Beta 1 integrins in third trimester human placentae: No differential expression in pathological pregnancy

Divers, Mike; Bulmer, Judith N.; Miller, D. H.; Lilford, Richard

doi:10.1016/0143-4004(95)90112-4

Cited by 36 publications

(18 citation statements)

References 13 publications

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“…Cell culture studies have shown that integrin β1 in trophoblast has a higher than expected molecular mass due to the presence of additional, or longer, polylactosamine chains [18]. A surprising finding is the presence of substantial amounts of β1 integrin in the syncytial MVM at term, with partner subunits α3, α5 and αIIb [8,19].…”

Section: Integrins and Adhesion To Extracellular Matrixmentioning

confidence: 94%

Adhesion Molecules in Human Trophoblast – A Review. I. Villous Trophoblast

Aplin¹,

Jones²,

Harris³

2009

Placenta

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In the placental villus, cells attach to basement membrane via integrin α6β4 and adhere both laterally and apically to their neighbours. The most prominent adhesive specialisation seen in the electron microscope is the desmosome, which connects cytotrophoblast cells (CTB) laterally and also contributes to the attachment of CTB to the overlying syncytium.However, numerous cadherins and other junctional proteins are also present in the corresponding plasma membrane domains, indicating a multiplicity of adhesive interactions.Integrins, tight junction components and cadherins are all found in the syncytial microvillous membrane, perhaps reflecting its ability to form intersyncytial bridges. There is a wide gulf to be filled between molecular anatomy and functional studies, with much to be learned about the role of adhesion molecules in regulating villous epithelial integrity, homeostasis and growth.3

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Section: Integrins and Adhesion To Extracellular Matrixmentioning

confidence: 94%

Adhesion Molecules in Human Trophoblast – A Review. I. Villous Trophoblast

Aplin¹,

Jones²,

Harris³

2009

Placenta

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“…These findings suggest that pre-eclampsia is associated with failure or delay of a CTB differentiation programme, with retention of cell adhesion molecules that under normal conditions are only expressed by villous progenitor cells and CTB in the proximal region of the cell column. However, another study has reported that expression of β1 integrins in trophoblast is similar in healthy women and women with pre-eclampsia or pre-115 term labour [37]. Some heterogeneity in the expression of different integrin α subunits was noted, with variation being observed in each study group.…”

Section: Integrinsmentioning

confidence: 96%

Adhesion Molecules in Human Trophoblast – A Review. II. Extravillous Trophoblast

2009

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“…[25][26][27][28] For example reported that VCAM-1, PECAM-1 and Eselectin are not expressed on villous cytotrophoblasts but VCAM-1 and PECAM-1 are upregulated during invasion and are expressed on cytotrophoblast within the uterine wall, on endovascular cytotrophoblasts and on maternal endothelium. In contrast, three studies [29][30][31] found that, while villous endothelial cells and endothelial cells of spiral arteries were PECAM positive, all cytotrophoblast cells in villous tissue and cytotrophoblast in the placental bed and associated with spiral arteries were PECAM negative. There are a number of possibilities for these conflicting findings.…”

Section: Invading Cytotrophoblast Cells Express Endothelial Cell Adhementioning

confidence: 78%

Mechanisms regulating cytotrophoblast invasion in normal pregnancy and pre‐eclampsia

Lyall

2006

Aust NZ J Obst Gynaeco

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The placental bed underlies the placenta and includes the decidua basalis and underlying myometrium containing the uterine spiral arteries. For successful human haemochorial placentation, the placental bed spiral arteries must undergo considerable alterations. These physiological modifications are thought to be brought about by the interaction of invasive cytotrophoblast with the spiral artery vessel wall. Failure of spiral artery transformation is thought to play an important role in the sequence of events that gives rise to pre-eclampsia. The mechanisms that control human trophoblast invasion in normal, let alone abnormal pregnancy, are still poorly understood. Much of the information on the early physiological changes within the placental bed comes from studies on intact hysterectomy specimens.(1) Details of such events in late pregnancy and in pregnancies complicated by pre-eclampsia and fetal growth restriction are principally derived from the study of placental bed biopsies taken at Caesarean section. The methods of sampling the placental bed have been reviewed elsewhere.(2) Many investigators have relied on in vitro models of trophoblast invasion. In vitro models can be extremely useful in dissecting out some of these processes but may be open to artefacts. The mechanisms underlying normal and failed trophoblast invasion appear to be complex. In this manuscript the mechanisms that control the invasion of trophoblast into the decidua and myometrium are reviewed. Along with this is a review of the purported mechanisms underlying failed spiral artery transformation. Particular emphasis has been placed on topics that have been best studied.

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Beta 1 integrins in third trimester human placentae: No differential expression in pathological pregnancy

Cited by 36 publications

References 13 publications

Adhesion Molecules in Human Trophoblast – A Review. I. Villous Trophoblast

Adhesion Molecules in Human Trophoblast – A Review. I. Villous Trophoblast

Adhesion Molecules in Human Trophoblast – A Review. II. Extravillous Trophoblast

Mechanisms regulating cytotrophoblast invasion in normal pregnancy and pre‐eclampsia

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