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Article: Osteopontin expression in progressive renal injury in remnant kidney: Role of angiotensin II

TitleOsteopontin expression in progressive renal injury in remnant kidney: Role of angiotensin II
Authors
KeywordsAdhesion molecule
Macrophages
Nephrectomy
Rampiril
Tubulointerstitial injury
Valsartan
Issue Date2000
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2000, v. 58 n. 4, p. 1469-1480 How to Cite?
AbstractBackground. Osteopontin (OPN) is a macrophage chemotactic and adhesion molecule and has been shown to play a role in glomerular and tubulointerstitial injury in several kidney disease models. Methods. The present study examined whether OPN expression is involved in the progression of renal disease following subtotal (5/6) nephrectomy (STNx) in rats and whether angiotensin II (Ang II) mediates the up-regulation of renal OPN expression and macrophage accumulation in this model by administering valsartan, an Ang II type I (AT1) receptor antagonist, or ramipril, an angiotensin-converting enzyme (ACE) inhibitor. Results. In normal and sham-operated rat kidneys, OPN was expressed in a few tubules (< 5%) and was absent in glomeruli. Following STNx (weeks 2 to 16), there was substantial up-regulation of OPN mRNA and protein expression in glomeruli [2 to 12 cells/glomerular cross section (gcs)] and tubular epithelial cells (20 to 75% OPN +). The up-regulation of OPN expression was associated with macrophage accumulation within the kidney, severe proteinuria, loss of renal function, and severe histologic damage, including tubulitis and tubulointerstitial fibrosis (all P < 0.001). Treatment with either valsartan or ramipril completely abrogated the up-regulation of OPN mRNA and protein expression in glomeruli and tubules. The reduction in OPN expression was associated with a significant inhibition of macrophage accumulation and progressive renal injury (P < 0.001). Conclusion. An up-regulation of OPN expression may play a role in progressive renal injury following STNx. Inhibition of OPN expression may be one of the mechanisms by which Ang II blockade attenuated renal injury after renal ablation.
Persistent Identifierhttp://hdl.handle.net/10722/76672
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, XQen_HK
dc.contributor.authorWu, LLen_HK
dc.contributor.authorHuang, XRen_HK
dc.contributor.authorYang, Nen_HK
dc.contributor.authorGilbert, REen_HK
dc.contributor.authorCooper, MEen_HK
dc.contributor.authorJohnson, RJen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorLan, HYen_HK
dc.date.accessioned2010-09-06T07:23:42Z-
dc.date.available2010-09-06T07:23:42Z-
dc.date.issued2000en_HK
dc.identifier.citationKidney International, 2000, v. 58 n. 4, p. 1469-1480en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76672-
dc.description.abstractBackground. Osteopontin (OPN) is a macrophage chemotactic and adhesion molecule and has been shown to play a role in glomerular and tubulointerstitial injury in several kidney disease models. Methods. The present study examined whether OPN expression is involved in the progression of renal disease following subtotal (5/6) nephrectomy (STNx) in rats and whether angiotensin II (Ang II) mediates the up-regulation of renal OPN expression and macrophage accumulation in this model by administering valsartan, an Ang II type I (AT1) receptor antagonist, or ramipril, an angiotensin-converting enzyme (ACE) inhibitor. Results. In normal and sham-operated rat kidneys, OPN was expressed in a few tubules (< 5%) and was absent in glomeruli. Following STNx (weeks 2 to 16), there was substantial up-regulation of OPN mRNA and protein expression in glomeruli [2 to 12 cells/glomerular cross section (gcs)] and tubular epithelial cells (20 to 75% OPN +). The up-regulation of OPN expression was associated with macrophage accumulation within the kidney, severe proteinuria, loss of renal function, and severe histologic damage, including tubulitis and tubulointerstitial fibrosis (all P < 0.001). Treatment with either valsartan or ramipril completely abrogated the up-regulation of OPN mRNA and protein expression in glomeruli and tubules. The reduction in OPN expression was associated with a significant inhibition of macrophage accumulation and progressive renal injury (P < 0.001). Conclusion. An up-regulation of OPN expression may play a role in progressive renal injury following STNx. Inhibition of OPN expression may be one of the mechanisms by which Ang II blockade attenuated renal injury after renal ablation.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subjectAdhesion moleculeen_HK
dc.subjectMacrophagesen_HK
dc.subjectNephrectomyen_HK
dc.subjectRampirilen_HK
dc.subjectTubulointerstitial injuryen_HK
dc.subjectValsartanen_HK
dc.titleOsteopontin expression in progressive renal injury in remnant kidney: Role of angiotensin IIen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0085-2538&volume=58&issue=4&spage=1469&epage=1480&date=2000&atitle=Osteopontin+expression+in+progressive+renal+injury+in+remnant+kidney:+role+of+angiotensin+IIen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1523-1755.2000.00309.xen_HK
dc.identifier.pmid11012882-
dc.identifier.scopuseid_2-s2.0-0033807278en_HK
dc.identifier.hkuros61553en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033807278&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume58en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1469en_HK
dc.identifier.epage1480en_HK
dc.identifier.isiWOS:000089626700010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYu, XQ=7404114196en_HK
dc.identifier.scopusauthoridWu, LL=7404904067en_HK
dc.identifier.scopusauthoridHuang, XR=7410248090en_HK
dc.identifier.scopusauthoridYang, N=7202173206en_HK
dc.identifier.scopusauthoridGilbert, RE=7401931892en_HK
dc.identifier.scopusauthoridCooper, ME=7404410528en_HK
dc.identifier.scopusauthoridJohnson, RJ=35398596600en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK

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