File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Reduced Clusterin (apo J) Content Of Low Density Lipoproteins Contribute To Endothelial Dysfunction In Adiponectin-Deficient Mice

TitleReduced Clusterin (apo J) Content Of Low Density Lipoproteins Contribute To Endothelial Dysfunction In Adiponectin-Deficient Mice
Authors
Issue Date2015
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
Citation
The 83rd European Atherosclerosis Society Congress (EAS Congress), Glasgow, UK, 22-25 March 2015. In Atherosclerosis, 2015, v. 241 n. 1, p. e4-e5 How to Cite?
AbstractAim: Low adiponectin and clusterin (apoJ) levels are risk factors of atherosclerosis. The present study aims to investigate the relationships of adiponectin with clusterin in lipoproteins and endothelial dysfunction. Methods: Wild type and adiponectin-deficient mice were fed high fat diet for at least 12 weeks. The recombinant adenoviruses encoding mouse adiponectin or luciferase (as control) were administrated into wild type and adiponectin-deficient mice through tail vein injection. Cholesterol and protein levels were measured in low and high density lipoproteins (LDL and HDL) separated by density gradient ultracentrifugation. Clusterin was detected in LDL and HDL by Western blotting using specific antibody. Vascular function were assessed in wild type and adiponectin-deficient mice using wire myography. Results: Circulating levels of total and LDL-cholesterols were significantly increased in adiponectin-deficient mice by 50.7% and 89.1%, respectively, compared with wild type mice (P < 0.05). Protein/cholesterol ratio in LDL particles was significantly lower in adiponectin-deficient mice than that in wild type mice (0.58±0.10 vs. 0.79±0.02, P < 0.05). Clusterin content in LDL particles were significantly decreased in adiponectin-deficient mice (fold change vs. wild type: 0.35±0.04, P < 0.05). The endothelium-dependent contraction was significantly enhanced in arteries from the adiponectin-deficient mice compared to the wild type controls. The endothelium-dependent relaxation was significantly attenuated by adiponectin deficiency. Treatment of recombinant adenoviruses encoding mouse adiponectin increased clusterin content in LDL by nearly 90% and ameliorated the endothelium-dependent vascular function in adiponectin-deficient mice. Conclusions: Adiponectin may exert anti-atherogenic effects and prevent endothelial dysfunction via its interactions with clusterin in LDL.
DescriptionOral Session- OR03: Endothelial Cells & Platelet Biology - Young Investigator Communication 2
Persistent Identifierhttp://hdl.handle.net/10722/209920
ISSN
2015 Impact Factor: 3.942
2015 SCImago Journal Rankings: 1.819

 

DC FieldValueLanguage
dc.contributor.authorDeng, HB-
dc.contributor.authorHuang, B-
dc.contributor.authorXu, C-
dc.contributor.authorPark, S-
dc.contributor.authorXu, A-
dc.contributor.authorLee, IK-
dc.contributor.authorWang, Y-
dc.date.accessioned2015-05-18T03:31:08Z-
dc.date.available2015-05-18T03:31:08Z-
dc.date.issued2015-
dc.identifier.citationThe 83rd European Atherosclerosis Society Congress (EAS Congress), Glasgow, UK, 22-25 March 2015. In Atherosclerosis, 2015, v. 241 n. 1, p. e4-e5-
dc.identifier.issn0021-9150-
dc.identifier.urihttp://hdl.handle.net/10722/209920-
dc.descriptionOral Session- OR03: Endothelial Cells & Platelet Biology - Young Investigator Communication 2-
dc.description.abstractAim: Low adiponectin and clusterin (apoJ) levels are risk factors of atherosclerosis. The present study aims to investigate the relationships of adiponectin with clusterin in lipoproteins and endothelial dysfunction. Methods: Wild type and adiponectin-deficient mice were fed high fat diet for at least 12 weeks. The recombinant adenoviruses encoding mouse adiponectin or luciferase (as control) were administrated into wild type and adiponectin-deficient mice through tail vein injection. Cholesterol and protein levels were measured in low and high density lipoproteins (LDL and HDL) separated by density gradient ultracentrifugation. Clusterin was detected in LDL and HDL by Western blotting using specific antibody. Vascular function were assessed in wild type and adiponectin-deficient mice using wire myography. Results: Circulating levels of total and LDL-cholesterols were significantly increased in adiponectin-deficient mice by 50.7% and 89.1%, respectively, compared with wild type mice (P < 0.05). Protein/cholesterol ratio in LDL particles was significantly lower in adiponectin-deficient mice than that in wild type mice (0.58±0.10 vs. 0.79±0.02, P < 0.05). Clusterin content in LDL particles were significantly decreased in adiponectin-deficient mice (fold change vs. wild type: 0.35±0.04, P < 0.05). The endothelium-dependent contraction was significantly enhanced in arteries from the adiponectin-deficient mice compared to the wild type controls. The endothelium-dependent relaxation was significantly attenuated by adiponectin deficiency. Treatment of recombinant adenoviruses encoding mouse adiponectin increased clusterin content in LDL by nearly 90% and ameliorated the endothelium-dependent vascular function in adiponectin-deficient mice. Conclusions: Adiponectin may exert anti-atherogenic effects and prevent endothelial dysfunction via its interactions with clusterin in LDL.-
dc.languageeng-
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis-
dc.relation.ispartofAtherosclerosis-
dc.titleReduced Clusterin (apo J) Content Of Low Density Lipoproteins Contribute To Endothelial Dysfunction In Adiponectin-Deficient Mice-
dc.typeConference_Paper-
dc.identifier.emailDeng, HB: hbdeng1@hku.hk-
dc.identifier.emailHuang, B: ianto@hku.hk-
dc.identifier.emailXu, C: xchku@hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.doi10.1016/j.atherosclerosis.2015.04.033-
dc.identifier.hkuros243119-
dc.identifier.hkuros243594-
dc.identifier.volume241-
dc.identifier.issue1-
dc.identifier.spagee4-
dc.identifier.epagee5-
dc.publisher.placeIreland-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats