Mechanisms of induction of adenosine receptor genes and its functional significance

Hilaire, Cynthia St.; Carroll, Shannon H.; Chen, Hongjie; Ravid, Katya

doi:10.1002/jcp.21579

Cited by 74 publications

(54 citation statements)

References 155 publications

(171 reference statements)

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“…In line with this, other C 60 fullerene reported effects are a reduced contractile response for acetylcholine, histamine, and 5-HT in muscle of guinea pig and rat which may be due to a change in postreceptor processes. 40 Recent studies on the mechanisms involved in the regulation of adenosine receptor expression have shed light on the participation of transcription factors, such as nuclear factorkappa B (NFκB), hypoxic-inducible factor 1, and cAMP-responsive element binding protein (CREB; for a review see ref 41). Thus, reactive oxygen species (ROS) can increase the expression of the A 1 receptor by activating NF kappa B regulatory site(s) on this gene and thereby enhance the cytoprotective role of adenosine.…”

Section: ' Discussionmentioning

confidence: 99%

Modulation of Adenosine Receptors by [60]Fullerene Hydrosoluble Derivative in SK-N-MC Cells

Giust

León

Ballesteros-Yáñez

et al. 2011

ACS Chem. Neurosci.

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The most known fullerenes are spherical carbon compounds composed of 60 carbon atoms. C60 fullerenes have shown biochemical and biomedical properties in the last years such as as blockade of apoptosis and neuroprotection. The nucleoside adenosine has a neuroprotective role mainly due to inhibition of glutamate release, which is a neurotransmitter related to excitotoxicity and cell death. In the present work, we have determined the presence of adenosine receptors in SK-N-MC cells, a neuroepithelioma human cell line, and analyzed the effect of fullerenes in these receptors by using radioligand binding, immunoblotting, and quantitative real time PCR assays. Results demonstrated that SK-N-MC cells endogenously express adenosine receptors. Fullerene exposure of these cells did not affect cell viability measured by MTT reduction assay. However, adenosine A1 and A2A receptors were both increased in SK-N-MC cells after treatment. These results suggest for the first time the modulation of adenosine receptors after C60 fullerenes exposure.

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Section: ' Discussionmentioning

confidence: 99%

Modulation of Adenosine Receptors by [60]Fullerene Hydrosoluble Derivative in SK-N-MC Cells

Giust

León

Ballesteros-Yáñez

et al. 2011

ACS Chem. Neurosci.

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“…MSCs and SOD3-transduced MSCs also inhibit IMQ-induced inflammation independent of TLR-7 signaling through regulation of the late-phase inflammatory responses IMQ is also shown to induce the activation of transcription factor NF-jB and the downstream production of proinflammatory cytokines, in the absence of TLR-7, through the adenosine receptor-dependent mechanism (48,49,53). To further investigate the cause and therapeutic effect of SOD3-transduced MSCs or MSCs in the IMQ-induced psoriasis mouse model, independent of TLR-7 signaling, we explored adenosine receptor activation and dependent mechanism.…”

Section: Sod3-transduced Mscs Efficiently Prevent Psoriasismentioning

confidence: 99%

Effects of Human Mesenchymal Stem Cells Transduced with Superoxide Dismutase on Imiquimod-Induced Psoriasis-Like Skin Inflammation in Mice

Sah

Kim

Yun

et al. 2016

Antioxidants & Redox Signaling

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Aims: The immunomodulatory and anti-inflammatory properties of mesenchymal stem cells (MSCs) have been proposed in several autoimmune diseases and successfully tested in animal models, but their contribution to psoriasis and underlying pathways remains elusive. Likewise, an increased or prolonged presence of reactive oxygen species and aberrant antioxidant systems in skin are known to contribute to the development of psoriasis and therefore effective antioxidant therapy is highly required. We explored the feasibility of using extracellular superoxide dismutase (SOD3)-transduced allogeneic MSCs as a novel therapeutic approach in a mouse model of imiquimod (IMQ)-induced psoriasis-like inflammation and investigated the poorly understood underlying mechanism. In addition, the chronicity and late-phase response of inflammation were evaluated during continued activation of antigen receptors by applying a booster dose of IMQ. Results: Subcutaneous injection of allogeneic SOD3-transduced MSCs significantly prevented psoriasis development in our IMQ-induced mouse model, likely through a suppression of proliferation and infiltration of various effector cells into skin with a concomitant modulated cytokine and chemokine expression and inhibition of signaling pathways such as tolllike receptor-7, nuclear factor-kappa B, p38 mitogen-activated kinase, and Janus kinase-signal transducer and activator of transcription, as well as adenosine receptor activation. Innovation and Conclusion: Our data offer a novel therapeutic approach to chronic inflammatory skin diseases such as psoriasis by leveraging immunomodulatory effects of MSCs as well as SOD3 expression. Antioxid. Redox Signal. 24, 233-248.

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“…This metabolite is produced and released under conditions of increased energy consumption, such as stress or hypoxia, where it then functions in an autocrine as well as paracrine fashion (10,14). The effects of adenosine are mediated through binding to four distinct GPCRs, the A1, A2a, A2b, and A3 receptors, which couple to Ptx sensitive Gi proteins (i.e., the A1 and A3 receptors), Gs (A2a and A2b receptors), or Gq/G11 (the A2b receptor) [reviewed in (15)]. Mast cells express different levels of the A2a, A2b, and A3 receptors (16), therefore marking those receptors as potential mediators of allergic and inflammatory processes.…”

Section: All1 Inhibits A3r-activated Erk Signaling In Purified Rpmcs mentioning

confidence: 99%

Activation of Mast Cells by Trimeric G Protein Gi3; Coupling to the A3 Adenosine Receptor Directly and upon T Cell Contact

Baram

Dekel

Mekori

et al. 2010

The Journal of Immunology

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Mast cells are key players in mediating and amplifying allergic and inflammatory reactions. Previously, we identified the G-protein, Gi3, as the cellular target of receptor mimetic basic secretagogues that activate mast cell independently of IgE. In this study, we demonstrate that Gi3 is the cellular target of the adenosine A3 receptor (A3R), a G-protein coupled receptor involved in inflammation and the pathophysiology of asthma. By using a cell permeable peptide comprising the C-terminal end of Gαi3 fused to an importation sequence (ALL1) as a selective inhibitor of Gi3 signaling, we show that by coupling to Gi3, the A3R stimulates multiple signaling pathways in human mast cells, leading to upregulation of cytokines, chemokines, and growth factors. We further show that after contact with activated T cell membranes, endogenous adenosine binds to and activates the A3R, resulting in Gi3-mediated signaling. Specifically, the majority of ERK1/2 signaling initiated by contact with activated T cell membranes, is mediated by Gi3, giving rise to ALL1-inhibitable cellular responses. These results unveil the physiological G-protein coupled receptor that couples to Gi3 and establish the important role played by this G-protein in inflammatory conditions that involve adenosine-activated mast cells.

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Mechanisms of induction of adenosine receptor genes and its functional significance

Cited by 74 publications

References 155 publications

Modulation of Adenosine Receptors by [60]Fullerene Hydrosoluble Derivative in SK-N-MC Cells

Modulation of Adenosine Receptors by [60]Fullerene Hydrosoluble Derivative in SK-N-MC Cells

Effects of Human Mesenchymal Stem Cells Transduced with Superoxide Dismutase on Imiquimod-Induced Psoriasis-Like Skin Inflammation in Mice

Activation of Mast Cells by Trimeric G Protein Gi3; Coupling to the A3 Adenosine Receptor Directly and upon T Cell Contact

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