scholarly journals Podocyte Density and Albuminuria in Aging Diabetic Ins2± Mice with or Without Adenosine A1 Receptor Signaling

2020 ◽  
Vol Volume 13 ◽  
pp. 19-26
Author(s):  
Robert Faulhaber-Walter ◽  
Lanping Jiang ◽  
Diane Mizel ◽  
Patricia Zerfas ◽  
Jeffrey B Kopp ◽  
...  
Keyword(s):  
Adenosine A1 Receptor ◽  
Receptor Signaling ◽  
Adenosine A1 ◽  
A1 Receptor

Role of EGFR in Adenosine A1 Receptor Signaling and Cardioprotection

2010 ◽  
Vol 19 ◽  
pp. S46
Author(s):  
G. Williams-Pritchard ◽  
M. Knight ◽  
L. See Hoe ◽  
J. Headrick ◽  
J. Peart
Keyword(s):  
Adenosine A1 Receptor ◽  
Receptor Signaling ◽  
Adenosine A1 ◽  
A1 Receptor

scholarly journals Clock genes Period1 and Period2 in the hippocampal CA1 mediate depression-like behaviors and rapid antidepressant response

2021 ◽  
Author(s):  
Xin-Ling Wang ◽  
Xiaoxing Liu ◽  
Kai Yuan ◽  
Ying Han ◽  
Yan-Xue Xue ◽  
...  
Keyword(s):  
Clock Genes ◽  
Critical Role ◽  
Adenosine A1 Receptor ◽  
Receptor Signaling ◽  
Promoter Regions ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Adenosine A1 ◽  
A1 Receptor

Accumulated reports have indicated that circadian rhythm is closely related to the pathogenesis of major depressive disorder (MDD). Recently, adenosine has been identified to modulate circadian clock via adenosine A1 and A2A receptor signaling pathways. Cyclic AMP-response element binding protein (CREB) is a convergent point that plays a critical role in the pathogenesis of depression and is a downstream molecule of adenosine A1 receptor signaling pathway as an endpoint that can regulate the expression of circadian genes Period1 (Per1) and Period2 (Per2). However, whether Per mediates the development of MDD via CREB has not been elucidated. We used chronic unpredictable stress (CUS) to induce depression-like behaviors and found that it could induce decrease in p-CREB and PER1 levels in the hippocampal CA1 region in rats. Both depression-like behaviors and the decreased protein levels could be rapidly rescued by the administration of adenosine A1 receptor agonist 2-Choro-N6-cyclopentyladenosine (CCPA). Furthermore, knockdown of Per1 in hippocampal CA1 region could also induce depression-like behaviors, which could also be rescued by CCPA. Interestingly, Per2 knockdown in hippocampal CA1 region resulted in potential antidepressant-like effect. In addition, knockout of CRE sequence in the promoter regions of either Per1 or Per2 led to depression-like behaviors, which could not be rescued by CCPA. These results indicated that clock genes Per1 and Per2 play critical roles in the pathophysiology of depression and CRE sequences in the promoter regions of Per1 and Per2 may be a critical antidepressant target.

scholarly journals Impaired Glucose Tolerance in the Absence of Adenosine A1 Receptor Signaling

Diabetes ◽  
2011 ◽  
Vol 60 (10) ◽  
pp. 2578-2587 ◽  
Author(s):  
R. Faulhaber-Walter ◽  
W. Jou ◽  
D. Mizel ◽  
L. Li ◽  
J. Zhang ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Adenosine A1 Receptor ◽  
Receptor Signaling ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine A1 Receptor Antagonist Up-regulates Casp3 and Stimulates Apoptosis Rate in Breast Cancer Cell Line T47D

2020 ◽  
Vol 9 (1) ◽  
pp. 14-20
Author(s):  
Mohammad Zamani Rarani ◽  
Fahimeh Zamani Rarani ◽  
Ali Valiani ◽  
Zeinolabedin Shrifian Dastjerdi ◽  
Elias Kargar Abargouei ◽  
...  
Keyword(s):  
Cell Line ◽  
Cancer Cell Line ◽  
P53 Gene ◽  
T47d Cell ◽  
Adenosine A1 Receptor ◽  
T47d Cells ◽  
Apoptosis Rate ◽  
Adenosine A1 ◽  
T47d Cell Line ◽  
A1 Receptor

Background: Adenosine receptor family, especially A1 type is-overexpressed in breast-derived tumor cells and the P53 gene is mutant in some of these cells while the casps gene is of wild type as well. The aim of this study was to evaluate the effect of the A1 receptor function on cell programmed death or proliferation, as well as the relationship between this receptor stimulation/inhibition and caspase 3 (casp3) expression in T47D cell line that has a mutant and non-functional P53 gene. Materials and Methods: The expression of casps3 was measured by real-time polymerase chain reaction and then flow cytometery and MTT assay were used to assess the apoptotic and proliferation cell rate after the treatment of T47D cells with specific agonist N6-cyclopentyladenosine (CPA) and antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) of this receptor 24, 48, and 72 hours after treatment. Result: Our results indicated that DPCPX significantly induces apoptosis in T47D cells and the rate of survival cell after the reduction of this treatment, especially 72 hours after treatment. Finally, the expression of casp3 was up-regulated by DPCPX treatment, especially in 72 hours while CPA treatment had opposite results (P>0.05). Conclusion: In general, DPCPX could up-regulate casp3 gene expression and subsequently increase the apoptosis rate in T47D cells with casp3 expression without the P53 gene interference. Therefore, adenosine A1 receptor antagonists may be introduced as anti-cancer agents.

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