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Results demonstrate that agonism of either peripheral A2AAR or central A2BAR causes hypothermia. Thus, agonism at any one of the four canonical adenosine receptors, A1AR, A2AAR, A2BAR, or A3AR can cause hypothermia. This four-fold redundancy in adenosine-mediated initiation of hypothermia may reflect the centrality of hypothermia as a protective response.
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Authors show that engagement of A2A adenosine receptor (A2AR) acts as a checkpoint that limits the maturation of natural killer (NK) cells. Both global and NK-cell-specific conditional deletion of A2AR enhanced proportions of terminally mature NK cells at homeostasis, following reconstitution, and in the tumor microenvironment.
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Results show that A2ARs are important molecules that are required for gammadelta T cells to exert their enhancing activation. Blockade of A2AR function on gammadelta T cells should allow us to tip the enhancing and inhibiting function of gammadelta T cells toward the latter.
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protective role in obesity-associated nonalcoholic fatty liver disease attributable to the direct effects of A2AR on altering inflammatory and metabolic responses of macrophages and hepatocytes
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Study demonstrates that cognitive functions, including spatial memory and mood, are impaired due to acute hypobaric hypoxia (HH); and demonstrate that genetic inactivation of A2AR prevented spatial memory impairment in acute HH model of mice. The underlying mechanism might include microglia-mediated neuroinflammation via A2AR activation in the hippocampus.
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Cigarette smoke impairs A2A adenosine receptor mediated wound repair through up-regulation of Duox-1 expression.
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The present study evaluates the behavioral effects of pharmacological manipulation and genetic blockade of A2A R and D2 R within the frame of such a predominant striatal heteromeric population.
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Early synaptic deficits in the APP/PS1 mouse model of Alzheimer's disease involve neuronal adenosine A2A receptors.
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importance for MC5r and A2Ar expression in EAU to promote the induction of protective regulatory immunity, and the expression of MC5r and A2Ar on human immune cells, suggests that it may be possible to utilize the melanocortin-adenosinergic pathways to induce protective immunity in uveitic patients
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Body weight was significantly smaller in A2AR-KO mice at the age of 6 months
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Results show overall cognitive impairments in A2A adenosine receptor knockout mice associated with a decrease in new-born hippocampal neuron proliferation and concomitant changes in synaptic protein expression, in both the prefrontal cortex and the hippocampus.
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aged mice have a lower ability to cope with inflammation due to C. albicans over-colonization, associated with an inability to adaptively adjust adenosine A2A receptors density
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A2AR activation enhances its interaction with endothelial glutamate transporters. Inhibition of A2AR rescued dysfunction of brain endothelial glutamate transporters.
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The astrocytic Lrp4 plays an important role in ischemic brain injury response. Lrp4 deficiency in astrocytes seems to be protective in response to ischemic brain injury, likely because of the increased ATP release and adenosine-A2AR signaling.
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the potential effects of the A2A adenosine receptor (A2AR) antagonist SCH 5826 (SCH) and agonist CGS 21680 (CGS) on behavior (self-grooming), hot plate test results, and expression levels of IL-17A(+), RORgammat(+), Foxp3(+), and IL-10(+) in CD4(+) T spleen cells in BTBR and C57BL/6 (B6) mice, were investigated.
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Compared to adults, young WT mice failed to control S. pneumoniae infection after vaccination and this was associated with lower levels of CD73 on innate B cells. We hypothesized that pharmacological activation of A2a receptor may improve Pneumovax 23 immunization in young WT mice
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Absence of A2AAR increases cochlear resistance to acoustic trauma.
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Behavioral, anatomical and neurochemical studies to assess psychotic-like symptoms in adult male and female A2AR KO and wild-type littermates. Results bolster the adenosine hypothesis of schizophrenia by demonstrating behavioral and anatomical alterations associated with the specific deletion of adenosine A2AR. These findings resemble most of the relevant phenotype features of the human disorder.
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Adenosine receptor A2A drives pathological angiogenesis in the oxygen-induced retinopathy mouse model by promoting glycolysis in endothelial cells via the ERK/Akt/HIF-1alpha pathway.
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it is concluded that the anxiolytic-like activities of rubimetide and typical agonist peptides of the FPR2 were mediated successively by the PGD2-DP1 receptor, adenosine-A2A receptor, and GABA-GABAA receptor systems downstream of the FPR2.
