Adenosine Metabolism in COPD: A Study on Adenosine Levels, 5′-Nucleotidase, Adenosine Deaminase and Its Isoenzymes Activity in Serum, Lymphocytes and Erythrocytes

Patidar, Bhagwan Singh; Meena, A. K.; Kumar, Manoj; Menon, Balakrishnan; Rohil, Vishwajeet; Bansal, Surendra K.

doi:10.1080/15412555.2018.1537365

Cited by 15 publications

(12 citation statements)

References 43 publications

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“…For example, the hypoxic-adenosinergic pathway is activated in IPF patients with pulmonary hypertension (PH), as marked by increased expression of HIF-1α, adenosine, adenosine A2B receptor, CD73, and ENT1 ( 124 ). Other studies showed that adenosine levels are increased in the serum, lymphocytes, and erythrocytes in healthy smokers compared to healthy non-smokers and continue to increase with the severity in COPD patients ( 134 ). The same study also demonstrated that patients with higher levels of adenosine tend to have reduced forced expiratory volume in one second (FEV1), suggesting a potential functional link ( 134 ).…”

Section: Adenosine At the Interphase Of Hypoxia And Inflammation In Lmentioning

confidence: 99%

“…Other studies showed that adenosine levels are increased in the serum, lymphocytes, and erythrocytes in healthy smokers compared to healthy non-smokers and continue to increase with the severity in COPD patients ( 134 ). The same study also demonstrated that patients with higher levels of adenosine tend to have reduced forced expiratory volume in one second (FEV1), suggesting a potential functional link ( 134 ). Furthermore, adenosine signaling is significantly enhanced in COPD as represented by increased CD73 activity and adenosine receptor levels in lung tissue from patients with COPD or in murine model of emphysema ( 135 , 136 ).…”

Section: Adenosine At the Interphase Of Hypoxia And Inflammation In Lmentioning

confidence: 99%

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Adenosine at the Interphase of Hypoxia and Inflammation in Lung Injury

Berg

Mills

et al. 2021

Front. Immunol.

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Hypoxia and inflammation often coincide in pathogenic conditions such as acute respiratory distress syndrome (ARDS) and chronic lung diseases, which are significant contributors to morbidity and mortality for the general population. For example, the recent global outbreak of Coronavirus disease 2019 (COVID-19) has placed viral infection-induced ARDS under the spotlight. Moreover, chronic lung disease ranks the third leading cause of death in the United States. Hypoxia signaling plays a diverse role in both acute and chronic lung inflammation, which could partially be explained by the divergent function of downstream target pathways such as adenosine signaling. Particularly, hypoxia signaling activates adenosine signaling to inhibit the inflammatory response in ARDS, while in chronic lung diseases, it promotes inflammation and tissue injury. In this review, we discuss the role of adenosine at the interphase of hypoxia and inflammation in ARDS and chronic lung diseases, as well as the current strategy for therapeutic targeting of the adenosine signaling pathway.

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Section: Adenosine At the Interphase Of Hypoxia And Inflammation In Lmentioning

confidence: 99%

Section: Adenosine At the Interphase Of Hypoxia And Inflammation In Lmentioning

confidence: 99%

Adenosine at the Interphase of Hypoxia and Inflammation in Lung Injury

Berg

Mills

et al. 2021

Front. Immunol.

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“…CD73 metabolizes AMP to adenosine. COPD and IPF patients exhibit increased CD73 activity (116) along with elevated adenosine levels (117, 118). CD39 and CD73 levels correlated with pulmonary hypertension severity in explanted lungs from patients with IPF (119).…”

Section: Purinergic Signaling In Chronic Pulmonary Inflammationmentioning

confidence: 99%

“…Adenosine was shown to induce airway hyper-responsiveness, causing bronchoconstriction, in patients with asthma (124) and COPD (125). Adenosine levels are also elevated in BALF and exhaled breath condensate of patients with COPD (116, 126) and are negatively correlated with pulmonary function.…”

Section: Purinergic Signaling In Chronic Pulmonary Inflammationmentioning

confidence: 99%

Purinergic Signaling in Pulmonary Inflammation

Berg

Harting

et al. 2019

Front. Immunol.

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Purine nucleotides and nucleosides are at the center of biologic reactions. In particular, adenosine triphosphate (ATP) is the fundamental energy currency of cellular activity and adenosine has been demonstrated to play essential roles in human physiology and pathophysiology. In this review, we examine the role of purinergic signaling in acute and chronic pulmonary inflammation, with emphasis on ATP and adenosine. ATP is released into extracellular space in response to cellular injury and necrosis. It is then metabolized to adenosine monophosphate (AMP) via ectonucleoside triphosphate diphosphohydrolase-1 (CD39) and further hydrolyzed to adenosine via ecto-5′-nucleotidase (CD73). Adenosine signals via one of four adenosine receptors to exert pro- or anti-inflammatory effects. Adenosine signaling is terminated by intracellular transport by concentrative or equilibrative nucleoside transporters (CNTs and ENTs), deamination to inosine by adenosine deaminase (ADA), or phosphorylation back into AMP via adenosine kinase (AK). Pulmonary inflammatory and hypoxic conditions lead to increased extracellular ATP, adenosine diphosphate (ADP) and adenosine levels, which translates to increased adenosine signaling. Adenosine signaling is central to the pulmonary injury response, leading to various effects on inflammation, repair and remodeling processes that are either tissue-protective or tissue destructive. In the acute setting, particularly through activation of adenosine 2A and 2B receptors, adenosine signaling serves an anti-inflammatory, tissue-protective role. However, excessive adenosine signaling in the chronic setting promotes pro-inflammatory, tissue destructive effects in chronic pulmonary inflammation.

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“…This potent chemokine attracting dendritic cells has previously been linked to the pathogenesis of COPD 3334 . ADA and MMP1, also among the most differential mRNAs, have also been associated with the pathogenesis of COPD [35][36][37] . In contrast to COPD, the relative RNA content is comparable in urine from bladder cancer patients and healthy volunteers, in CSF from glioblastoma patients and hydrocephalus patient, and in saliva from diabetes patients and healthy volunteers ( Fig.…”

Section: Assessment Of the Tissues Of Origin And Deconvolution Of Panmentioning

confidence: 99%

Charting extracellular transcriptomes in The Human Biofluid RNA Atlas

Hulstaert

Morlion

Cobos

et al. 2019

Preprint

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Extracellular RNAs present in biofluids have emerged as potential biomarkers for disease.Where most studies focus on plasma or serum, other biofluids may contain more informative RNA molecules, depending on the type of disease. Here, we present an unprecedented atlas of messenger, circular and small RNA transcriptomes of a comprehensive collection of 20 different human biofluids. By means of synthetic spike-in controls, we compared RNA content across biofluids, revealing a more than 10 000-fold difference in RNA concentration. The circular RNA fraction is increased in nearly all biofluids compared to tissues. Each biofluid transcriptome is enriched for RNA molecules derived from specific tissues and cell types. In addition, a subset of biofluids, including stool, sweat, saliva and sputum, contains high levels of bacterial RNAs. Our atlas enables a more informed selection of the most relevant biofluid to monitor particular diseases. To verify the biomarker potential in these biofluids, four validation cohorts representing a broad spectrum of diseases were profiled, revealing numerous differential RNAs between case and control subjects. Taken together, our results reveal novel insights in the RNA content of human biofluids and may serve as a valuable resource for future biomarker studies.

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Adenosine Metabolism in COPD: A Study on Adenosine Levels, 5′-Nucleotidase, Adenosine Deaminase and Its Isoenzymes Activity in Serum, Lymphocytes and Erythrocytes

Cited by 15 publications

References 43 publications

Adenosine at the Interphase of Hypoxia and Inflammation in Lung Injury

Adenosine at the Interphase of Hypoxia and Inflammation in Lung Injury

Purinergic Signaling in Pulmonary Inflammation

Charting extracellular transcriptomes in The Human Biofluid RNA Atlas

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