Antihyperalgesic activity of nucleoside transport inhibitors in models of inflammatory pain in guinea pigs

Maes, Sabine S; Pype, Stefan; Hoffmann, Vincent; Biermans, Maria; Meert, Theo

doi:10.2147/jpr.s35108

Cited by 13 publications

(9 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We identified a compound known as soluflazine that has been demonstrated to have 20-to 100-fold increased specificity for ENT2 relative to ENT1 in vitro (49)(50)(51). In vivo studies demonstrate that soluflazine is efficacious via increasing extracellular adenosine (77). Continuous delivery of soluflazine mimicked the protective effect observed with dipyridamole treatment in murine colitis.…”

Section: Figure 9 Genetic or Pharmacologic Ent2 Inhibition Does Not mentioning

confidence: 83%

Coordination of ENT2-dependent adenosine transport and signaling dampens mucosal inflammation

Aherne¹,

Collins²,

Rapp³

et al. 2018

JCI Insight

View full text Add to dashboard Cite

Section: Figure 9 Genetic or Pharmacologic Ent2 Inhibition Does Not mentioning

confidence: 83%

Coordination of ENT2-dependent adenosine transport and signaling dampens mucosal inflammation

Aherne¹,

Collins²,

Rapp³

et al. 2018

JCI Insight

View full text Add to dashboard Cite

“…in various inflammatory pain models (Maes et al 2012). In addition, adenosine also mediates the analgesic mechanism of acupunctures via peripheral A1 receptors (Goldman et al 2010).…”

Section: Discussionmentioning

confidence: 99%

CD73 Controls Extracellular Adenosine Generation in the Trigeminal Nociceptive Nerves

Liu

Zhang

et al. 2017

J Dent Res

View full text Add to dashboard Cite

Purinergic signaling is involved in pain generation and modulation in the nociceptive sensory nervous system. Adenosine triphosphate (ATP) induces pain via activation of ionotropic P2X receptors while adenosine mediates analgesia via activation of metabotropic P1 receptors. These purinergic signaling are determined by ecto-nucleotidases that control ATP degradation and adenosine generation. Using enzymatic histochemistry, we detected ecto-AMPase activity in dental pulp, trigeminal ganglia (TG) neurons, and their nerve fibers. Using immunofluorescence staining, we confirmed the expression of ecto-5'-nucleotidase (CD73) in trigeminal nociceptive neurons and their axonal fibers, including the nociceptive nerve fibers projecting into the brainstem. In addition, we detected the existence of CD73 and ecto-AMPase activity in the nociceptive lamina of the trigeminal subnucleus caudalis (TSNC) in the brainstem. Furthermore, we demonstrated that incubation with specific anti-CD73 serum significantly reduced the ecto-AMPase activity in the nociceptive lamina in the brainstem. Our results indicate that CD73 might participate in nociceptive modulation by affecting extracellular adenosine generation in the trigeminal nociceptive pathway. Disruption of TG neuronal ecto-nucleotidase expression and axonal terminal localization under certain circumstances such as chronic inflammation, oxidant stress, local constriction, and injury in trigeminal nerves may contribute to the pathogenesis of orofacial neuropathic pain.

show abstract

“…Maes et al demonstrated that systemic administration of ENT-1 inhibitors can reverse hyperalgesia in guinea pig inflammatory pain models [ 188 ]. The mechanism underlying this analgesia seems to be the blocking of adenosine reuptake into cells, allowing greater activation of A 1 and A 2 AR [ 188 ]. These results show that it is necessary to investigate the potential therapeutic effect of ENT inhibition.…”

Section: Perspectives Of Atp and Adenosine Signaling Modulation: Pmentioning

confidence: 99%

Purinergic Signaling in Endometriosis-Associated Pain

Trapero

Martı́n-Satué

2020

IJMS

View full text Add to dashboard Cite

Endometriosis is an estrogen-dependent gynecological disease, with an associated chronic inflammatory component, characterized by the presence of endometrial tissue outside the uterine cavity. Its predominant symptom is pain, a condition notably altering the quality of life of women with the disease. This review is intended to exhaustively gather current knowledge on purinergic signaling in endometriosis-associated pain. Altered extracellular ATP hydrolysis, due to changes in ectonucleotidase activity, has been reported in endometriosis; the resulting accumulation of ATP in the endometriotic microenvironment points to sustained activation of nucleotide receptors (P2 receptors) capable of generating a persistent pain message. P2X3 receptor, expressed in sensory neurons, mediates nociceptive, neuropathic, and inflammatory pain, and is enrolled in endometriosis-related pain. Pharmacological inhibition of P2X3 receptor is under evaluation as a pain relief treatment for women with endometriosis. The role of other ATP receptors is also discussed here, e.g., P2X4 and P2X7 receptors, which are involved in inflammatory cell–nerve and microglia–nerve crosstalk, and therefore in inflammatory and neuropathic pain. Adenosine receptors (P1 receptors), by contrast, mainly play antinociceptive and anti-inflammatory roles. Purinome-targeted drugs, including nucleotide receptors and metabolizing enzymes, are potential non-hormonal therapeutic tools for the pharmacological management of endometriosis-related pain.

show abstract

Antihyperalgesic activity of nucleoside transport inhibitors in models of inflammatory pain in guinea pigs

Cited by 13 publications

References 45 publications

Coordination of ENT2-dependent adenosine transport and signaling dampens mucosal inflammation

Coordination of ENT2-dependent adenosine transport and signaling dampens mucosal inflammation

CD73 Controls Extracellular Adenosine Generation in the Trigeminal Nociceptive Nerves

Purinergic Signaling in Endometriosis-Associated Pain

Contact Info

Product

Resources

About