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Article: LMO2 promotes angiogenesis probably by up-regulation of bFGF in endothelial cells: An implication of its pathophysiological role in infantile haemangioma

TitleLMO2 promotes angiogenesis probably by up-regulation of bFGF in endothelial cells: An implication of its pathophysiological role in infantile haemangioma
Authors
KeywordsBFGF
Endothelial cells
Infantile haemangiomas
LMO2
Issue Date2010
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HIS
Citation
Histopathology, 2010, v. 57 n. 4, p. 622-632 How to Cite?
AbstractAims: Infantile haemangiomas (IHs) are common benign vascular tumours distinctive for their perinatal presentation, rapid growth during the first year of life and subsequent slow involution. Recent research has indicated that endothelial cells of haemangiomas express LIM-only protein 2 (LMO2). The aim of this study was to investigate the role of LMO2 in the pathogenesis of IHs was investigated.Methods and results: Immunoreactivity of LMO2 was assessed in specimens of 19 IH. Stable transfection of LMO2 into human endothelial cell lines (EAhy926) was performed to evaluate the role of LMO2 in terms of the change in cell proliferation, cell cycle and cell migration as well as the expression level of angiogenic factors. Immunoreactivity for LMO2 was detected in all IH specimens, specifically in the nucleus of the endothelial cells. The intensity of LMO2 immunostaining decreased significantly from proliferative to involuting stages. Furthermore, the overexpression of LMO2 enhanced the proliferation and migration of the endothelial cells and promoted G0/G1-S-phase transition in vitro, together with an up-regulation of bFGF expression.Conclusions: LMO2 probably promotes angiogenesis by up-regulation of bFGF expression and thereby consequently influences progression of IH. © 2010 Blackwell Publishing Limited.
Persistent Identifierhttp://hdl.handle.net/10722/134986
ISSN
2014 Impact Factor: 3.453
2014 SCImago Journal Rankings: 1.291
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China30600712
30872894
30973330
Funding Information:

This work was supported by grants from the National Natural Science Foundation of China (30600712) to Dr Z J Sun and (30872894 and 30973330) to Dr Y F Zhao. We thank Dr Roger A Zwahlen of The Faculty of Dentistry, The University of Hong Kong for his kind assistance in editing.

References

 

DC FieldValueLanguage
dc.contributor.authorSun, ZJen_HK
dc.contributor.authorCai, Yen_HK
dc.contributor.authorChen, Gen_HK
dc.contributor.authorWang, Ren_HK
dc.contributor.authorJia, Jen_HK
dc.contributor.authorChen, XMen_HK
dc.contributor.authorZheng, LWen_HK
dc.contributor.authorZhao, YFen_HK
dc.date.accessioned2011-07-27T01:25:24Z-
dc.date.available2011-07-27T01:25:24Z-
dc.date.issued2010en_HK
dc.identifier.citationHistopathology, 2010, v. 57 n. 4, p. 622-632en_HK
dc.identifier.issn0309-0167en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134986-
dc.description.abstractAims: Infantile haemangiomas (IHs) are common benign vascular tumours distinctive for their perinatal presentation, rapid growth during the first year of life and subsequent slow involution. Recent research has indicated that endothelial cells of haemangiomas express LIM-only protein 2 (LMO2). The aim of this study was to investigate the role of LMO2 in the pathogenesis of IHs was investigated.Methods and results: Immunoreactivity of LMO2 was assessed in specimens of 19 IH. Stable transfection of LMO2 into human endothelial cell lines (EAhy926) was performed to evaluate the role of LMO2 in terms of the change in cell proliferation, cell cycle and cell migration as well as the expression level of angiogenic factors. Immunoreactivity for LMO2 was detected in all IH specimens, specifically in the nucleus of the endothelial cells. The intensity of LMO2 immunostaining decreased significantly from proliferative to involuting stages. Furthermore, the overexpression of LMO2 enhanced the proliferation and migration of the endothelial cells and promoted G0/G1-S-phase transition in vitro, together with an up-regulation of bFGF expression.Conclusions: LMO2 probably promotes angiogenesis by up-regulation of bFGF expression and thereby consequently influences progression of IH. © 2010 Blackwell Publishing Limited.en_HK
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HISen_HK
dc.relation.ispartofHistopathologyen_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subjectBFGFen_HK
dc.subjectEndothelial cellsen_HK
dc.subjectInfantile haemangiomasen_HK
dc.subjectLMO2en_HK
dc.subject.meshDNA-Binding Proteins - metabolism-
dc.subject.meshEndothelial Cells - metabolism-
dc.subject.meshFibroblast Growth Factor 2 - biosynthesis-
dc.subject.meshHemangioma, Capillary - metabolism-
dc.subject.meshMetalloproteins - metabolism-
dc.titleLMO2 promotes angiogenesis probably by up-regulation of bFGF in endothelial cells: An implication of its pathophysiological role in infantile haemangiomaen_HK
dc.typeArticleen_HK
dc.identifier.emailZheng, LW:lwzheng@hku.hken_HK
dc.identifier.authorityZheng, LW=rp01411en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2559.2010.03676.xen_HK
dc.identifier.pmid20955387en_HK
dc.identifier.scopuseid_2-s2.0-78650504772en_HK
dc.identifier.hkuros188022en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78650504772&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume57en_HK
dc.identifier.issue4en_HK
dc.identifier.spage622en_HK
dc.identifier.epage632en_HK
dc.identifier.isiWOS:000283078300015-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridSun, ZJ=35316325300en_HK
dc.identifier.scopusauthoridCai, Y=35214334700en_HK
dc.identifier.scopusauthoridChen, G=36046344700en_HK
dc.identifier.scopusauthoridWang, R=37062256500en_HK
dc.identifier.scopusauthoridJia, J=7202343447en_HK
dc.identifier.scopusauthoridChen, XM=15219054500en_HK
dc.identifier.scopusauthoridZheng, LW=11241247300en_HK
dc.identifier.scopusauthoridZhao, YF=35249951900en_HK
dc.identifier.citeulike8049268-

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