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Article: Lipocalin-2 derived from adipose tissue mediates aldosterone-induced renal injury

TitleLipocalin-2 derived from adipose tissue mediates aldosterone-induced renal injury
Authors
KeywordsAdipose tissue
Inflammation
Mouse models
Nephrology
Issue Date2018
PublisherAmerican Society for Clinical Investigation . The Journal's web site is located at https://insight.jci.org/
Citation
Journal of Clinical Investigation Insight, 2018, v. 3 n. 17, article no. 120196 How to Cite?
AbstractLipocalin-2 is not only a sensitive biomarker but also contributes to the pathogenesis of renal injuries. The present study demonstrates that adipose tissue-derived lipocalin-2 plays a critical role in causing both chronic and acute renal injuries. Four-weeks treatment with aldosterone and high salt after uninephrectomy (ANS) significantly increased both circulating and urinary lipocalin-2, and induced glomerular and tubular injuries in kidneys of wild type (WT) mice. Despite increased renal expression of lcn2 and urinary excretion of lipocalin-2, mice with selective deletion of lcn2 alleles in adipose tissue (Adipo-LKO) are protected from ANS- or aldosterone-induced renal injuries. By contrast, selective deletion of lcn2 alleles in kidney did not prevent aldosterone- or ANS-induced renal injuries. Transplantation of fat pads from WT donors increased the sensitivity of mice without lipocalin-2 (LKO) to aldosterone-induced renal injuries. Aldosterone promoted the urinary excretion of a human lipocalin-2 variant, R81E, in turn causing renal injuries in LKO mice. Chronic treatment with R81E triggered significant renal injuries in LKO, resembling those observed in WT mice following ANS challenge. Taken in conjunction, the present results demonstrate that lipocalin-2 derived from adipose tissue causes acute and chronic renal injuries, largely independent of local lcn2 expression in kidney.
Persistent Identifierhttp://hdl.handle.net/10722/259380
ISSN
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSun, WY-
dc.contributor.authorBai, B-
dc.contributor.authorLuo, C-
dc.contributor.authorYang, K-
dc.contributor.authorLI, D-
dc.contributor.authorWu, D-
dc.contributor.authorFeletou, M-
dc.contributor.authorVilleneuve, N-
dc.contributor.authorZhou, Y-
dc.contributor.authorYang, J-
dc.contributor.authorXu, A-
dc.contributor.authorVanhoutte, PMGR-
dc.contributor.authorWang, Y-
dc.date.accessioned2018-09-03T04:06:28Z-
dc.date.available2018-09-03T04:06:28Z-
dc.date.issued2018-
dc.identifier.citationJournal of Clinical Investigation Insight, 2018, v. 3 n. 17, article no. 120196-
dc.identifier.issn2379-3708-
dc.identifier.urihttp://hdl.handle.net/10722/259380-
dc.description.abstractLipocalin-2 is not only a sensitive biomarker but also contributes to the pathogenesis of renal injuries. The present study demonstrates that adipose tissue-derived lipocalin-2 plays a critical role in causing both chronic and acute renal injuries. Four-weeks treatment with aldosterone and high salt after uninephrectomy (ANS) significantly increased both circulating and urinary lipocalin-2, and induced glomerular and tubular injuries in kidneys of wild type (WT) mice. Despite increased renal expression of lcn2 and urinary excretion of lipocalin-2, mice with selective deletion of lcn2 alleles in adipose tissue (Adipo-LKO) are protected from ANS- or aldosterone-induced renal injuries. By contrast, selective deletion of lcn2 alleles in kidney did not prevent aldosterone- or ANS-induced renal injuries. Transplantation of fat pads from WT donors increased the sensitivity of mice without lipocalin-2 (LKO) to aldosterone-induced renal injuries. Aldosterone promoted the urinary excretion of a human lipocalin-2 variant, R81E, in turn causing renal injuries in LKO mice. Chronic treatment with R81E triggered significant renal injuries in LKO, resembling those observed in WT mice following ANS challenge. Taken in conjunction, the present results demonstrate that lipocalin-2 derived from adipose tissue causes acute and chronic renal injuries, largely independent of local lcn2 expression in kidney.-
dc.languageeng-
dc.publisherAmerican Society for Clinical Investigation . The Journal's web site is located at https://insight.jci.org/-
dc.relation.ispartofJournal of Clinical Investigation Insight-
dc.subjectAdipose tissue-
dc.subjectInflammation-
dc.subjectMouse models-
dc.subjectNephrology-
dc.titleLipocalin-2 derived from adipose tissue mediates aldosterone-induced renal injury-
dc.typeArticle-
dc.identifier.emailSun, WY: kiwisun@hku.hk-
dc.identifier.emailBai, B: baibohku@hku.hk-
dc.identifier.emailLuo, C: cuiting@hku.hk-
dc.identifier.emailYang, K: yangkm@hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authorityVanhoutte, PMGR=rp00238-
dc.identifier.authorityWang, Y=rp00239-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1172/jci.insight.120196-
dc.identifier.pmid30185654-
dc.identifier.pmcidPMC6171815-
dc.identifier.hkuros288680-
dc.identifier.volume3-
dc.identifier.issue17-
dc.identifier.spagearticle no. 120196-
dc.identifier.epagearticle no. 120196-
dc.identifier.isiWOS:000443880600005-
dc.publisher.placeUnited States-

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