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Promotion of Wound Healing by an Agonist of Adenosine A2A Receptor Is Dependent on Tissue Plasminogen Activator.
Montesinos, M Carmen; Desai-Merchant, Avani; Cronstein, Bruce N.
Afiliación
  • Montesinos MC; Department of Medicine, New York University School of Medicine, 550 First Avenue, MSB251, New York, NY, 10016, USA. m.carmen.montesinos@uv.es.
  • Desai-Merchant A; Instituto de Reconocimiento Molecular y Desarrollo Tecnológico, Centro Mixto Universidad Politécnica de Valencia, Universidad de Valencia, Valencia, Spain. m.carmen.montesinos@uv.es.
  • Cronstein BN; Department de Farmacologia, Universitat de València, Ave. Vicent Andrès Estellès s/n, 46100 Burjassot, Valencia, Spain. m.carmen.montesinos@uv.es.
Inflammation ; 38(6): 2036-41, 2015 Dec.
Article en En | MEDLINE | ID: mdl-25991438
Impaired wound healing, as it occurs in diabetes mellitus or long-term corticoid treatment, is commonly associated with disability, diminished quality of life, and high economic costs. Selective agonists of the A2A receptor subtype of adenosine, an endogenous regulator of inflammation, promote tissue repair in animal models, both healthy and with impaired healing. Plasmin-mediated proteolysis of fibrin and other matrix proteins is essential for cell migration at sites of injury. Since adenosine A2A receptor activation increases plasminogen activator release from macrophages and mast cells, we studied the effect of a selective agonist, CGS-21680, on full-thickness excisional wound closure in wild-type, urokinase plasminogen activator (uPA)-deficient, and tissue plasminogen activator (tPA)-deficient mice. Wound closure was impaired in tPA- and uPA-deficient mice as compared with wild-type mice, and topical application of CGS-21680 significantly increased the rate at which wounds closed in wild-type mice and uPA-deficient mice, but not in tPA-deficient mice. Immunostaining of tissue sections showed that tPA was present in endothelial cells and histiocytes by day 3 post-wound and also by day 6. In contrast, uPA was more prominent in these cell types only by day 6 post-wound. Our results confirm that plasminogen activation contributes to wound repair and are consistent with the hypothesis that adenosine A2A receptor activation promotes wound closure by a mechanism that depends upon tPA, but not uPA. Moreover, our results suggest that topical adenosine A2A receptor agonists may be useful in promotion of wound closure in patients with impaired wound healing.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fenetilaminas / Piel / Cicatrización de Heridas / Heridas Penetrantes / Adenosina / Activador de Tejido Plasminógeno / Receptor de Adenosina A2A / Agonistas del Receptor de Adenosina A2 Tipo de estudio: Prognostic_studies Aspecto: Patient_preference Límite: Animals Idioma: En Revista: Inflammation Año: 2015 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fenetilaminas / Piel / Cicatrización de Heridas / Heridas Penetrantes / Adenosina / Activador de Tejido Plasminógeno / Receptor de Adenosina A2A / Agonistas del Receptor de Adenosina A2 Tipo de estudio: Prognostic_studies Aspecto: Patient_preference Límite: Animals Idioma: En Revista: Inflammation Año: 2015 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos