File Download

There are no files associated with this item.

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

Conference Paper: Role of lipocalin-2 in dietary and aldosterone-induced renal damages

TitleRole of lipocalin-2 in dietary and aldosterone-induced renal damages
Authors
Issue Date2017
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Experimental Biology 2017 Annual Meeting Abstracts: Transforming the future through science, Chicago, USA, 22-26 April 2017. In The FASEB Journal, 2017, v. 31 n. 1, Suppl , abstract no. 998.10 How to Cite?
AbstractStudy objective Both high fat diet and aldosterone challenge can cause significant renal damage, either as a primary cause or as co-morbidities with other diseases (e.g. cardiovascular diseases and diabetes). Angiotensin-converting-enzyme inhibitor (ACEi) and mineralocorticoid receptor inhibitor (MRi; e.g. spinronolactone and eplerenone) are commonly used in these patients. However their mortality is still high and such treatments are not suitable for all patients. Thus, a new therapeutic approach is warranted for renal damages. Herein, we hypothesize that lipocalin-2 plays a detrimental role in both dietary and aldosterone-induced renal injuries, and thus could be a novel drug target for therapeutic development. Methods Wild-type (WT), lipocalin-2 knockout (LKO) and lipocalin-2 tissue specific knockout in adipose tissue (ADN-Cre) mice were subjected to eight weeks of high fat diet treatment or to nephrectomy followed by four weeks of aldosterone/nephrectomy/1% saline treatment (ANS). MRi (either spinronolactone or eplerenone) was administered in ANS-treated groups to compare its efficacy versus lipocalin-2 deficiency mice in terms of anti-hypertensive effect, renal damages and fibrosis, and small resistance artery stiffness and tone. Adipose tissue of all mice was also collected for further analysis. Results Compared to MRi-treated wildtype mice, LKO and ADN-Cre mice showed a better protection against ANS-induced renal damages, as evidenced by: (1) attenuation of tissue fibrosis, (2) decreased infiltration of macrophages, (3) reduced levels of molecular injury markers, such as kidney injury marker (KIM)-1, monocyte chemoattractant protein (MCP)-1, transforming growth factor (TFG)-β and collagen I. In addition, LKO and ADN-Cre mice treated with high fat diet showed significant protection from renal damages and reduced adipose tissue fibrosis when compared to controls. As regards small resistance artery stiffness and compliance, ADN-Cre mice were protected against ANS and high fat diet challenge. Conclusion Lipocalin-2 is involved in the development of the metabolic-renal syndrome. Targeting its expression and/or signalling pathways could be a novel therapeutic approach to combat these medical complications.
Description998. Renal Pharmacology and Disease - Poster - Cardiovascular Pharmacology - no. D182 998.10
Persistent Identifierhttp://hdl.handle.net/10722/246349
ISSN
2017 Impact Factor: 5.595
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorSun, WY-
dc.contributor.authorYang, K-
dc.contributor.authorLuo, C-
dc.contributor.authorFeletou, M-
dc.contributor.authorVilleneuve, N-
dc.contributor.authorVanhoutte, PMGR-
dc.contributor.authorXu, C-
dc.contributor.authorWang, Y-
dc.date.accessioned2017-09-18T02:26:57Z-
dc.date.available2017-09-18T02:26:57Z-
dc.date.issued2017-
dc.identifier.citationExperimental Biology 2017 Annual Meeting Abstracts: Transforming the future through science, Chicago, USA, 22-26 April 2017. In The FASEB Journal, 2017, v. 31 n. 1, Suppl , abstract no. 998.10-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/246349-
dc.description998. Renal Pharmacology and Disease - Poster - Cardiovascular Pharmacology - no. D182 998.10-
dc.description.abstractStudy objective Both high fat diet and aldosterone challenge can cause significant renal damage, either as a primary cause or as co-morbidities with other diseases (e.g. cardiovascular diseases and diabetes). Angiotensin-converting-enzyme inhibitor (ACEi) and mineralocorticoid receptor inhibitor (MRi; e.g. spinronolactone and eplerenone) are commonly used in these patients. However their mortality is still high and such treatments are not suitable for all patients. Thus, a new therapeutic approach is warranted for renal damages. Herein, we hypothesize that lipocalin-2 plays a detrimental role in both dietary and aldosterone-induced renal injuries, and thus could be a novel drug target for therapeutic development. Methods Wild-type (WT), lipocalin-2 knockout (LKO) and lipocalin-2 tissue specific knockout in adipose tissue (ADN-Cre) mice were subjected to eight weeks of high fat diet treatment or to nephrectomy followed by four weeks of aldosterone/nephrectomy/1% saline treatment (ANS). MRi (either spinronolactone or eplerenone) was administered in ANS-treated groups to compare its efficacy versus lipocalin-2 deficiency mice in terms of anti-hypertensive effect, renal damages and fibrosis, and small resistance artery stiffness and tone. Adipose tissue of all mice was also collected for further analysis. Results Compared to MRi-treated wildtype mice, LKO and ADN-Cre mice showed a better protection against ANS-induced renal damages, as evidenced by: (1) attenuation of tissue fibrosis, (2) decreased infiltration of macrophages, (3) reduced levels of molecular injury markers, such as kidney injury marker (KIM)-1, monocyte chemoattractant protein (MCP)-1, transforming growth factor (TFG)-β and collagen I. In addition, LKO and ADN-Cre mice treated with high fat diet showed significant protection from renal damages and reduced adipose tissue fibrosis when compared to controls. As regards small resistance artery stiffness and compliance, ADN-Cre mice were protected against ANS and high fat diet challenge. Conclusion Lipocalin-2 is involved in the development of the metabolic-renal syndrome. Targeting its expression and/or signalling pathways could be a novel therapeutic approach to combat these medical complications.-
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.titleRole of lipocalin-2 in dietary and aldosterone-induced renal damages-
dc.typeConference_Paper-
dc.identifier.emailSun, WY: kiwisun@hku.hk-
dc.identifier.emailLuo, C: cuiting@hku.hk-
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hk-
dc.identifier.emailXu, C: xchku@hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityVanhoutte, PMGR=rp00238-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.hkuros276443-
dc.identifier.hkuros276444-
dc.identifier.volume31-
dc.identifier.issue1, Suppl-
dc.identifier.spageabstract no. 998.10-
dc.identifier.epageabstract no. 998.10-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats