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Conference Paper: The role of visfatin in intermittent hypoxia-induced inflammation and endothelial dysfunction

TitleThe role of visfatin in intermittent hypoxia-induced inflammation and endothelial dysfunction
Authors
KeywordsMedical sciences
Respiratory diseases
Issue Date2014
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
The 2014 International Conference of the American Thoracic Society (ATS 2014), San Diego, CA., 16-21 May 2014. In American Journal of Respiratory and Critical Care Medicine, 2014, v. 189 n. 1_Meeting Abstracts, abstract no. A2409 How to Cite?
AbstractRATIONALE: Intermittent hypoxia (IH), a hallmark feature in obstructive sleep apnea (OSA) associated with transient cessation of breathing during sleep, may be the main culprit underlying endothelial dysfunction, a risk factor for atherosclerosis. Visfatin is a multifaceted adipokine, the extracellular form of which can exert various effects on the vascular endothelium including inflammation, proliferation and endothelium-dependent relaxation. However, little is known about the role of visfatin in inflammation and endothelial dysfunction induced by IH. This study is aimed to compare the effects of visfatin on inflammation and endothelial function between IH and normoxia in endothelial cells. METHODS: IH exposure was performed in the hypoxic chamber in which O2 levels were alternated between 1% for 10 min and 21% for 5 min in one complete cycle and CO2 levels were maintained at 5%. Intermittent normoxia (IN;21% O2 and 5% CO2) exposure was carried out simultaneously in control cell cultures. Endothelial EA.hy926 cells were exposed to IN or IH for 96 cycles with two concentrations of visfatin (10ng/ml and 100ng/ml). Supernatants were collected after treatment to measure the levels of inflammatory markers, interleukin (IL)-8 and monocyte chemoattractant protein (MCP)-1, using commercial ELISA kits. Cellular proteins were extracted to determine the expression ofa key enzyme regulating endothelial function, nitric oxide synthase (eNOS) and its activity in terms of phosphorylation at ser1177 [p-eNOS (Ser1177)] using Western blot. RESULTS: IH exposure induced elevation of IL-8 and MCP-1 levels (p<0.05). Visfatin attenuated IH-induced elevation of IL-8 and MCP-1 levels in a dose-dependent manner. Visfatin alone had no effects on basal levels of IL-8 and MCP-1. Western blot analysis revealed that IH exposure significantly suppressed p-eNOS expression but not eNOS expression in EA.hy926 cells. In the presence of visfatin, no differences were found in the basal expression of p-eNOS and eNOS or in IH-induced suppression of p-eNOS. CONCLUSION: These results provided evidence that visfatin might play a pivotal role in IH-induced endothelial inflammation but not in reversing endothelial dysfunction in OSA.
DescriptionPoster Session: A109 - The Impact of Sleep Disordered Breathing on the Heart and other Organ Systems: no. A2409
Persistent Identifierhttp://hdl.handle.net/10722/212212
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832

 

DC FieldValueLanguage
dc.contributor.authorWang, Y-
dc.contributor.authorLee, MYK-
dc.contributor.authorIp, MS-
dc.contributor.authorMak, JC-
dc.date.accessioned2015-07-21T02:27:48Z-
dc.date.available2015-07-21T02:27:48Z-
dc.date.issued2014-
dc.identifier.citationThe 2014 International Conference of the American Thoracic Society (ATS 2014), San Diego, CA., 16-21 May 2014. In American Journal of Respiratory and Critical Care Medicine, 2014, v. 189 n. 1_Meeting Abstracts, abstract no. A2409-
dc.identifier.issn1073-449X-
dc.identifier.urihttp://hdl.handle.net/10722/212212-
dc.descriptionPoster Session: A109 - The Impact of Sleep Disordered Breathing on the Heart and other Organ Systems: no. A2409-
dc.description.abstractRATIONALE: Intermittent hypoxia (IH), a hallmark feature in obstructive sleep apnea (OSA) associated with transient cessation of breathing during sleep, may be the main culprit underlying endothelial dysfunction, a risk factor for atherosclerosis. Visfatin is a multifaceted adipokine, the extracellular form of which can exert various effects on the vascular endothelium including inflammation, proliferation and endothelium-dependent relaxation. However, little is known about the role of visfatin in inflammation and endothelial dysfunction induced by IH. This study is aimed to compare the effects of visfatin on inflammation and endothelial function between IH and normoxia in endothelial cells. METHODS: IH exposure was performed in the hypoxic chamber in which O2 levels were alternated between 1% for 10 min and 21% for 5 min in one complete cycle and CO2 levels were maintained at 5%. Intermittent normoxia (IN;21% O2 and 5% CO2) exposure was carried out simultaneously in control cell cultures. Endothelial EA.hy926 cells were exposed to IN or IH for 96 cycles with two concentrations of visfatin (10ng/ml and 100ng/ml). Supernatants were collected after treatment to measure the levels of inflammatory markers, interleukin (IL)-8 and monocyte chemoattractant protein (MCP)-1, using commercial ELISA kits. Cellular proteins were extracted to determine the expression ofa key enzyme regulating endothelial function, nitric oxide synthase (eNOS) and its activity in terms of phosphorylation at ser1177 [p-eNOS (Ser1177)] using Western blot. RESULTS: IH exposure induced elevation of IL-8 and MCP-1 levels (p<0.05). Visfatin attenuated IH-induced elevation of IL-8 and MCP-1 levels in a dose-dependent manner. Visfatin alone had no effects on basal levels of IL-8 and MCP-1. Western blot analysis revealed that IH exposure significantly suppressed p-eNOS expression but not eNOS expression in EA.hy926 cells. In the presence of visfatin, no differences were found in the basal expression of p-eNOS and eNOS or in IH-induced suppression of p-eNOS. CONCLUSION: These results provided evidence that visfatin might play a pivotal role in IH-induced endothelial inflammation but not in reversing endothelial dysfunction in OSA.-
dc.languageeng-
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org-
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicine-
dc.subjectMedical sciences-
dc.subjectRespiratory diseases-
dc.titleThe role of visfatin in intermittent hypoxia-induced inflammation and endothelial dysfunction-
dc.typeConference_Paper-
dc.identifier.emailLee, MYK: leemary@hku.hk-
dc.identifier.emailIp, MS: msmip@hku.hk-
dc.identifier.emailMak, JC: judithmak@hku.hk-
dc.identifier.authorityIp, MS=rp00347-
dc.identifier.authorityMak, JC=rp00352-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros245898-
dc.identifier.volume189-
dc.identifier.issue1_Meeting Abstracts-
dc.publisher.placeUnited States-

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