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Conference Paper: Reduced Clusterin Contents Contribute to The Pro-Inflammatory and Pro-Senescent Activity of Low Density Lipoprotein Particles in Adiponectin Deficient Mice

TitleReduced Clusterin Contents Contribute to The Pro-Inflammatory and Pro-Senescent Activity of Low Density Lipoprotein Particles in Adiponectin Deficient Mice
Authors
Issue Date2014
Citation
The 9th Congress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases (APSAVD) & 16th Diabetes and Cardiovascular Risk Factors – East Meets West Symposium (EMW), Hong Kong, China, 25-28 September 2014, abstract no. Ab153 How to Cite?
AbstractPurpose of the study Low adiponectin level is associated with highly oxidized low density lipoprotein (LDL) in patients with coronary heart disease. Clusterin inhibits LDL-induced monocyte chemotactic activity in artery wall. In the present study, we aim to investigate the relationship between adiponectin and clusterin in regulating the pathophysiological function of LDL. Methods Cholesterol and protein levels in LDL, HDL2 and HDL3 fractions were measured in serum from wild type and adiponectin-deficient mice after separation of these fractions by density gradient ultracentrifugation. Clusterin was detected in each lipoprotein fraction by Western blotting using specific antibody. LDL-induced endothelial cell senescence were determined by senescence-associated beta-galactosidase staining. Vascular functions were assessed in wild type and adiponectin-deficient mice using wire myography. Summary of the results Circulating levels of total, LDL- and HDL2-cholesterols were significantly increased in adiponectin-deficient mice by 64.7%, 32.5%, 36.1% compared with wild type control mice (All P < 0.05). Protein concentrations of these lipoprotein particles were similar between adiponectin-deficient and wild type mice. However, the clusterin levels were significantly decreased in LDL particles from adiponectin-deficient mice (fold change in protein expression: 0.2). Cellular senescence was significantly higher in primary porcine endothelial cells treated with the clusterin-poor LDL from adiponectin-deficient mice than that with the control LDL from wild type mice. In mice with dietary obesity, the endothelium-dependent contractions were significantly enhanced in arteries from the adiponectin-deficient mice compared to their wild type controls. Endothelium dependent relaxation were significantly attenuated by adiponectin deficiency. Conclusions Adiponectin exerts its anti-inflammatory and anti-atherogenic effects via regulating the function of LDL particles through its interactions with clusterin.
DescriptionOral Presentation 2B
Persistent Identifierhttp://hdl.handle.net/10722/204298

 

DC FieldValueLanguage
dc.contributor.authorDeng, Hen_US
dc.contributor.authorHuang, Ben_US
dc.contributor.authorXu, Cen_US
dc.contributor.authorPark, Sen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorLee, IKen_US
dc.contributor.authorWang, Yen_US
dc.date.accessioned2014-09-19T21:43:26Z-
dc.date.available2014-09-19T21:43:26Z-
dc.date.issued2014en_US
dc.identifier.citationThe 9th Congress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases (APSAVD) & 16th Diabetes and Cardiovascular Risk Factors – East Meets West Symposium (EMW), Hong Kong, China, 25-28 September 2014, abstract no. Ab153en_US
dc.identifier.urihttp://hdl.handle.net/10722/204298-
dc.descriptionOral Presentation 2B-
dc.description.abstractPurpose of the study Low adiponectin level is associated with highly oxidized low density lipoprotein (LDL) in patients with coronary heart disease. Clusterin inhibits LDL-induced monocyte chemotactic activity in artery wall. In the present study, we aim to investigate the relationship between adiponectin and clusterin in regulating the pathophysiological function of LDL. Methods Cholesterol and protein levels in LDL, HDL2 and HDL3 fractions were measured in serum from wild type and adiponectin-deficient mice after separation of these fractions by density gradient ultracentrifugation. Clusterin was detected in each lipoprotein fraction by Western blotting using specific antibody. LDL-induced endothelial cell senescence were determined by senescence-associated beta-galactosidase staining. Vascular functions were assessed in wild type and adiponectin-deficient mice using wire myography. Summary of the results Circulating levels of total, LDL- and HDL2-cholesterols were significantly increased in adiponectin-deficient mice by 64.7%, 32.5%, 36.1% compared with wild type control mice (All P < 0.05). Protein concentrations of these lipoprotein particles were similar between adiponectin-deficient and wild type mice. However, the clusterin levels were significantly decreased in LDL particles from adiponectin-deficient mice (fold change in protein expression: 0.2). Cellular senescence was significantly higher in primary porcine endothelial cells treated with the clusterin-poor LDL from adiponectin-deficient mice than that with the control LDL from wild type mice. In mice with dietary obesity, the endothelium-dependent contractions were significantly enhanced in arteries from the adiponectin-deficient mice compared to their wild type controls. Endothelium dependent relaxation were significantly attenuated by adiponectin deficiency. Conclusions Adiponectin exerts its anti-inflammatory and anti-atherogenic effects via regulating the function of LDL particles through its interactions with clusterin.en_US
dc.languageengen_US
dc.relation.ispartofCongress of the Asian-Pacific Society of Atherosclerosis and Vascular Diseases (APSAVD) & Diabetes and Cardiovascular Risk Factors – East Meets West Symposium (EMW)en_US
dc.titleReduced Clusterin Contents Contribute to The Pro-Inflammatory and Pro-Senescent Activity of Low Density Lipoprotein Particles in Adiponectin Deficient Miceen_US
dc.typeConference_Paperen_US
dc.identifier.emailDeng, H: hbdeng1@hku.hken_US
dc.identifier.emailHuang, B: ianto@hku.hken_US
dc.identifier.emailXu, C: xchku@hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailWang, Y: yuwanghk@hku.hken_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityWang, Y=rp00239en_US
dc.identifier.hkuros239963en_US

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