Placenta 26 : 491 497.
25. Salafia, C.M. et al. 1995. Intrauterine growth restriction in infants of less than thirty-two weeks' gestation: associated placental pathologic features. Am. J. Obstet. Gynecol. 173 : 1049 1057.
26. Salafia, C.M. et al. 1997. Placental pathology of absent and reversed end-diastolic flow in growth-restricted fetuses. Obstet. Gynecol. 90 : 830 836.
27. Estelles, A. et al. 1989. Changes in the plasma levels of type 1 and type 2 plasminogen activator inhibitors in normal pregnancy and in patients with severe preeclampsia. Blood 74 : 1332 1338.
28. Estelles, A. et al. 1994. Altered expression of plasminogen activator inhibitor type 1 in placentas from pregnant women with preeclampsia and/or intrauterine fetal growth retardation. Blood 84 : 143 150.
29. Estelles, A. et al. 1996. Abnormal expression of plasminogen activator inhibitors in patients with gestational trophoblastic disease. Am. J. Pathol. 149 : 1229 139.
30. Grancha, S. et al. 1996. Decreased expression of PAI-2 mRNA and protein in pregnancies complicated with intrauterine fetal growth retardation. Thromb. Haemost. 76 : 761 767.
31. Di Santo, S. et al. 2007. Dual in vitro perfusion of an isolated cotyledon as a model to study the implication of changes in the third trimester placenta on preeclampsia. Placenta 28 (Suppl A S23 32.
32. Guller, S. et al. 2007. Differential release of plasminogen activator inhibitors (PAIs) during dual perfusion of human placenta: implications in preeclampsia. Placenta 28 : 278 285.