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Article: Angiotensin II induces interleukin-6 synthesis in osteoblasts through ERK1/2 pathway via AT1 receptor

TitleAngiotensin II induces interleukin-6 synthesis in osteoblasts through ERK1/2 pathway via AT1 receptor
Authors
KeywordsAngiotensin II
Extracellular signal-regulated kinase
Interleukin-6
Osteoblast
Issue Date2011
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/archoralbio
Citation
Archives Of Oral Biology, 2011, v. 56 n. 3, p. 205-211 How to Cite?
AbstractBackground: Interleukin-6 (IL-6) is a potent stimulator of osteoclastic bone resorption. Osteoblast secretion of IL-6 plays an important role in the regulation of bone metabolism. Angiotensin II (Ang II) has been shown to regulate the expression of potent inflammatory factors, including MCP-1 and IL-6, by stimulating endothelia cells, vascular smooth muscle cells (VSMC) and monocytes. However, of the mechanism by which Ang II regulates IL-6 expression in osteoblasts is unknown. Aims: The present study was designed to investigate the effect of Ang II on IL-6 expression in osteoblasts isolated from mice. The receptor(s) required and the potential role of extracellular signal-regulated kinase 1/2 (ERK1/2) activation in Ang II-induced IL-6 synthesis was also examined in these cells. Methods: The osteoblasts were isolated from the calvaria of mice and cultured in α-MEM medium. IL-6 mRNA expression and protein synthesis was determined by qPCR and ELISA analyses. ERK1/2 kinase activation was determined by western blot. Results: The results indicate that Ang II induced IL-6 mRNA expression and protein synthesis in cultured osteoblasts. However, these effects were abolished by pre-treatment with Ang II type 1 (AT1) receptor antagonist, losartan, and the ERK1/2 inhibitor, U0126, inhibited Ang II-mediated IL-6 expression and the phosphorylation of ERK1/2. Conclusion: Ang II induces the synthesis of IL-6 in osteoblasts through activation of the ERK1/2 pathway via the AT1 receptor. Crown Copyright © 2010 Published by Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/133570
ISSN
2015 Impact Factor: 1.733
2015 SCImago Journal Rankings: 0.713
ISI Accession Number ID
Funding AgencyGrant Number
Public Welfare Foundation of the Sichuan Science and Technology Department of China2008FN0174
Funding Information:

This study was supported by the Public Welfare Foundation of the Sichuan Science and Technology Department of China (No. 2008FN0174).

References

 

DC FieldValueLanguage
dc.contributor.authorGuo, Len_HK
dc.contributor.authorWang, Men_HK
dc.contributor.authorZhang, ZYen_HK
dc.contributor.authorHao, Len_HK
dc.contributor.authorLou, BYen_HK
dc.contributor.authorLi, XYen_HK
dc.contributor.authorLoo, WTYen_HK
dc.contributor.authorJin, Len_HK
dc.contributor.authorCheung, MNBen_HK
dc.date.accessioned2011-05-24T02:10:46Z-
dc.date.available2011-05-24T02:10:46Z-
dc.date.issued2011en_HK
dc.identifier.citationArchives Of Oral Biology, 2011, v. 56 n. 3, p. 205-211en_HK
dc.identifier.issn0003-9969en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133570-
dc.description.abstractBackground: Interleukin-6 (IL-6) is a potent stimulator of osteoclastic bone resorption. Osteoblast secretion of IL-6 plays an important role in the regulation of bone metabolism. Angiotensin II (Ang II) has been shown to regulate the expression of potent inflammatory factors, including MCP-1 and IL-6, by stimulating endothelia cells, vascular smooth muscle cells (VSMC) and monocytes. However, of the mechanism by which Ang II regulates IL-6 expression in osteoblasts is unknown. Aims: The present study was designed to investigate the effect of Ang II on IL-6 expression in osteoblasts isolated from mice. The receptor(s) required and the potential role of extracellular signal-regulated kinase 1/2 (ERK1/2) activation in Ang II-induced IL-6 synthesis was also examined in these cells. Methods: The osteoblasts were isolated from the calvaria of mice and cultured in α-MEM medium. IL-6 mRNA expression and protein synthesis was determined by qPCR and ELISA analyses. ERK1/2 kinase activation was determined by western blot. Results: The results indicate that Ang II induced IL-6 mRNA expression and protein synthesis in cultured osteoblasts. However, these effects were abolished by pre-treatment with Ang II type 1 (AT1) receptor antagonist, losartan, and the ERK1/2 inhibitor, U0126, inhibited Ang II-mediated IL-6 expression and the phosphorylation of ERK1/2. Conclusion: Ang II induces the synthesis of IL-6 in osteoblasts through activation of the ERK1/2 pathway via the AT1 receptor. Crown Copyright © 2010 Published by Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/archoralbioen_HK
dc.relation.ispartofArchives of Oral Biologyen_HK
dc.subjectAngiotensin IIen_HK
dc.subjectExtracellular signal-regulated kinaseen_HK
dc.subjectInterleukin-6en_HK
dc.subjectOsteoblasten_HK
dc.subject.meshAngiotensin II - physiology-
dc.subject.meshInterleukin-6 - biosynthesis - secretion-
dc.subject.meshMitogen-Activated Protein Kinase 1 - antagonists and inhibitors - metabolism-
dc.subject.meshMitogen-Activated Protein Kinase 3 - antagonists and inhibitors - metabolism-
dc.subject.meshOsteoblasts - metabolism-
dc.titleAngiotensin II induces interleukin-6 synthesis in osteoblasts through ERK1/2 pathway via AT1 receptoren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0003-9969&volume=56&issue=3&spage=205&epage=211&date=2011&atitle=Angiotensin+II+induces+interleukin-6+synthesis+in+osteoblasts+through+ERK1/2+pathway+via+AT1+receptor-
dc.identifier.emailJin, L:ljjin@hkucc.hku.hken_HK
dc.identifier.authorityJin, L=rp00028en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.archoralbio.2010.09.016en_HK
dc.identifier.pmid21109230-
dc.identifier.scopuseid_2-s2.0-79951855395en_HK
dc.identifier.hkuros185238en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79951855395&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume56en_HK
dc.identifier.issue3en_HK
dc.identifier.spage205en_HK
dc.identifier.epage211en_HK
dc.identifier.isiWOS:000288474400001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridGuo, L=37161549100en_HK
dc.identifier.scopusauthoridWang, M=36079147700en_HK
dc.identifier.scopusauthoridZhang, ZY=41862888700en_HK
dc.identifier.scopusauthoridHao, L=37016273300en_HK
dc.identifier.scopusauthoridLou, BY=15829719900en_HK
dc.identifier.scopusauthoridLi, XY=36014403800en_HK
dc.identifier.scopusauthoridLoo, WTY=7003567474en_HK
dc.identifier.scopusauthoridJin, L=7403328850en_HK
dc.identifier.scopusauthoridCheung, MNB=7201897548en_HK
dc.identifier.citeulike8366099-

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