Tofacitinib improved peripheral endothelial dysfunction and brain‐derived neurotrophic factor levels in the rat adjuvant‐induced arthritis model

Totoson, Perle; Peyronnel, C.; Quirié, Aurore; Pedard, Martin; Cefis, Marina; Bermont, Laurent; Prigent‐Tessier, Anne; Prati, Clément; Tournier, Maude; Wendling, Daniel; Marie, Christine; Demougeot, Céline

doi:10.1111/fcp.12731

Cited by 4 publications

(1 citation statement)

References 49 publications

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“…Animals were habituated to the activity chambers in three 30-min sessions and locomotor activity was recorded for 30 min. The rats were returned to their home cages after each experimental session had been completed [26].…”

Section: Locomotor Activitymentioning

confidence: 99%

Activation of spinal ephrin‐B3/EphBs signaling induces hyperalgesia through a PLP‐mediated mechanism

Zhang

Qiao

Shu

et al. 2021

Fundamemntal Clinical Pharma

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Ephrin B/EphB signaling pathway is involved in the regulation of pain caused by spinal cord injury. However, the role of ephrin-B3/EphBs signaling in regulation of nociceptive information is poorly understood. In the present study, formalin-induced inflammatory pain, mechanical allodynia and thermal hyperalgesia, was measured using Efnb3 mutant mice (Efnb3 À/À ) and wild-type (Efnb3 +/+ ) mice. The spinal cord (L4-6) was selected for molecular and cellular identification by western blotting and immunofluorescence. Efnb3 mutant mice showed a significant increased the thermal and mechanical threshold, followed by aberrant thin myelin sheath. Furthermore, expression of proteolipid protein (PLP) was significantly lower in L4-6 spinal cord of Efnb3 À/À mice. These morphological and behavioral abnormalities in mutant mice were rescued by conditional knock-in of wild-type ephrin-B3. Intrathecal administration of specific PLP siRNA significantly increased the thermal and mechanical threshold hyperalgesia in wild-type mice. However, overexpressing PLP protein by AAV9-PLP could decrease the sensitivity of mice to thermal and mechanical stimuli in Efnb3 À/À mice, compared with scrabble Efnb3 À/À mice. Further, Efnb3 lacz mice, which have activities to initiate forward signaling, but transduce reverse signals by ephrin-B3, shows normal acute pain behavior, compared with wild type mice. These findings indicate that a key molecule Efnb3 act as a prominent contributor to hyperalgesia and essential roles of ephrin-B3/EphBs in nociception through a myelin-mediated mechanism.Eph/ephrin receptor is currently the largest family of tyrosine kinase receptors, divided into two subfamilies, A and B, which form high-affinity protein by binding to ephrin A and ephrin B ligands, respectively [1]. Both the Eph receptor and the ephrin ligand are anchored on the surface of the cell, and ephrin A has only the extracellular region, which is directly anchored to the cell membrane by a glycosyl group, whereas ephrin B has a hydrophobic transmembrane region and intracellular region, which can transmit intracellular signals through

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Section: Locomotor Activitymentioning

confidence: 99%