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Conference Paper: Modification of circulating and cardiac expressions of adiponectin and CINC-1 by intermittent hypoxia in vivo

TitleModification of circulating and cardiac expressions of adiponectin and CINC-1 by intermittent hypoxia in vivo
Authors
KeywordsMedical sciences
Respiratory diseases
Issue Date2010
PublisherAmerican Thoracic Society. The Conference Abstracts' web site is located at http://www.atsjournals.org/series/ajrccm-conference
Citation
The 106th International Conference of the American Thoracic Society (ATS 2010), San Diego, CA., 15-20 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2010, v. 181 meeting abstracts, no. A3702 How to Cite?
AbstractRATIONALE: Adiponectin is an adipokine that exerts anti-inflammatory and cardiovascular protective properties. Obstructive sleep apnea (OSA), characterized by recurrent intermittent hypoxia (IH), is highly associated with cardiovascular diseases. This study aimed to explore the effects of IH on circulating and cardiac expressions of adiponectin and cytokine induced neutrophil chemoattractant (CINC)-1 in the rat model in vivo, thus identifying possible links between OSA and cardiovascular risks. METHODS: Male Sprague-Dawley rats were randomly divided into two groups: control and IH exposed. The IH exposure was performed using OxyCycler A84 System (BioSpherix, Redfield, NY, USA) daily, and composed of cycles of 4 min hypoxia (10% O2) followed by 2 min normoxia (21% O2) for 6 hours. After 14 or 28 days, sera and heart tissues were collected. Circulating and heart tissue levels of adiponectin and CINC-1 were measured by ELISA. RESULTS: IH caused a decrease in serum adiponectin level at 28 days (6.09 ± 0.37 vs 8.24 ± 0.82 μg/ml for IH and control groups respectively; p < 0.05) but not at 14 days, and significant increases in serum CINC-1 level at both 14 days (1.4-fold) and 28 days (1.7-fold). However, cardiac adiponectin level showed a trend of decrease at 14 days but a significant increase at 28 days (0.60 ± 0.048 vs 0.45 ± 0.04 μg/mg protein for IH and control groups respectively; p < 0.05). Cardiac CINC-1 level showed no significant differences at both time points. CONCLUSION: This study suggests that IH-induced reduction in adiponectin and elevation in CINC-1 in serum levels may serve as the possible underlying mechanisms of OSA-related cardiovascular diseases.
DescriptionSession - B73 Sleep Disordered Breathing and Control of Ventilation: Basic and Translational Aspects
Persistent Identifierhttp://hdl.handle.net/10722/133305
ISSN
2023 Impact Factor: 19.3
2023 SCImago Journal Rankings: 5.336

 

DC FieldValueLanguage
dc.contributor.authorHan, Q-
dc.contributor.authorYeung, SC-
dc.contributor.authorIp, MS-
dc.contributor.authorMak, JC-
dc.date.accessioned2011-05-11T06:58:05Z-
dc.date.available2011-05-11T06:58:05Z-
dc.date.issued2010-
dc.identifier.citationThe 106th International Conference of the American Thoracic Society (ATS 2010), San Diego, CA., 15-20 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2010, v. 181 meeting abstracts, no. A3702-
dc.identifier.issn1073-449X-
dc.identifier.urihttp://hdl.handle.net/10722/133305-
dc.descriptionSession - B73 Sleep Disordered Breathing and Control of Ventilation: Basic and Translational Aspects-
dc.description.abstractRATIONALE: Adiponectin is an adipokine that exerts anti-inflammatory and cardiovascular protective properties. Obstructive sleep apnea (OSA), characterized by recurrent intermittent hypoxia (IH), is highly associated with cardiovascular diseases. This study aimed to explore the effects of IH on circulating and cardiac expressions of adiponectin and cytokine induced neutrophil chemoattractant (CINC)-1 in the rat model in vivo, thus identifying possible links between OSA and cardiovascular risks. METHODS: Male Sprague-Dawley rats were randomly divided into two groups: control and IH exposed. The IH exposure was performed using OxyCycler A84 System (BioSpherix, Redfield, NY, USA) daily, and composed of cycles of 4 min hypoxia (10% O2) followed by 2 min normoxia (21% O2) for 6 hours. After 14 or 28 days, sera and heart tissues were collected. Circulating and heart tissue levels of adiponectin and CINC-1 were measured by ELISA. RESULTS: IH caused a decrease in serum adiponectin level at 28 days (6.09 ± 0.37 vs 8.24 ± 0.82 μg/ml for IH and control groups respectively; p < 0.05) but not at 14 days, and significant increases in serum CINC-1 level at both 14 days (1.4-fold) and 28 days (1.7-fold). However, cardiac adiponectin level showed a trend of decrease at 14 days but a significant increase at 28 days (0.60 ± 0.048 vs 0.45 ± 0.04 μg/mg protein for IH and control groups respectively; p < 0.05). Cardiac CINC-1 level showed no significant differences at both time points. CONCLUSION: This study suggests that IH-induced reduction in adiponectin and elevation in CINC-1 in serum levels may serve as the possible underlying mechanisms of OSA-related cardiovascular diseases.-
dc.languageeng-
dc.publisherAmerican Thoracic Society. The Conference Abstracts' web site is located at http://www.atsjournals.org/series/ajrccm-conference-
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicine-
dc.subjectMedical sciences-
dc.subjectRespiratory diseases-
dc.titleModification of circulating and cardiac expressions of adiponectin and CINC-1 by intermittent hypoxia in vivoen_US
dc.typeConference_Paperen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1073-449X&volume=181: A3702&spage=&epage=&date=2010&atitle=Modification+of+circulating+and+cardiac+expressions+of+adiponectin+and+CINC-1+by+intermittent+hypoxia+in+vivo-
dc.identifier.emailHan, Q: hanqian@hkusua.hku.hk, hanqian1020@yahoo.com-
dc.identifier.emailYeung, SC: h0294069@graduate.hku.hk-
dc.identifier.emailIp, MS: msmip@hku.hk-
dc.identifier.emailMak, JC: judymak@HKUCC.hku.hk-
dc.identifier.hkuros171676-
dc.identifier.volume181-
dc.identifier.issuemeeting abstracts-
dc.description.otherInternational Conference of the American Thoracic Society (ATS) 2009, San Diego, CA., 15-20 May 2010. In American Journal of Respiratory and Critical Care Medicine, 2010, v. 181 (Meeting abstracts), no. A3702-
dc.identifier.issnl1073-449X-

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