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- Publisher Website: 10.1016/j.bbrc.2004.03.050
- Scopus: eid_2-s2.0-1842426689
- PMID: 15063765
- WOS: WOS:000220922200009
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Article: Regulatory role of vHL/HIF-1α in hypoxia-induced VEGF production in hepatic stellate cells
Title | Regulatory role of vHL/HIF-1α in hypoxia-induced VEGF production in hepatic stellate cells |
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Authors | |
Keywords | COX-2 HIF-1α Hypoxic T6-HSCs VEGF vHL |
Issue Date | 2004 |
Publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description |
Citation | Biochemical And Biophysical Research Communications, 2004, v. 317 n. 2, p. 358-362 How to Cite? |
Abstract | Activated hepatic stellate cells (HSCs) produce cyclooxygenase-2 (COX-2) protein to induce vascular endothelial growth factor (VEGF) production that participates in angiogenesis in injured liver. To reveal the unknown regulatory mechanism, we used hypoxic atmosphere mimicking injured-tissue microenvironment to induce VEGF expression in a rat hepatic stellate cell line (T6-HSCs). The present study showed that hypoxia up-regulated the protein levels of COX-2 and hypoxia-inducible factor-1-α (HIF-1α), but rapidly effected degradation of von Hippel-Lindau (vHL) protein. As a result, expression of VEGF in HSCs was markedly elevated; and pretreatment with COX-2 inhibitors (nimesulide or indomethacin) could significantly ameliorate the angiogenic event. Collectively, hypoxic HSCs increased accumulation of HIF-1α protein and induced VEGF expression in a time-dependent manner. Inhibition of COX-2 activities would prevent vHL protein from degradation and suppress HIF-1α up-regulation. Thus, vHL/HIF-1α has a regulatory role in COX-2-mediated VEGF production in hypoxic stellate cells in injured liver. © 2004 Elsevier Inc. All rights reserved. |
Persistent Identifier | http://hdl.handle.net/10722/172870 |
ISSN | 2023 Impact Factor: 2.5 2023 SCImago Journal Rankings: 0.770 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wang, YQ | en_HK |
dc.contributor.author | Luk, JM | en_HK |
dc.contributor.author | Ikeda, K | en_HK |
dc.contributor.author | Man, K | en_HK |
dc.contributor.author | Chu, AC | en_HK |
dc.contributor.author | Kaneda, K | en_HK |
dc.contributor.author | Fan, ST | en_HK |
dc.date.accessioned | 2012-10-30T06:25:25Z | - |
dc.date.available | 2012-10-30T06:25:25Z | - |
dc.date.issued | 2004 | en_HK |
dc.identifier.citation | Biochemical And Biophysical Research Communications, 2004, v. 317 n. 2, p. 358-362 | en_HK |
dc.identifier.issn | 0006-291X | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/172870 | - |
dc.description.abstract | Activated hepatic stellate cells (HSCs) produce cyclooxygenase-2 (COX-2) protein to induce vascular endothelial growth factor (VEGF) production that participates in angiogenesis in injured liver. To reveal the unknown regulatory mechanism, we used hypoxic atmosphere mimicking injured-tissue microenvironment to induce VEGF expression in a rat hepatic stellate cell line (T6-HSCs). The present study showed that hypoxia up-regulated the protein levels of COX-2 and hypoxia-inducible factor-1-α (HIF-1α), but rapidly effected degradation of von Hippel-Lindau (vHL) protein. As a result, expression of VEGF in HSCs was markedly elevated; and pretreatment with COX-2 inhibitors (nimesulide or indomethacin) could significantly ameliorate the angiogenic event. Collectively, hypoxic HSCs increased accumulation of HIF-1α protein and induced VEGF expression in a time-dependent manner. Inhibition of COX-2 activities would prevent vHL protein from degradation and suppress HIF-1α up-regulation. Thus, vHL/HIF-1α has a regulatory role in COX-2-mediated VEGF production in hypoxic stellate cells in injured liver. © 2004 Elsevier Inc. All rights reserved. | en_HK |
dc.language | eng | en_US |
dc.publisher | Academic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description | en_HK |
dc.relation.ispartof | Biochemical and Biophysical Research Communications | en_HK |
dc.subject | COX-2 | en_HK |
dc.subject | HIF-1α | en_HK |
dc.subject | Hypoxic T6-HSCs | en_HK |
dc.subject | VEGF | en_HK |
dc.subject | vHL | en_HK |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Carrier Proteins - Metabolism | en_US |
dc.subject.mesh | Cell Hypoxia - Drug Effects - Physiology | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Cyclooxygenase 2 | en_US |
dc.subject.mesh | Dose-Response Relationship, Drug | en_US |
dc.subject.mesh | Gene Expression Regulation - Drug Effects - Physiology | en_US |
dc.subject.mesh | Hepatocytes - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Homeostasis - Physiology | en_US |
dc.subject.mesh | Hypoxia-Inducible Factor 1, Alpha Subunit | en_US |
dc.subject.mesh | Indomethacin - Pharmacology | en_US |
dc.subject.mesh | Isoenzymes - Antagonists & Inhibitors - Metabolism | en_US |
dc.subject.mesh | Prostaglandin-Endoperoxide Synthases - Metabolism | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Sulfonamides - Pharmacology | en_US |
dc.subject.mesh | Transcription Factors - Metabolism | en_US |
dc.subject.mesh | Vascular Endothelial Growth Factor A - Metabolism | en_US |
dc.title | Regulatory role of vHL/HIF-1α in hypoxia-induced VEGF production in hepatic stellate cells | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Luk, JM: jmluk@hkucc.hku.hk | en_HK |
dc.identifier.email | Man, K: kwanman@hku.hk | en_HK |
dc.identifier.email | Chu, AC: bcccy@hkucc.hku.hk | en_HK |
dc.identifier.email | Fan, ST: stfan@hku.hk | en_HK |
dc.identifier.authority | Luk, JM=rp00349 | en_HK |
dc.identifier.authority | Man, K=rp00417 | en_HK |
dc.identifier.authority | Chu, AC=rp00505 | en_HK |
dc.identifier.authority | Fan, ST=rp00355 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/j.bbrc.2004.03.050 | en_HK |
dc.identifier.pmid | 15063765 | - |
dc.identifier.scopus | eid_2-s2.0-1842426689 | en_HK |
dc.identifier.hkuros | 85943 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-1842426689&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 317 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 358 | en_HK |
dc.identifier.epage | 362 | en_HK |
dc.identifier.isi | WOS:000220922200009 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Wang, YQ=37074971500 | en_HK |
dc.identifier.scopusauthorid | Luk, JM=7006777791 | en_HK |
dc.identifier.scopusauthorid | Ikeda, K=7404890758 | en_HK |
dc.identifier.scopusauthorid | Man, K=7101754072 | en_HK |
dc.identifier.scopusauthorid | Chu, AC=24343085700 | en_HK |
dc.identifier.scopusauthorid | Kaneda, K=7202540217 | en_HK |
dc.identifier.scopusauthorid | Fan, ST=7402678224 | en_HK |
dc.identifier.issnl | 0006-291X | - |