Adenosine and blood platelets

Abstract

Adenosine is an important regulatory metabolite and an inhibitor of platelet activation. Adenosine released from different cells or generated through the activity of cellsurface ectoenzymes exerts its effects through the binding of four different G-protein-coupled adenosine receptors. In platelets, binding of A 2 subtypes (A 2A or A 2B ) leads to consequent elevation of intracellular cyclic adenosine monophosphate, an inhibitor of platelet activation. The significance of this ligand and its receptors for platelet activation is addressed in this review, including how adenosine metabolism and its A 2 subtype receptors impact the expression and activity of adenosine diphosphate receptors. The expression of A 2 adenosine receptors is induced by conditions such as oxidative stress, a hallmark of aging. The effect of adenosine receptors on platelet activation during aging is also discussed, as well as potential therapeutic applications.Keywords Adenosine . A 2B adenosine receptor . A 2A adenosine receptor . ADP-mediated platelet activation and aggregation . Cyclic adenosine monophosphate (cAMP)

Platelets and von Willebrand factor in atherogenesis

“…[1][2][3][4][5][6][7][8] One of the earliest events in atherosclerosis is the loss of normal endothelial function, including disruption of antiplatelet mechanisms. [1][2][3][4][5][6] Later in this review, we discuss how abnormalities in VWF regulation are likely a contributing factor to atherosclerosis through the subsequent recruitment of platelets. However, other mechanisms may be operative that involve increased activation state of platelets triggered by classical risk factors of smoking, elevated lowdensity lipoprotein cholesterol, reduced high-density lipoprotein cholesterol, and insulin resistance.…”

Adenosine-associated delivery systems

“…Nevertheless, due to cardiovascular side effects, and liver toxicity of ADK disruption the systemic administration of adenosine is not practical (Olsson and Pearson, 1990, Boison et al, 2002b, Fredholm et al, 2005). Another interesting application for adenosine is antiplatelet therapy, which has not yet been clinically used because of adenosine short half-life (Johnston-Cox and Ravid, 2011). …”

Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies

“…Adenosine is centrally involved in the signaling cascade of related events, including anti-inflammatory actions, angiogenesis, oxygen supply/demand ratio, and ischemic pre-and post-conditioning [3]. Under these circumstances, the local levels of extracellular adenosine are increased due to the increased need for energy supplied by ATP [4].…”

“…These receptors can be distinguished based on their affinities for adenosine agonists and antagonists. In addition, these receptors are classified based on their mechanism of signal Journal of Neuroimmunology 264 (2013) [54][55][56][57][58][59][60][61][62][63][64] Abbreviations: TON, traumatic optic neuropathy; TNF-α, tumor necrosis factor-α; ELISA, Enzyme-linked immunosorbent assay; ROS, reactive oxygen species; MAP kinase, Mitogenactivated protein kinase; ERK, extracellular signal-regulated kinase; AR, adenosine receptor; CGS21680, 2-p- phenethylamino-5′-N-ethylcarboxamidoadenosine; LPS, lipopolysaccharides; NECA, 5′-N-Ethylcarboxamidoadenosine; ZM241385, 4-(2-[7-Amino-2-(2-furyl) [1,2,4]triazolo [2,3-a] [1,3,5] …”

“…These stimuli associated with the injured RGCs often activate retinal microglia, which release pro-inflammatory cytokines and cytotoxic molecules to further exacerbate the degenerative process [2]. These findings suggest that pharmacological interventions that reduce inflammation may be effective neuroprotectants for TON.Adenosine is centrally involved in the signaling cascade of related events, including anti-inflammatory actions, angiogenesis, oxygen supply/demand ratio, and ischemic pre-and post-conditioning [3]. Under these circumstances, the local levels of extracellular adenosine are increased due to the increased need for energy supplied by ATP [4].…”