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Conference Paper: The potential role of brain-derived neurotrophic factor (BDNF) in angiogenesis

TitleThe potential role of brain-derived neurotrophic factor (BDNF) in angiogenesis
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research
Citation
AACR 98th Annual Meeting, Los Angeles, CA, 14–18 April 2007. In Cancer Research, 2007, v. 67 n. 9S, p. 4617 How to Cite?
AbstractBackground and Aim: Hepatocellular carcinoma is a hypervascularized solid tumor, in which angiogenesis plays an essential role. The present study aims to investigate the potential role of brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, in the angiogenic behavior of endothelial cells. Materials and Methods: One normal mouse endothelial cell line and one tumor-derived endothelial cell line were used in an in vitro setting. These two cell lines were treated with recombinant BDNF protein, TrkB blocker-K252a or in combination. In addition, BDNF level was up-regulated in the normal endothelial cells by transfection. The viability of cells was determined by MTT assay, and the percentage of apoptotic cells was quantified by Annexin V labeling. Cell motility was assessed by cell migration assay. The expression of BDNF, HIF-1α, and VEGF was detected by semi-quantitative RT-PCR and Western blot. Results: Firstly, the two cell lines expressed different levels of endogenous BDNF. The tumor-derived endothelial cells with a higher level of endogenous BDNF, demonstrated a higher proliferation rate than that in the normal endothelial cells, which had a lower endogenous BDNF level. Secondly, exogenous BDNF administration could promote cell proliferation in both cell lines. Thirdly, exogenous BDNF up-regulated the expression of HIF-1α and VEGF in the tumor-derived endothelial cells, and augmented the expression of BDNF and VEGF in the normal endothelial cells. Lastly, up-regulation of BDNF by transfection promoted cell migration and abrogated serum-starvation induced apoptosis. Conclusion: The present study suggested the potential role of BDNF in physiological and pathological angiogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/107641
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorLam, CTen_HK
dc.contributor.authorYang, Zen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorPoon, RTPen_HK
dc.date.accessioned2010-09-26T00:06:15Z-
dc.date.available2010-09-26T00:06:15Z-
dc.date.issued2007en_HK
dc.identifier.citationAACR 98th Annual Meeting, Los Angeles, CA, 14–18 April 2007. In Cancer Research, 2007, v. 67 n. 9S, p. 4617-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/107641-
dc.description.abstractBackground and Aim: Hepatocellular carcinoma is a hypervascularized solid tumor, in which angiogenesis plays an essential role. The present study aims to investigate the potential role of brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, in the angiogenic behavior of endothelial cells. Materials and Methods: One normal mouse endothelial cell line and one tumor-derived endothelial cell line were used in an in vitro setting. These two cell lines were treated with recombinant BDNF protein, TrkB blocker-K252a or in combination. In addition, BDNF level was up-regulated in the normal endothelial cells by transfection. The viability of cells was determined by MTT assay, and the percentage of apoptotic cells was quantified by Annexin V labeling. Cell motility was assessed by cell migration assay. The expression of BDNF, HIF-1α, and VEGF was detected by semi-quantitative RT-PCR and Western blot. Results: Firstly, the two cell lines expressed different levels of endogenous BDNF. The tumor-derived endothelial cells with a higher level of endogenous BDNF, demonstrated a higher proliferation rate than that in the normal endothelial cells, which had a lower endogenous BDNF level. Secondly, exogenous BDNF administration could promote cell proliferation in both cell lines. Thirdly, exogenous BDNF up-regulated the expression of HIF-1α and VEGF in the tumor-derived endothelial cells, and augmented the expression of BDNF and VEGF in the normal endothelial cells. Lastly, up-regulation of BDNF by transfection promoted cell migration and abrogated serum-starvation induced apoptosis. Conclusion: The present study suggested the potential role of BDNF in physiological and pathological angiogenesis.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleThe potential role of brain-derived neurotrophic factor (BDNF) in angiogenesisen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailYang, Z: zfyang@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.hkuros159422en_HK

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