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Article: Impaired angiogenesis, delayed wound healing and retarded tumor growth in Perlecan heparan sulfate-deficient mice

TitleImpaired angiogenesis, delayed wound healing and retarded tumor growth in Perlecan heparan sulfate-deficient mice
Authors
Issue Date2004
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2004, v. 64 n. 14, p. 4699-4702 How to Cite?
AbstractPerlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes. It sequesters growth factors such as fibroblast growth factor 2 (FGF-2) and regulates the ligand-receptor interactions on the cell surface, and thus it has been implicated in the control of angiogenesis. Both stimulatory and inhibitory effects of perlecan on FGF-2 signaling have been reported. To understand the in vivo function of HS carried by perlecan, the perlecan gene heparan sulfate proteoglycan 2 (Hspg2) was mutated in mouse by gene targeting. The HS at the NH2 terminus of perlecan was removed while the core protein remained intact. Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis. In the mouse corneal angiogenesis model, FGF-2-induced neovascularization was significantly impaired in Hspg2 Δ3/Δ3 mutant mice. Our results suggest that HS in perlecan positively regulates the angiogenesis in vivo.
Persistent Identifierhttp://hdl.handle.net/10722/134122
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Zen_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorCao, Ren_HK
dc.contributor.authorMorita, Hen_HK
dc.contributor.authorSoininen, Ren_HK
dc.contributor.authorChan, KMen_HK
dc.contributor.authorLiu, Ben_HK
dc.contributor.authorCao, Yen_HK
dc.contributor.authorTryggvason, Ken_HK
dc.date.accessioned2011-06-13T07:19:35Z-
dc.date.available2011-06-13T07:19:35Z-
dc.date.issued2004en_HK
dc.identifier.citationCancer Research, 2004, v. 64 n. 14, p. 4699-4702en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134122-
dc.description.abstractPerlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes. It sequesters growth factors such as fibroblast growth factor 2 (FGF-2) and regulates the ligand-receptor interactions on the cell surface, and thus it has been implicated in the control of angiogenesis. Both stimulatory and inhibitory effects of perlecan on FGF-2 signaling have been reported. To understand the in vivo function of HS carried by perlecan, the perlecan gene heparan sulfate proteoglycan 2 (Hspg2) was mutated in mouse by gene targeting. The HS at the NH2 terminus of perlecan was removed while the core protein remained intact. Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis. In the mouse corneal angiogenesis model, FGF-2-induced neovascularization was significantly impaired in Hspg2 Δ3/Δ3 mutant mice. Our results suggest that HS in perlecan positively regulates the angiogenesis in vivo.en_HK
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBasement Membrane - pathologyen_HK
dc.subject.meshBlood Vessels - pathologyen_HK
dc.subject.meshCell Division - physiologyen_HK
dc.subject.meshCornea - blood supplyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFibroblast Growth Factor 2 - genetics - physiologyen_HK
dc.subject.meshHeparan Sulfate Proteoglycans - deficiency - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshNIH 3T3 Cellsen_HK
dc.subject.meshNeoplasms, Experimental - blood supply - genetics - pathologyen_HK
dc.subject.meshNeovascularization, Pathologic - pathologyen_HK
dc.subject.meshNeovascularization, Physiologic - physiologyen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshWound Healing - physiologyen_HK
dc.titleImpaired angiogenesis, delayed wound healing and retarded tumor growth in Perlecan heparan sulfate-deficient miceen_HK
dc.typeArticleen_HK
dc.identifier.emailZhou, Z: zhongjun@hkucc.hku.hken_HK
dc.identifier.emailChan, KM: ming616@graduate.hku.hken_HK
dc.identifier.emailLiu, B: ppliew@hku.hken_HK
dc.identifier.authorityZhou, Z=rp00503en_HK
dc.identifier.authorityChan, KM=rp01757en_HK
dc.identifier.authorityLiu, B=rp01485en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1158/0008-5472.CAN-04-0810en_HK
dc.identifier.pmid15256433-
dc.identifier.scopuseid_2-s2.0-3142682314en_HK
dc.identifier.hkuros95437-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3142682314&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume64en_HK
dc.identifier.issue14en_HK
dc.identifier.spage4699en_HK
dc.identifier.epage4702en_HK
dc.identifier.isiWOS:000222674700003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhou, Z=8631856300en_HK
dc.identifier.scopusauthoridWang, J=8631854400en_HK
dc.identifier.scopusauthoridCao, R=7103341338en_HK
dc.identifier.scopusauthoridMorita, H=55722033000en_HK
dc.identifier.scopusauthoridSoininen, R=7003955362en_HK
dc.identifier.scopusauthoridChan, KM=8631854500en_HK
dc.identifier.scopusauthoridLiu, B=7408693394en_HK
dc.identifier.scopusauthoridCao, Y=7404524342en_HK
dc.identifier.scopusauthoridTryggvason, K=7102025185en_HK

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