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- W2103984309 abstract "Adenosine has been described as playing a role in the control of inflammation, but it has not been certain which of its receptors mediate this effect. Here, we generated an A2B adenosine receptor-knockout/reporter gene-knock-in (A2BAR-knockout/reporter gene-knock-in) mouse model and showed receptor gene expression in the vasculature and macrophages, the ablation of which causes low-grade inflammation compared with age-, sex-, and strain-matched control mice. Augmentation of proinflammatory cytokines, such as TNF-alpha, and a consequent downregulation of IkappaB-alpha are the underlying mechanisms for an observed upregulation of adhesion molecules in the vasculature of these A2BAR-null mice. Intriguingly, leukocyte adhesion to the vasculature is significantly increased in the A2BAR-knockout mice. Exposure to an endotoxin results in augmented proinflammatory cytokine levels in A2BAR-null mice compared with control mice. Bone marrow transplantations indicated that bone marrow (and to a lesser extent vascular) A2BARs regulate these processes. Hence, we identify the A2BAR as a new critical regulator of inflammation and vascular adhesion primarily via signals from hematopoietic cells to the vasculature, focusing attention on the receptor as a therapeutic target." @default.
- W2103984309 created "2016-06-24" @default.
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- W2103984309 date "2006-07-03" @default.
- W2103984309 modified "2023-10-17" @default.
- W2103984309 title "The A2B adenosine receptor protects against inflammation and excessive vascular adhesion" @default.
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- W2103984309 doi "https://doi.org/10.1172/jci27933" @default.
- W2103984309 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1483170" @default.
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