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Article: Glycodelin-A as a paracrine regulator in early pregnancy

TitleGlycodelin-A as a paracrine regulator in early pregnancy
Authors
KeywordsFetal tolerance
Glycodelin-A
Glycosylation
Immunoendocrinology
Placentation
Issue Date2011
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/jri
Citation
Journal Of Reproductive Immunology, 2011, v. 90 n. 1, p. 29-34 How to Cite?
AbstractGlycodelin-A (GdA) is a glycoprotein secreted from the endometrial glands and decidual glandular epithelium. Given its abundance and ubiquitous distribution in the first trimester uterus, GdA may be involved in early placental development via its modulatory effect on immune and trophoblast cells. GdA inhibits activation and proliferation, and induces apoptosis of T cells. By selectively inducing Th1 cell death, GdA may shift the Th1/Th2 ratio at the feto-maternal interface. This is also achieved indirectly through enhanced expression of Fas in the Th1 cells, thus making them vulnerable to cell death through Fas ligand expressed on trophoblast, endometrial, and activated T helper cells. GdA also promotes secretion of the Th2 cytokines IL-6 and IL-13 from NK cells, and induces immunological tolerance of dendritic cells and apoptosis of monocytes. Specific glycosylation is a prerequisite for the biological activities of GdA. Reduction in α2-6 sialylation of GdA, as in gestational diabetes, is associated with impairment of its T cell apoptosis-inducing activities. This review integrates recent studies on GdA and its role as a paracrine regulator in early pregnancy. © 2011 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/135678
ISSN
2015 Impact Factor: 3.202
2015 SCImago Journal Rankings: 1.233
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, CLen_HK
dc.contributor.authorLam, KKWen_HK
dc.contributor.authorKoistinen, Hen_HK
dc.contributor.authorSeppala, Men_HK
dc.contributor.authorKurpisz, Men_HK
dc.contributor.authorFernandez, Nen_HK
dc.contributor.authorPang, RTKen_HK
dc.contributor.authorYeung, WSBen_HK
dc.contributor.authorChiu, PCNen_HK
dc.date.accessioned2011-07-27T01:39:13Z-
dc.date.available2011-07-27T01:39:13Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Reproductive Immunology, 2011, v. 90 n. 1, p. 29-34en_HK
dc.identifier.issn0165-0378en_HK
dc.identifier.urihttp://hdl.handle.net/10722/135678-
dc.description.abstractGlycodelin-A (GdA) is a glycoprotein secreted from the endometrial glands and decidual glandular epithelium. Given its abundance and ubiquitous distribution in the first trimester uterus, GdA may be involved in early placental development via its modulatory effect on immune and trophoblast cells. GdA inhibits activation and proliferation, and induces apoptosis of T cells. By selectively inducing Th1 cell death, GdA may shift the Th1/Th2 ratio at the feto-maternal interface. This is also achieved indirectly through enhanced expression of Fas in the Th1 cells, thus making them vulnerable to cell death through Fas ligand expressed on trophoblast, endometrial, and activated T helper cells. GdA also promotes secretion of the Th2 cytokines IL-6 and IL-13 from NK cells, and induces immunological tolerance of dendritic cells and apoptosis of monocytes. Specific glycosylation is a prerequisite for the biological activities of GdA. Reduction in α2-6 sialylation of GdA, as in gestational diabetes, is associated with impairment of its T cell apoptosis-inducing activities. This review integrates recent studies on GdA and its role as a paracrine regulator in early pregnancy. © 2011 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/jrien_HK
dc.relation.ispartofJournal of Reproductive Immunologyen_HK
dc.subjectFetal toleranceen_HK
dc.subjectGlycodelin-Aen_HK
dc.subjectGlycosylationen_HK
dc.subjectImmunoendocrinologyen_HK
dc.subjectPlacentationen_HK
dc.subject.meshFas Ligand Protein - immunology - metabolism-
dc.subject.meshGlycoproteins - metabolism-
dc.subject.meshPlacenta - metabolism-
dc.subject.meshPregnancy Proteins - metabolism-
dc.subject.meshTrophoblasts - immunology - metabolism-
dc.titleGlycodelin-A as a paracrine regulator in early pregnancyen_HK
dc.typeArticleen_HK
dc.identifier.emailPang, RTK: rtkpang@hku.hken_HK
dc.identifier.emailChiu, PCN: pchiucn@hku.hken_HK
dc.identifier.authorityPang, RTK=rp01761en_HK
dc.identifier.authorityChiu, PCN=rp00424en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jri.2011.04.007en_HK
dc.identifier.pmid21641661-
dc.identifier.scopuseid_2-s2.0-79960001031en_HK
dc.identifier.hkuros188137en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79960001031&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume90en_HK
dc.identifier.issue1en_HK
dc.identifier.spage29en_HK
dc.identifier.epage34en_HK
dc.identifier.eissn1872-7603-
dc.identifier.isiWOS:000293324100006-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridLee, CL=9277221100en_HK
dc.identifier.scopusauthoridLam, KKW=25637362300en_HK
dc.identifier.scopusauthoridKoistinen, H=7003612125en_HK
dc.identifier.scopusauthoridSeppala, M=35475165300en_HK
dc.identifier.scopusauthoridKurpisz, M=7006744359en_HK
dc.identifier.scopusauthoridFernandez, N=7102523519en_HK
dc.identifier.scopusauthoridPang, RTK=7004376636en_HK
dc.identifier.scopusauthoridYeung, WSB=55763794895en_HK
dc.identifier.scopusauthoridChiu, PCN=25959969200en_HK
dc.identifier.citeulike9492750-

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