File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL

Conference Paper: Lipocalin-2 Deficiency Protects against Aldosterone-Induced Hypertension and Organ Damages by Inhibiting Mineralocorticoid Receptor Signaling

TitleLipocalin-2 Deficiency Protects against Aldosterone-Induced Hypertension and Organ Damages by Inhibiting Mineralocorticoid Receptor Signaling
Authors
Issue Date2016
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2016 Annual Meeting of Experimental Biology (EB 2016), San Diego, CA., 2-6 April 2016. In The FASEB Journal, 2016, v. 30 meeting abstracts, abstarct no. 942.6 How to Cite?
AbstractLipocalin-2, an adipokine dysregulated in cardiometabolic syndrome, is causatively involved in the development of obesity-related endothelial dysfunction and hypertension. The present study investigated the contribution of lipocalin-2 to aldosterone-induced pathologies involving mineralocorticoid receptors (MR). Mice were treated during four weeks with vehicle, angiotensin II or challenged with the combination of aldosterone plus uninephrectomy and administration of 1% saline in the drinking water (ANS). In mice without lipocalin-2 (LKO), the gene expression levels of MR in heart, kidney, adipose tissue and aorta are significantly lower than those of wild-type (WT) controls. ANS significantly increased arterial blood pressures in WT but not LKO mice. Moreover, lipocalin-2 deficiency prevented ANS-induced fibrotic damages in heart and kidneys. Treatment with the MR antagonist, spironolactone, protected mice against ANS-induced hypertension and organ damages to a similar extent as lipocalin-2-deficiency. On the other hand, angiotensin II-induced elevation of blood pressure was not affected significantly by either lipocalin-2-deficiency or MR inhibition. The mechanistic involvement of lipocalin-2 in aldosterone-stimulated MR expression and/or activation was further investigated. Collectively, the results demonstrate that lipocalin-2 plays a critical role in the cardiovascular damage induced by activation of the aldosterone-MR signaling axis.
DescriptionPharmacology - Session 942. Pathobiology of Blood Pressure Control: no. 942.6
Persistent Identifierhttp://hdl.handle.net/10722/226480
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorYang, K-
dc.contributor.authorLuo, C-
dc.contributor.authorCheung, BMY-
dc.contributor.authorFeletou, M-
dc.contributor.authorVilaine, JP-
dc.contributor.authorVilleneuve, N-
dc.contributor.authorXu, A-
dc.contributor.authorVanhoutte, PM-
dc.contributor.authorWang, Y-
dc.date.accessioned2016-06-17T07:44:25Z-
dc.date.available2016-06-17T07:44:25Z-
dc.date.issued2016-
dc.identifier.citationThe 2016 Annual Meeting of Experimental Biology (EB 2016), San Diego, CA., 2-6 April 2016. In The FASEB Journal, 2016, v. 30 meeting abstracts, abstarct no. 942.6-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/226480-
dc.descriptionPharmacology - Session 942. Pathobiology of Blood Pressure Control: no. 942.6-
dc.description.abstractLipocalin-2, an adipokine dysregulated in cardiometabolic syndrome, is causatively involved in the development of obesity-related endothelial dysfunction and hypertension. The present study investigated the contribution of lipocalin-2 to aldosterone-induced pathologies involving mineralocorticoid receptors (MR). Mice were treated during four weeks with vehicle, angiotensin II or challenged with the combination of aldosterone plus uninephrectomy and administration of 1% saline in the drinking water (ANS). In mice without lipocalin-2 (LKO), the gene expression levels of MR in heart, kidney, adipose tissue and aorta are significantly lower than those of wild-type (WT) controls. ANS significantly increased arterial blood pressures in WT but not LKO mice. Moreover, lipocalin-2 deficiency prevented ANS-induced fibrotic damages in heart and kidneys. Treatment with the MR antagonist, spironolactone, protected mice against ANS-induced hypertension and organ damages to a similar extent as lipocalin-2-deficiency. On the other hand, angiotensin II-induced elevation of blood pressure was not affected significantly by either lipocalin-2-deficiency or MR inhibition. The mechanistic involvement of lipocalin-2 in aldosterone-stimulated MR expression and/or activation was further investigated. Collectively, the results demonstrate that lipocalin-2 plays a critical role in the cardiovascular damage induced by activation of the aldosterone-MR signaling axis.-
dc.languageeng-
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journal-
dc.titleLipocalin-2 Deficiency Protects against Aldosterone-Induced Hypertension and Organ Damages by Inhibiting Mineralocorticoid Receptor Signaling-
dc.typeConference_Paper-
dc.identifier.emailLuo, C: cuiting@hku.hk-
dc.identifier.emailCheung, BMY: mycheung@hkucc.hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityCheung, BMY=rp01321-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authorityVanhoutte, PM=rp00238-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.hkuros258316-
dc.identifier.volume30-
dc.identifier.issuemeeting abstracts-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats