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Article: Effects of vascular endothelial growth factor (VEGF) on MC3T3-E1

TitleEffects of vascular endothelial growth factor (VEGF) on MC3T3-E1
Authors
KeywordsBone remodeling
Osteoblast
VEGF
Issue Date2010
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1601-6335&site=1
Citation
Orthodontics And Craniofacial Research, 2010, v. 13 n. 4, p. 223-228 How to Cite?
AbstractObjective - To investigate whether VEGF has direct effects on bone cells activities and to better understand how VEGF promotes bone remodeling. Materials and Methods - MC3T3-E1 cell line was cultured with and without VEGF in vitro. The cells in both control and test groups were collected at different culture time points of 24, 48 and 72 h. Real-time polymerase chain reaction (qPCR) was carried out to quantify the mRNA expression of VEGF receptor (VEGFR2), alkaline phosphatase (ALP) and osteocalcin (OCN), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa β ligand (RANKL). Results - The expression of VEGFR2 significantly increased by 53% at 24 h and remained increased by 8% at 72 h compared to control (p < 0.05). ALP showed an early increase by 73% at 24 h (p < 0.001), but dropped by 14 and 41% at 48 and 72 h, respectively (p < 0.05). OCN was down-regulated by 41% at 24 h but then up-regulated by 149% at 72 h (p < 0.001). The expression of OPG significantly decreased by 7% at 24 h (p < 0.001) while dramatically increased by 133% at 72 h (p < 0.001). RANKL remained unchanged at all three time points (p > 0.05). Conclusion - VEGF promotes bone remodeling by direct effects on osteoblastic cells via regulating gene expression of ALP, OCN, and OPG through VEGFR2 signaling pathway. © 2010 John Wiley & Sons A/S.
Persistent Identifierhttp://hdl.handle.net/10722/133543
ISSN
2021 Impact Factor: 2.563
2020 SCImago Journal Rankings: 0.664
ISI Accession Number ID
Funding AgencyGrant Number
Basic Research HKU200803159006
Funding Information:

This work is supported by Seed Funding Programme for Basic Research HKU (200803159006). We thank Mr. Raymond Tong and Mr. Shadow Yeung for their technical assistance.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorTan, YYen_HK
dc.contributor.authorYang, YQen_HK
dc.contributor.authorChai, Len_HK
dc.contributor.authorWong, RWKen_HK
dc.contributor.authorRabie, ABMen_HK
dc.date.accessioned2011-05-19T07:12:59Z-
dc.date.available2011-05-19T07:12:59Z-
dc.date.issued2010en_HK
dc.identifier.citationOrthodontics And Craniofacial Research, 2010, v. 13 n. 4, p. 223-228en_HK
dc.identifier.issn1601-6335en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133543-
dc.description.abstractObjective - To investigate whether VEGF has direct effects on bone cells activities and to better understand how VEGF promotes bone remodeling. Materials and Methods - MC3T3-E1 cell line was cultured with and without VEGF in vitro. The cells in both control and test groups were collected at different culture time points of 24, 48 and 72 h. Real-time polymerase chain reaction (qPCR) was carried out to quantify the mRNA expression of VEGF receptor (VEGFR2), alkaline phosphatase (ALP) and osteocalcin (OCN), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa β ligand (RANKL). Results - The expression of VEGFR2 significantly increased by 53% at 24 h and remained increased by 8% at 72 h compared to control (p < 0.05). ALP showed an early increase by 73% at 24 h (p < 0.001), but dropped by 14 and 41% at 48 and 72 h, respectively (p < 0.05). OCN was down-regulated by 41% at 24 h but then up-regulated by 149% at 72 h (p < 0.001). The expression of OPG significantly decreased by 7% at 24 h (p < 0.001) while dramatically increased by 133% at 72 h (p < 0.001). RANKL remained unchanged at all three time points (p > 0.05). Conclusion - VEGF promotes bone remodeling by direct effects on osteoblastic cells via regulating gene expression of ALP, OCN, and OPG through VEGFR2 signaling pathway. © 2010 John Wiley & Sons A/S.en_HK
dc.languageeng-
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1601-6335&site=1en_HK
dc.relation.ispartofOrthodontics and Craniofacial Researchen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectBone remodelingen_HK
dc.subjectOsteoblasten_HK
dc.subjectVEGFen_HK
dc.subject.mesh3T3 Cells-
dc.subject.meshAlkaline Phosphatase - analysis - drug effects-
dc.subject.meshOsteoblasts - drug effects-
dc.subject.meshOsteogenesis - drug effects-
dc.subject.meshVascular Endothelial Growth Factor A - pharmacology-
dc.titleEffects of vascular endothelial growth factor (VEGF) on MC3T3-E1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1601-6335&volume=13&issue=4&spage=223&epage=228&date=2010&atitle=Effects+of+vascular+endothelial+growth+factor+(VEGF)+on+MC3T3-E1-
dc.identifier.emailYang, YQ: yangyanq@hkucc.hku.hken_HK
dc.identifier.emailRabie, ABM: rabie@hku.hken_HK
dc.identifier.authorityYang, YQ=rp00045en_HK
dc.identifier.authorityRabie, ABM=rp00029en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1111/j.1601-6343.2010.01498.xen_HK
dc.identifier.pmid21040465-
dc.identifier.scopuseid_2-s2.0-77958111867en_HK
dc.identifier.hkuros183183-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77958111867&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue4en_HK
dc.identifier.spage223en_HK
dc.identifier.epage228en_HK
dc.identifier.eissn1601-6343-
dc.identifier.isiWOS:000282569200005-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectEffects and signal pathway of vascular endothelial growth factor (VEGF) on osteoblastic cell line of MC3T3-E1 in vitro-
dc.identifier.scopusauthoridTan, YY=37075994500en_HK
dc.identifier.scopusauthoridYang, YQ=36623085300en_HK
dc.identifier.scopusauthoridChai, L=36196100600en_HK
dc.identifier.scopusauthoridWong, RWK=36642905800en_HK
dc.identifier.scopusauthoridRabie, ABM=7007172734en_HK
dc.identifier.issnl1601-6335-

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