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Article: Endocrine gland-derived vascular endothelial growth factor stimulates proliferation and tube formation in human uterine microvascular endothelial cell through the mitogen-activated protein kinase but not through the Akt pathway

TitleEndocrine gland-derived vascular endothelial growth factor stimulates proliferation and tube formation in human uterine microvascular endothelial cell through the mitogen-activated protein kinase but not through the Akt pathway
Authors
Keywordsangiogenesis
cell-signaling pathways
EG-VEGF
PKR1
PKR2
UtMVEC-Myo
Issue Date2009
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/fertnstert
Citation
Fertility And Sterility, 2009, v. 91 n. 5 SUPPL., p. 2163-2171 How to Cite?
AbstractObjective: To study the angiogenic functions of endocrine gland-derived vascular endothelial growth factor (EG-VEGF) on a normal myometrial uterine microvascular endothelial cell line (UtMVEC-Myo) and the signaling pathways elicited by EG-VEGF in UtMVEC-Myo. Design: Experimental laboratory study. Setting: University gynecology unit. Patient(s): Infertile women undergoing diagnostic laparoscopy for assessment of tubal patency. Intervention(s): Real-time polymerase chain reaction (PCR) analysis of mRNA of EG-VEGF and its receptors, PKR1 and PKR2, in UtMVEC-Myo and endometrial samples. The effects of EG-VEGF on the cell proliferation, tube formation, and cell signaling pathways of UtMVEC-Myo were studied. Main Outcome Measure(s): Cell proliferation, tube formation, and molecules of cell-signaling pathways in the treated UtMVEC-Myo. Result(s): UtMVEC-Myo cells had PKR1 and PKR2 but not EG-VEGF mRNA. EG-VEGF significantly stimulated cell proliferation and tube formation in UtMVEC-Myo cells. EG-VEGF activated p44/42 mitogen-activated protein kinase (MAPK) but not Akt signaling pathway. The effects of EG-VEGF on p44/42 MAPK phosphorylation and cell proliferation were nullified by the specific MAPK inhibitor, PD98059. Conclusion(s): EG-VEGF has a direct angiogenic effect on UtMVEC-Myo that expresses EG-VEGF receptors (PKR1 and PKR2) and modulates cell proliferation and sprouting of the endothelial cells. It is suggested that EG-VEGF enhanced cell proliferation through the activation of MAPK pathway but not through the Akt pathway. © 2009 American Society for Reproductive Medicine.
Persistent Identifierhttp://hdl.handle.net/10722/60351
ISSN
2015 Impact Factor: 4.426
2015 SCImago Journal Rankings: 2.156
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, YLen_HK
dc.contributor.authorChan, YLen_HK
dc.contributor.authorChow, WNen_HK
dc.contributor.authorNg, EHYen_HK
dc.contributor.authorLee, KFen_HK
dc.contributor.authorYeung, WSBen_HK
dc.contributor.authorHo, PCen_HK
dc.date.accessioned2010-05-31T04:08:54Z-
dc.date.available2010-05-31T04:08:54Z-
dc.date.issued2009en_HK
dc.identifier.citationFertility And Sterility, 2009, v. 91 n. 5 SUPPL., p. 2163-2171en_HK
dc.identifier.issn0015-0282en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60351-
dc.description.abstractObjective: To study the angiogenic functions of endocrine gland-derived vascular endothelial growth factor (EG-VEGF) on a normal myometrial uterine microvascular endothelial cell line (UtMVEC-Myo) and the signaling pathways elicited by EG-VEGF in UtMVEC-Myo. Design: Experimental laboratory study. Setting: University gynecology unit. Patient(s): Infertile women undergoing diagnostic laparoscopy for assessment of tubal patency. Intervention(s): Real-time polymerase chain reaction (PCR) analysis of mRNA of EG-VEGF and its receptors, PKR1 and PKR2, in UtMVEC-Myo and endometrial samples. The effects of EG-VEGF on the cell proliferation, tube formation, and cell signaling pathways of UtMVEC-Myo were studied. Main Outcome Measure(s): Cell proliferation, tube formation, and molecules of cell-signaling pathways in the treated UtMVEC-Myo. Result(s): UtMVEC-Myo cells had PKR1 and PKR2 but not EG-VEGF mRNA. EG-VEGF significantly stimulated cell proliferation and tube formation in UtMVEC-Myo cells. EG-VEGF activated p44/42 mitogen-activated protein kinase (MAPK) but not Akt signaling pathway. The effects of EG-VEGF on p44/42 MAPK phosphorylation and cell proliferation were nullified by the specific MAPK inhibitor, PD98059. Conclusion(s): EG-VEGF has a direct angiogenic effect on UtMVEC-Myo that expresses EG-VEGF receptors (PKR1 and PKR2) and modulates cell proliferation and sprouting of the endothelial cells. It is suggested that EG-VEGF enhanced cell proliferation through the activation of MAPK pathway but not through the Akt pathway. © 2009 American Society for Reproductive Medicine.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/fertnsterten_HK
dc.relation.ispartofFertility and Sterilityen_HK
dc.rightsFertility and Sterility. Copyright © Elsevier Inc.en_HK
dc.subjectangiogenesisen_HK
dc.subjectcell-signaling pathwaysen_HK
dc.subjectEG-VEGFen_HK
dc.subjectPKR1en_HK
dc.subjectPKR2en_HK
dc.subjectUtMVEC-Myoen_HK
dc.titleEndocrine gland-derived vascular endothelial growth factor stimulates proliferation and tube formation in human uterine microvascular endothelial cell through the mitogen-activated protein kinase but not through the Akt pathwayen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0015-0282&volume=91&spage=2163&epage=2171&date=2009&atitle=Endocrine+gland-derived+vascular+endothelial+growth+factor+stimulates+proliferation+and+tube+formation+in+human+uterine+microvascular+endothelial+cell+through+the+mitogen-activated+protein+kinase+but+not+through+the+Akt+pathwayen_HK
dc.identifier.emailLee, YL:h9316321@hku.hken_HK
dc.identifier.emailNg, EHY:nghye@hkucc.hku.hken_HK
dc.identifier.emailLee, KF:ckflee@hku.hken_HK
dc.identifier.emailYeung, WSB:wsbyeung@hkucc.hku.hken_HK
dc.identifier.emailHo, PC:pcho@hku.hken_HK
dc.identifier.authorityLee, YL=rp00308en_HK
dc.identifier.authorityNg, EHY=rp00426en_HK
dc.identifier.authorityLee, KF=rp00458en_HK
dc.identifier.authorityYeung, WSB=rp00331en_HK
dc.identifier.authorityHo, PC=rp00325en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.fertnstert.2008.03.076en_HK
dc.identifier.pmid18571163-
dc.identifier.scopuseid_2-s2.0-65049089509en_HK
dc.identifier.hkuros157972en_HK
dc.identifier.hkuros148602-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65049089509&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume91en_HK
dc.identifier.issue5 SUPPL.en_HK
dc.identifier.spage2163en_HK
dc.identifier.epage2171en_HK
dc.identifier.isiWOS:000265969300027-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, YL=15033851800en_HK
dc.identifier.scopusauthoridChan, YL=36989095800en_HK
dc.identifier.scopusauthoridChow, WN=35200386900en_HK
dc.identifier.scopusauthoridNg, EHY=35238184300en_HK
dc.identifier.scopusauthoridLee, KF=26643097500en_HK
dc.identifier.scopusauthoridYeung, WSB=7102370745en_HK
dc.identifier.scopusauthoridHo, PC=7402211440en_HK

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