Association Analysis of Adenosine A2a Receptor 1976T>C Polymorphisms and Alzheimer’s Disease

2005 ◽  
Vol 53 (2) ◽  
pp. 99-100 ◽  
Author(s):  
Hsiu-Chih Liu ◽  
Chen-Jee Hong ◽  
Tsung-Yun Liu ◽  
Shih-Jen Tsai
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Analysis ◽  
Adenosine A2a Receptor ◽  
A2a Receptor ◽  
Adenosine A2a

scholarly journals Different Adenosine A2A Receptor Expression in Peripheral Cells from Elderly Patients with Vascular Dementia and Alzheimer's Disease

2014 ◽  
Vol 40 (1) ◽  
pp. 45-49 ◽  
Author(s):  
Cristina Gussago ◽  
Beatrice Arosio ◽  
Martina Casati ◽  
Evelyn Ferri ◽  
Federica Gualandris ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Elderly Patients ◽  
Vascular Dementia ◽  
Adenosine A2a Receptor ◽  
Receptor Expression ◽  
A2a Receptor ◽  
Adenosine A2a ◽  
Peripheral Cells

scholarly journals Adenosine A2A Receptor Antagonists Affects NMDA Glutamate Receptor Function. Potential to Address Neurodegeneration in Alzheimer’s Disease

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1075 ◽  
Author(s):  
Rafael Franco ◽  
Rafael Rivas-Santisteban ◽  
Mireia Casanovas ◽  
Alejandro Lillo ◽  
Carlos A. Saura ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glutamate Receptor ◽  
Expression System ◽  
Primary Cultures ◽  
Adenosine A2a Receptor ◽  
A2a Receptors ◽  
Adenosine A2a Receptor Antagonists ◽  
A2a Receptor ◽  
Adenosine A2a

(1) Background. N-methyl d-aspartate (NMDA) ionotropic glutamate receptor (NMDAR), which is one of the main targets to combat Alzheimer’s disease (AD), is expressed in both neurons and glial cells. The aim of this paper was to assess whether the adenosine A2A receptor (A2AR), which is a target in neurodegeneration, may affect NMDAR functionality. (2) Methods. Immuno-histo/cytochemical, biophysical, biochemical and signaling assays were performed in a heterologous cell expression system and in primary cultures of neurons and microglia (resting and activated) from control and the APPSw,Ind transgenic mice. (3) Results. On the one hand, NMDA and A2A receptors were able to physically interact forming complexes, mainly in microglia. Furthermore, the amount of complexes was markedly enhanced in activated microglia. On the other hand, the interaction resulted in a novel functional entity that displayed a cross-antagonism, that could be useful to prevent the exacerbation of NMDAR function by using A2AR antagonists. Interestingly, the amount of complexes was markedly higher in the hippocampal cells from the APPSw,Ind than from the control mice. In neurons, the number of complexes was lesser, probably due to NMDAR not interacting with the A2AR. However, the activation of the A2AR receptors resulted in higher NMDAR functionality in neurons, probably by indirect mechanisms. (4) Conclusions. A2AR antagonists such as istradefylline, which is already approved for Parkinson’s disease (Nouriast® in Japan and Nourianz® in the US), have potential to afford neuroprotection in AD in a synergistic-like fashion. i.e., via both neurons and microglia.

Synthesis of the Adenosine A2A Receptor Fluorescent Agonist MRS5424

BIO-PROTOCOL ◽  
2014 ◽  
Vol 4 (6) ◽  
Author(s):  
Kenneth Jacobson ◽  
Francisco Ciruela
Keyword(s):  
Adenosine A2a Receptor ◽  
A2a Receptor ◽  
Adenosine A2a

Optimization of the Human Adenosine A2a Receptor Yields in Saccharomyces cerevisiae

2008 ◽  
Vol 22 (5) ◽  
pp. 1249-1255 ◽  
Author(s):  
Alison Wedekind ◽  
Michelle A. O'Malley ◽  
Ronald T. Niebauer ◽  
Anne S. Robinson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Adenosine A2a Receptor ◽  
A2a Receptor ◽  
Adenosine A2a

scholarly journals A Cellular Assay for the Identification and Characterization of Connexin Gap Junction Modulators

2021 ◽  
Vol 22 (3) ◽  
pp. 1417
Author(s):  
Azeem Danish ◽  
Robin Gedschold ◽  
Sonja Hinz ◽  
Anke C. Schiedel ◽  
Dominik Thimm ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Small Molecules ◽  
High Throughput Screening ◽  
Cell Communication ◽  
Receptor Activation ◽  
Adenosine A2a Receptor ◽  
Intracellular Camp ◽  
Donor Cells ◽  
A2a Receptor ◽  
Adenosine A2a

Connexin gap junctions (Cx GJs) enable the passage of small molecules and ions between cells and are therefore important for cell-to-cell communication. Their dysfunction is associated with diseases, and small molecules acting as modulators of GJs may therefore be useful as therapeutic drugs. To identify GJ modulators, suitable assays are needed that allow compound screening. In the present study, we established a novel assay utilizing HeLa cells recombinantly expressing Cx43. Donor cells additionally expressing the Gs protein-coupled adenosine A2A receptor, and biosensor cells expressing a cAMP-sensitive GloSensor luciferase were established. Adenosine A2A receptor activation in the donor cells using a selective agonist results in intracellular cAMP production. The negatively charged cAMP migrates via the Cx43 gap junctions to the biosensor cells and can there be measured by the cAMP-dependent luminescence signal. Cx43 GJ modulators can be expected to impact the transfer of cAMP from the donor to the biosensor cells, since cAMP transit is only possible via GJs. The new assay was validated by testing the standard GJ inhibitor carbenoxolon, which showed a concentration-dependent inhibition of the signal and an IC50 value that was consistent with previously reported values. The assay was demonstrated to be suitable for high-throughput screening.

scholarly journals Correlation between low adenosine A2A receptor expression and hypercholesterolemia: A new component of the cardiovascular risk?

2021 ◽  
Vol 1866 (2) ◽  
pp. 158850
Author(s):  
Donato Vairo ◽  
Carola Giacobbe ◽  
Claire Guiol ◽  
Marie-Charlotte Chaptal ◽  
Maria Donata Di Taranto ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Adenosine A2a Receptor ◽  
Receptor Expression ◽  
A2a Receptor ◽  
Adenosine A2a

scholarly journals Adenosine A2A receptor signaling promotes FoxO associated autophagy in chondrocytes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Benjamin Friedman ◽  
Carmen Corciulo ◽  
Cristina M. Castro ◽  
Bruce N. Cronstein
Keyword(s):  
Cell Line ◽  
Metabolic Stress ◽  
Human Cell Line ◽  
Adenosine A2a Receptor ◽  
Autophagic Flux ◽  
A2a Receptor ◽  
Adenosine A2a ◽  
A2ar Agonist

AbstractAutophagy, a homeostatic pathway upregulated during cellular stress, is decreased in osteoarthritic chondrocytes and this reduction in autophagy is thought to contribute to the development and progression of osteoarthritis (OA). The adenosine A2A receptor (A2AR) is a potent anti-inflammatory receptor and deficiency of this receptor leads to the development of OA in mice. Moreover, treatment using liposomally conjugated adenosine or a specific A2AR agonist improved joint scores significantly in both rats with post-traumatic OA (PTOA) and mice subjected to a high fat diet obesity induced OA. Importantly, A2AR ligation is beneficial for mitochondrial health and metabolism in vitro in primary and the TC28a2 human cell line. An additional set of metabolic, stress-responsive, and homeostatic mediators include the Forkhead box O transcription factors (FoxOs). Data has shown that mouse FoxO knockouts develop early OA with reduced cartilage autophagy, indicating that FoxO-induced homeostasis is important for articular cartilage. Given the apparent similarities between A2AR and FoxO signaling, we tested the hypothesis that A2AR stimulation improves cartilage function through activation of the FoxO proteins leading to increased autophagy in chondrocytes. We analyzed the signaling pathway in the human TC28a2 cell line and corroborated these findings in vivo in a metabolically relevant obesity-induced OA mouse model. We found that A2AR stimulation increases activation and nuclear localization of FoxO1 and FoxO3, promotes an increase in autophagic flux, improves metabolic function in chondrocytes, and reduces markers of apoptosis in vitro and reduced apoptosis by TUNEL assay in vivo. A2AR ligation additionally enhances in vivo activation of FoxO1 and FoxO3 with evidence of enhanced autophagic flux upon injection of the liposome-associated A2AR agonist in a mouse obesity-induced OA model. These findings offer further evidence that A2AR may be an excellent target for promoting chondrocyte and cartilage homeostasis.

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