Role of Adenosine on Intestinal Ischemia-Reperfusion Injury in Rabbits

Taha, Murched Omar; Miranda-Ferreira, Regiane; Simões, Ricardo Santos; Abrão, Marianne Sales; Oliveira-Júnior, Itamar Souza; Monteiro, Hugo P.; Santos, João Paulo Fernandes; Rodrigues, Paulo Henrique Mazza; Rodrigues, João Valença; Alves, A.E.M.; Nascimento, Elisandra C.C.; Silva, T.L.B.; Zeviani, W.M.; Caricati‐Neto, Afonso

doi:10.1016/j.transproceed.2010.01.019

Cited by 6 publications

(5 citation statements)

References 12 publications

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“…The earliest link of extracellular adenosine to immunosuppression include studies on the anti-inflammatory activity of methotrexate (49) and seminal studies revealing A2AR signaling as essential in suppressing tissue-devastating inflammation (50). Extracellular adenosine protects tissues by dampening inflammation with myocardial injury (51)(52)(53), acute lung injury (54)(55)(56)(57)(58), intestinal ischemia-reperfusion injury (59)(60)(61), and inflammatory bowel disease (62)(63)(64)(65). Tumors exploit extracellular adenosine' to protect the cancer cells.…”

Section: Cd73 and Adenosine Receptor Activity Promotes Immunosuppressionmentioning

confidence: 99%

CD73's Potential as an Immunotherapy Target in Gastrointestinal Cancers

et al. 2020

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CD73, a cell surface 5 ′ nucleotidase that generates adenosine, has emerged as an attractive therapeutic target for reprogramming cancer cells and the tumor microenvironment to dampen antitumor immune cell evasion. Decades of studies have paved the way for these findings, starting with the discovery of adenosine signaling, particularly adenosine A2A receptor (A2AR) signaling, as a potent suppressor of tissue-devastating immune cell responses, and evolving with studies focusing on CD73 in breast cancer, melanoma, and non-small cell lung cancer. Gastrointestinal (GI) cancers are a major cause of cancer-related deaths. Evidence is mounting that shows promise for improving patient outcomes through incorporation of immunomodulatory strategies as single agents or in combination with current treatment options. Recently, several immune checkpoint inhibitors received FDA approval for use in GI cancers; however, clinical benefit is limited. Investigating molecular mechanisms promoting immunosuppression, such as CD73, in GI cancers can aid in current efforts to extend the efficacy of immunotherapy to more patients. In this review, we discuss current clinical and basic research studies on CD73 in GI cancers, including gastric, liver, pancreatic, and colorectal cancer, with special focus on the potential of CD73 as an immunotherapy target in these cancers. We also present a summary of current clinical studies targeting CD73 and/or A2AR and combination of these therapies with immune checkpoint inhibitors.

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Section: Cd73 and Adenosine Receptor Activity Promotes Immunosuppressionmentioning

confidence: 99%

CD73's Potential as an Immunotherapy Target in Gastrointestinal Cancers

et al. 2020

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“…ATP-MgCl 2 reduces intestinal permeability during mesenteric ischemia (Kreienberg et al, 1996). Both adenosine and ATP were reported to attenuate intestinal dysfunction produced by ischemia but not that caused by reperfusion (Taha et al, 2010a(Taha et al, , 2010b. A more recent study showed that treatment with adenosine attenuated small bowel motor and neural malfunctions produced by ischemia and reperfusion in rats (Haddad et al, 2012).…”

Section: Ischemiamentioning

confidence: 99%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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“…Similar, A2BR antagonism enhances intestinal inflammation and injury during I/R in wild-type mice (26), whereas A2BR agonist treatment protects from intestinal injury, inflammation, and barrier breakdown (26). Adenosine treatment also attenuates intestinal I/R injury (27, 28). In general, CD73 and A2BR deficient mice experience more severe tissue injury with I/R (22, 26), and ischemia results in a robust increase in HIFs (15).…”

Section: Intestinal Ischemia/reperfusion Injurymentioning

confidence: 99%

The Hypoxia–Adenosine Link during Intestinal Inflammation

Bowser

Phan

Eltzschig

2018

The Journal of Immunology

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Intestinal inflammation is a key element in inflammatory bowel disease and is related to a combination of factors, including genetics, mucosal barrier dysfunction, bacteria translocation, deleterious host-microbe interactions, and dysregulated immune responses. Over the past decade, it has been appreciated that these inflammatory lesions are associated with profound tissue hypoxia. Interestingly, an endogenous adaptive response under the control of hypoxia signaling is enhancement in adenosine signaling, which impacts these different endpoints, including promoting barrier function and encouraging anti-inflammatory activity. In this review, we discuss the hypoxia-adenosine link in inflammatory bowel disease, intestinal ischemia/reperfusion injury, and colon cancer. In addition, we provide a summary of clinical implications of hypoxia and adenosine signaling in intestinal inflammation and disease.

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Role of Adenosine on Intestinal Ischemia-Reperfusion Injury in Rabbits

Cited by 6 publications

References 12 publications

CD73's Potential as an Immunotherapy Target in Gastrointestinal Cancers

CD73's Potential as an Immunotherapy Target in Gastrointestinal Cancers

Purinergic Signaling and Blood Vessels in Health and Disease

The Hypoxia–Adenosine Link during Intestinal Inflammation

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