scholarly journals Biochemical and Pharmacological Role of A1 Adenosine Receptors and Their Modulation as Novel Therapeutic Strategy

2017 ◽  
pp. 193-232 ◽  
Author(s):  
Katia Varani ◽  
Fabrizio Vincenzi ◽  
Stefania Merighi ◽  
Stefania Gessi ◽  
Pier Andrea Borea
Keyword(s):  
Adenosine Receptors ◽  
Therapeutic Strategy ◽  
A1 Adenosine Receptors ◽  
Novel Therapeutic

The Role of TGF-β in Radiation and Chemotherapy Induced Pulmonary Fibrosis: Inhibition of TGF-β as a Novel Therapeutic Strategy

2008 ◽  
pp. 629-647
Author(s):  
Patricia J. Sime ◽  
R. Matthew Kottmann ◽  
Heather F. Lakatos ◽  
Thomas H. Thatcher
Keyword(s):  
Pulmonary Fibrosis ◽  
Therapeutic Strategy ◽  
Novel Therapeutic

Role of A1 adenosine receptors in regulation of vascular tone

2005 ◽  
Vol 288 (3) ◽  
pp. H1411-H1416 ◽  
Author(s):  
Huda E. Tawfik ◽  
J. Schnermann ◽  
Peter J. Oldenburg ◽  
S. Jamal Mustafa
Keyword(s):  
Adenosine Receptors ◽  
Vascular Tone ◽  
Receptor Subtypes ◽  
Vascular Relaxation ◽  
Response Curves ◽  
Cgs 21680 ◽  
A1 Adenosine Receptors ◽  
The Impact ◽  
Regulation Of Vascular Tone

The vascular response to adenosine and its analogs is mediated by four adenosine receptors (ARs), namely, A1, A2A, A2B, and A3. A2AARs and/or A2BARs are involved in adenosine-mediated vascular relaxation of coronary and aortic beds. However, the role of A1ARs in the regulation of vascular tone is less well substantiated. The aim of this study was to determine the role of A1ARs in adenosine-mediated regulation of vascular tone. A1AR-knockout [A1AR(−/−)] mice and available pharmacological tools were used to elucidate the function of A1ARs and the impact of these receptors on the regulation of vascular tone. Isolated aortic rings from A1AR(−/−) and wild-type [A1AR(+/+)] mice were precontracted with phenylephrine, and concentration-response curves for adenosine and its analogs, 5′- N-ethyl-carboxamidoadenosine (NECA, nonselective), 2-chloro- N6-cyclopentyladenosine (CCPA, A1AR selective), 2-(2-carboxyethyl)phenethyl amino-5′- N-ethylcarboxamido-adenosine (CGS-21680, A2A selective), and 2-chloro- N6-3-iodobenzyladenosine-5′- N-methyluronamide (Cl-IBMECA, A3 selective) were obtained to determine relaxation. Adenosine and NECA (0.1 μM) caused small contractions of 13.9 ± 3.0 and 16.4 ± 6.4%, respectively, and CCPA at 0.1 and 1.0 μM caused contractions of 30.8 ± 4.3 and 28.1 ± 3.9%, respectively, in A1AR(+/+) rings. NECA- and CCPA-induced contractions were eliminated by 100 nM of 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, selective A1AR antagonist). Adenosine, NECA, and CGS-21680 produced an increase in maximal relaxation in A1AR(−/−) compared with A1AR(+/+) rings, whereas Cl-IBMECA did not produce contraction in either A1AR(+/+) or A1AR(−/−) rings. CCPA-induced contraction at 1.0 μM was eliminated by the PLC inhibitor U-73122. These data suggest that activation of A1ARs causes contraction of vascular smooth muscle through PLC pathways and negatively modulates the vascular relaxation mediated by other adenosine receptor subtypes.

A potential role of central A1 adenosine receptors in the responses to hypothalamic stimulation in the anaesthetized cat

1994 ◽  
Vol 49 (1) ◽  
pp. 15-19 ◽  
Author(s):  
M.S. Dawid-Milner ◽  
L. Silva-Carvalho ◽  
G.R. Goldsmith ◽  
K.M. Spyer
Keyword(s):  
Adenosine Receptors ◽  
Potential Role ◽  
Hypothalamic Stimulation ◽  
A1 Adenosine Receptors

A novel mechanism of renal blood flow autoregulation and the autoregulatory role of A1 adenosine receptors in mice

2007 ◽  
Vol 293 (5) ◽  
pp. F1489-F1500 ◽  
Author(s):  
Armin Just ◽  
William J. Arendshorst
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Adenosine Receptors ◽  
Time Course ◽  
Tubuloglomerular Feedback ◽  
The Third ◽  
A1 Adenosine Receptors ◽  
The Impact ◽  
Renal Blood Flow Autoregulation

Autoregulation of renal blood flow (RBF) is mediated by a fast myogenic response (MR; ∼5 s), a slower tubuloglomerular feedback (TGF; ∼25 s), and potentially additional mechanisms. A1 adenosine receptors (A1AR) mediate TGF in superficial nephrons and contribute to overall autoregulation, but the impact on the other autoregulatory mechanisms is unknown. We studied dynamic autoregulatory responses of RBF to rapid step increases of renal artery pressure in mice. MR was estimated from autoregulation within the first 5 s, TGF from that at 5–25 s, and a third mechanism from 25–100 s. Genetic deficiency of A1AR (A1AR−/−) reduced autoregulation at 5–25 s by 50%, indicating a residual fourth mechanism resembling TGF kinetics but independent of A1AR. MR and third mechanism were unaltered in A1AR−/−. Autoregulation in A1AR−/− was faster at 5–25 than at 25–100 s suggesting two separate mechanisms. Furosemide in wild-type mice (WT) eliminated the third mechanism and enhanced MR, indicating TGF-MR interaction. In A1AR−/−, furosemide did not further impair autoregulation at 5–25 s, but eliminated the third mechanism and enhanced MR. The resulting time course was the same as during furosemide in WT, indicating that A1AR do not affect autoregulation during furosemide inhibition of TGF. We conclude that at least one novel mechanism complements MR and TGF in RBF autoregulation, that is slower than MR and TGF and sensitive to furosemide, but not mediated by A1AR. A fourth mechanism with kinetics similar to TGF but independent of A1AR and furosemide might also contribute. A1AR mediate classical TGF but not TGF-MR interaction.

The Role of Vascular Cell Senescence in Atherosclerosis: Antisenescence as a Novel Therapeutic Strategy for Vascular Aging

2004 ◽  
Vol 2 (2) ◽  
pp. 141-148 ◽  
Author(s):  
Tohru Minamino ◽  
Hideyuki Miyauchi ◽  
Toshihiko Yoshida ◽  
Kaoru Tateno ◽  
Issei Komuro
Keyword(s):  
Therapeutic Strategy ◽  
Cell Senescence ◽  
Vascular Aging ◽  
Vascular Cell ◽  
Novel Therapeutic ◽  
Vascular Cell Senescence

Effect of SSH1/SSH2 expression changes by shRNA in glioma cell lines on response to radiotherapy and cofilin-1 reactivation.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e13505-e13505
Author(s):  
Hong Xiao
Keyword(s):  
Protein Phosphatase ◽  
Glioma Cell ◽  
Therapeutic Strategy ◽  
Glioma Cells ◽  
Protein Phosphatase 1 ◽  
Migration And Invasion ◽  
Radiation Induced ◽  
U373 Cells ◽  
Novel Therapeutic

e13505 Background: Radiotherapy has become the most important treatment for malignant glioma following surgery. However, development of radioresistance in glioma cells limits therapeutic efficacy. The slingshot (SSH) family of phosphatases is a potent regulator of Cofilin-1 activation. Methods: We investigate the role of SSH1(slingshot protein phosphatase 1) and SSH2 in radioresistance via using shRNA to block SSH1/2 expression in U251 and U373 cells as well as established radioresistant U251 (RR-U251) and U373 (RR-U373) cells. Results: We found that both SSH1 and SSH2-shRNA efficiently sensitized glioma cells to radiation with a sensitization enhancement ratio (SER) of 1.01-1.73. In SSH1-silenced cells, the cell viability, migration, and invasion abilities following radiation were remarkably reduced and radiation induced cell apoptosis was markedly enhanced compared with control cells. While in SSH2-silenced cells, the alterations were not as significant. Furthermore, the result of Western-blot suggested that radiosensization of SSH1/SSH2 silencing was mediated by inhibiting reactivation of phosphorylated CFL-1. Conclusions: Our study demonstrated that SSH1 and SSH2 are valid radiosensitizing targets in not only normal glioma cells but radioresistant lines, suggesting a novel therapeutic strategy to improve the efficacy of radiotherapy in patients with glioma.

Positive allosteric modulation of A1 adenosine receptors as a novel and promising therapeutic strategy for anxiety

2016 ◽  
Vol 111 ◽  
pp. 283-292 ◽  
Author(s):  
Fabrizio Vincenzi ◽  
Annalisa Ravani ◽  
Silvia Pasquini ◽  
Stefania Merighi ◽  
Stefania Gessi ◽  
...  
Keyword(s):  
Adenosine Receptors ◽  
Therapeutic Strategy ◽  
Allosteric Modulation ◽  
A1 Adenosine Receptors

Role of PGE2 and EP Receptors in the Pathogenesis of Rheumatoid Arthritis and as a Novel Therapeutic Strategy

2006 ◽  
Vol 6 (4) ◽  
pp. 383-394 ◽  
Author(s):  
Jun Akaogi ◽  
Toshiko Nozaki ◽  
Minoru Satoh ◽  
Hidehiro Yamada
Keyword(s):  
Rheumatoid Arthritis ◽  
Therapeutic Strategy ◽  
Ep Receptors ◽  
Novel Therapeutic

Possible role of A1 adenosine receptors in the control of atrial natriuretic factor release in the rat

1990 ◽  
Vol 22 ◽  
pp. 389
Author(s):  
M. Perfumi ◽  
C. Polidori ◽  
A. Saija ◽  
G. Costa ◽  
G. Cristalli ◽  
...  
Keyword(s):  
Adenosine Receptors ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
A1 Adenosine Receptors ◽  
Factor Release ◽  
Atrial Natriuretic

scholarly journals Predominant role of A1 adenosine receptors in mediating adenosine induced vasodilatation of rat diaphragmatic arterioles: involvement of nitric oxide and the ATP-dependent K+ channels

1997 ◽  
Vol 121 (7) ◽  
pp. 1355-1363 ◽  
Author(s):  
Gawiyou Danialou ◽  
Eric Vicaut ◽  
Abdoulaye Sambe ◽  
Michel Aubier ◽  
Jorge Boczkowski
Keyword(s):  
Nitric Oxide ◽  
Adenosine Receptors ◽  
Predominant Role ◽  
K Channels ◽  
A1 Adenosine Receptors
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