An immunohistologic study of endothelialization of uteroplacental vessels in human pregnancy--evidence that endothelium is focally disrupted by trophoblast in preeclampsia
- PMID: 1530034
- DOI: 10.1016/s0002-9378(11)91583-x
An immunohistologic study of endothelialization of uteroplacental vessels in human pregnancy--evidence that endothelium is focally disrupted by trophoblast in preeclampsia
Abstract
Objective: Our objective was to study the endothelial status of the luminal lining of uteroplacental vessels in the human placental bed in normal and abnormal pregnancy in the third trimester.
Study design: Six placental basal plates from uncomplicated pregnancies and five from pregnancies complicated by preeclampsia (n = 3), preeclampsia and a small-for-gestational-age infant (n = 1), and diabetes mellitus (n = 1) were accessioned from the archives because of documentation of their containing uteroplacental vessels. Five placental bed biopsy specimens with intraluminal endovascular trophoblast in the third trimester were also studied. Sections were subjected to immunohistochemical analysis with monoclonal and polyclonal antibodies labeling endothelium and trophoblast.
Results: In third-trimester normal uncomplicated pregnancies the uteroplacental arteries and veins were completely endothelialized with no disruption of the endothelium. In third-trimester abnormal pregnancies the uteroplacental veins were also completely endothelialized. However, intraluminal endovascular trophoblast was seen within the uteroplacental arteries in eight of the 10 complicated pregnancies; this finding was associated with disruption of the endothelium.
Conclusion: In preeclampsia there is an aberrant wave of endovascular trophoblast migration in the third trimester, resulting in focal disruption of the endothelium. This may be responsible for the endothelial cell dysfunction thought to be of pathogenetic importance in preeclampsia.
Similar articles
-
Human trophoblast invasion and spiral artery transformation: the role of PECAM-1 in normal pregnancy, preeclampsia, and fetal growth restriction.Am J Pathol. 2001 May;158(5):1713-21. doi: 10.1016/S0002-9440(10)64127-2. Am J Pathol. 2001. PMID: 11337369 Free PMC article.
-
Endovascular trophoblast invasion: implications for the pathogenesis of intrauterine growth retardation and preeclampsia.Biol Reprod. 2003 Jul;69(1):1-7. doi: 10.1095/biolreprod.102.014977. Epub 2003 Mar 5. Biol Reprod. 2003. PMID: 12620937 Review.
-
Intercellular adhesion molecule-1 (ICAM-1) and HLA-DR antigens are expressed on endovascular cytotrophoblasts in abnormal pregnancies.Am J Reprod Immunol. 1995 Jan;33(1):47-53. doi: 10.1111/j.1600-0897.1995.tb01137.x. Am J Reprod Immunol. 1995. PMID: 7619233
-
[Pathophysiology of preeclampsia].J Gynecol Obstet Biol Reprod (Paris). 2008 Feb;37(1):16-23. doi: 10.1016/j.jgyn.2007.08.003. Epub 2007 Nov 26. J Gynecol Obstet Biol Reprod (Paris). 2008. PMID: 18036745 Review. French.
-
Divergent trophoblast invasion and apoptosis in placental bed spiral arteries from pregnancies complicated by maternal anemia and early-onset preeclampsia/intrauterine growth restriction.Am J Obstet Gynecol. 2006 Feb;194(2):557-63. doi: 10.1016/j.ajog.2005.07.035. Am J Obstet Gynecol. 2006. PMID: 16458661
Cited by
-
Failure of physiologic transformation of spiral arteries, endothelial and trophoblast cell activation, and acute atherosis in the basal plate of the placenta.Am J Obstet Gynecol. 2017 Mar;216(3):287.e1-287.e16. doi: 10.1016/j.ajog.2016.12.029. Epub 2016 Dec 27. Am J Obstet Gynecol. 2017. PMID: 28034657 Free PMC article.
-
Human trophoblast invasion and spiral artery transformation: the role of PECAM-1 in normal pregnancy, preeclampsia, and fetal growth restriction.Am J Pathol. 2001 May;158(5):1713-21. doi: 10.1016/S0002-9440(10)64127-2. Am J Pathol. 2001. PMID: 11337369 Free PMC article.
-
Biomarkers for Early Prediction and Management of Preeclampsia: A Comprehensive Review.Med Sci Monit. 2024 May 23;30:e944104. doi: 10.12659/MSM.944104. Med Sci Monit. 2024. PMID: 38781124 Free PMC article. Review.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Medical