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Article: Cotinine exposure increases fallopian tube PROKR1 expression via nicotinic AChRα-7: A potential mechanism explaining the link between smoking and tubal ectopic pregnancy

TitleCotinine exposure increases fallopian tube PROKR1 expression via nicotinic AChRα-7: A potential mechanism explaining the link between smoking and tubal ectopic pregnancy
Authors
Issue Date2010
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 2010, v. 177 n. 5, p. 2509-2515 How to Cite?
AbstractTubal ectopic pregnancy (EP) is the most common cause of maternal mortality in the first trimester of pregnancy; however, its etiology is uncertain. In EP, embryo retention within the Fallopian tube (FT) is thought to be due to impaired smooth muscle contractility (SMC) and alterations in the tubal microenvironment. Smoking is a major risk factor for EP. FTs from women with EP exhibit altered prokineticin receptor-1 (PROKR1) expression, the receptor for prokineticins (PROK). PROK1 is angiogenic, regulates SMC, and is involved in intrauterine implantation. We hypothesized that smoking predisposes women to EP by altering tubal PROKR1 expression. Sera/FT were collected at hysterectomy (n = 21). Serum levels of the smoking metabolite, cotinine, were measured by enzyme-linked immunosorbent assay. FTs were analyzed by q-RT-PCR, immunohistochemistry, and Western blotting for expression of PROKR1 and the predicted cotinine receptor, nicotinic acetylcholine receptor α-7 (AChRα-7). FT explants (n = 4) and oviductal epithelial cells (cell line OE-E6/E7) were treated with cotinine and an nAChRα-7 antagonist. PROKR1 transcription was higher in FTs from smokers (P < 0.01). nAChRα-7 expression was demonstrated in FT epithelium. Cotinine treatment of FT explants and OE-E6/E7 cells increased PROKR1 expression (P < 0.05), which was negated by cotreatment with nAChRα-7 antagonist. Smoking targets human FTs via nAChRα-7 to increase tubal PROKR1, leading to alterations in the tubal microenvironment that could predispose to EP. Copyright © American Society for Investigative Pathology.
Persistent Identifierhttp://hdl.handle.net/10722/139905
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Wellbeing of Women ProjectRG993
Medical Research Council (MAC)U.1276.00.004.00002.02
Scottish Government Rural and Environment Research and Analysis Directorate (RERAD)
MRC
Funding Information:

Supported by a Wellbeing of Women Project grant (RG993 to A.W.H.). H.N.J. was supported by Medical Research Council (MAC) Core Funding (U.1276.00.004.00002.02). G.E. was funded by the Scottish Government Rural and Environment Research and Analysis Directorate (RERAD). A.W.H. is supported by an MRC Clinician Scientist Fellowship.

References

 

DC FieldValueLanguage
dc.contributor.authorShaw, JLVen_HK
dc.contributor.authorOliver, Een_HK
dc.contributor.authorLee, KFen_HK
dc.contributor.authorEntrican, Gen_HK
dc.contributor.authorJabbour, HNen_HK
dc.contributor.authorCritchley, HODen_HK
dc.contributor.authorHorne, AWen_HK
dc.date.accessioned2011-09-23T06:00:00Z-
dc.date.available2011-09-23T06:00:00Z-
dc.date.issued2010en_HK
dc.identifier.citationAmerican Journal Of Pathology, 2010, v. 177 n. 5, p. 2509-2515en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139905-
dc.description.abstractTubal ectopic pregnancy (EP) is the most common cause of maternal mortality in the first trimester of pregnancy; however, its etiology is uncertain. In EP, embryo retention within the Fallopian tube (FT) is thought to be due to impaired smooth muscle contractility (SMC) and alterations in the tubal microenvironment. Smoking is a major risk factor for EP. FTs from women with EP exhibit altered prokineticin receptor-1 (PROKR1) expression, the receptor for prokineticins (PROK). PROK1 is angiogenic, regulates SMC, and is involved in intrauterine implantation. We hypothesized that smoking predisposes women to EP by altering tubal PROKR1 expression. Sera/FT were collected at hysterectomy (n = 21). Serum levels of the smoking metabolite, cotinine, were measured by enzyme-linked immunosorbent assay. FTs were analyzed by q-RT-PCR, immunohistochemistry, and Western blotting for expression of PROKR1 and the predicted cotinine receptor, nicotinic acetylcholine receptor α-7 (AChRα-7). FT explants (n = 4) and oviductal epithelial cells (cell line OE-E6/E7) were treated with cotinine and an nAChRα-7 antagonist. PROKR1 transcription was higher in FTs from smokers (P < 0.01). nAChRα-7 expression was demonstrated in FT epithelium. Cotinine treatment of FT explants and OE-E6/E7 cells increased PROKR1 expression (P < 0.05), which was negated by cotreatment with nAChRα-7 antagonist. Smoking targets human FTs via nAChRα-7 to increase tubal PROKR1, leading to alterations in the tubal microenvironment that could predispose to EP. Copyright © American Society for Investigative Pathology.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.subject.meshCotinine - blood - pharmacology-
dc.subject.meshFallopian Tubes - anatomy and histology - drug effects - metabolism-
dc.subject.meshPregnancy, Ectopic - etiology-
dc.subject.meshReceptors, Nicotinic - metabolism-
dc.subject.meshSmoking - adverse effects-
dc.titleCotinine exposure increases fallopian tube PROKR1 expression via nicotinic AChRα-7: A potential mechanism explaining the link between smoking and tubal ectopic pregnancyen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, KF:ckflee@hku.hken_HK
dc.identifier.authorityLee, KF=rp00458en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.2353/ajpath.2010.100243en_HK
dc.identifier.pmid20864676-
dc.identifier.pmcidPMC2966807-
dc.identifier.scopuseid_2-s2.0-78149343879en_HK
dc.identifier.hkuros196021en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78149343879&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume177en_HK
dc.identifier.issue5en_HK
dc.identifier.spage2509en_HK
dc.identifier.epage2515en_HK
dc.identifier.isiWOS:000284182900036-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShaw, JLV=7403899035en_HK
dc.identifier.scopusauthoridOliver, E=37067616100en_HK
dc.identifier.scopusauthoridLee, KF=26643097500en_HK
dc.identifier.scopusauthoridEntrican, G=7003339226en_HK
dc.identifier.scopusauthoridJabbour, HN=7005209265en_HK
dc.identifier.scopusauthoridCritchley, HOD=7006731536en_HK
dc.identifier.scopusauthoridHorne, AW=8067885000en_HK

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