Adiponectin suppresses IκB kinase activation induced by tumor necrosis factor-α or high glucose in endothelial cells: Role of cAMP and AMP kinase signaling

dc.contributor.author Wu, Xiangdong
dc.contributor.author Mahadev, Kalyankar
dc.contributor.author Fuchsel, Lauren
dc.contributor.author Ouedraogo, Raogo
dc.contributor.author Xu, Shi Qiong
dc.contributor.author Goldstein, Barry J.
dc.date.accessioned 2022-03-27T04:11:27Z
dc.date.available 2022-03-27T04:11:27Z
dc.date.issued 2007-12-01
dc.description.abstract Adiponectin is a protein secreted from adipocytes that exhibits salutary effects in the vascular endothelium by signaling mechanisms that are not well understood. In obesity-related disease states and type 2 diabetes, circulating substances, including tumor necrosis factor-α (TNFα) and high glucose, activate IκB kinase (IKK)β and reduce the abundance of its substrate, inhibitor of κB (IκB)α, leading to nuclear translocation of the transcription factor NF-κB and stimulation of an inflammatory signaling cascade closely associated with endothelial dysfunction. The present study demonstrates that the globular domain of adiponectin (gAd) potently suppresses the activation of IKKβ by either TNFα or high glucose in human umbilical vein endothelial cells and ameliorates the associated loss of IκBα protein. Interestingly, activation of AMP kinase was substantially more effective than cAMP signaling in suppressing high glucose-induced IKKβ activity, whereas both pathways were comparably active in suppressing the TNFα-induced increase in IKKβ. Both cAMP/protein kinase A signaling and activation of the AMP kinase pathway played a role in the suppression by gAd of TNFα- and high glucose-mediated IKKβ activation. These findings support an important role for adiponectin in anti-inflammatory signaling in the endothelium and also imply that multiple pathways are involved in the cellular effects of adiponectin. Copyright © 2007 the American Physiological Society.
dc.identifier.citation American Journal of Physiology - Endocrinology and Metabolism. v.293(6)
dc.identifier.issn 01931849
dc.identifier.uri 10.1152/ajpendo.00115.2007
dc.identifier.uri https://www.physiology.org/doi/10.1152/ajpendo.00115.2007
dc.identifier.uri https://dspace.uohyd.ac.in/handle/1/6754
dc.subject Endothelial dysfunction
dc.subject Inflammation
dc.subject Insulin resistance
dc.subject NF-κB
dc.title Adiponectin suppresses IκB kinase activation induced by tumor necrosis factor-α or high glucose in endothelial cells: Role of cAMP and AMP kinase signaling
dc.type Journal. Article
dspace.entity.type
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