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Pseudopterosins appear to enhance the wound healing process through an adenosine receptor mediated mechanism
Author(s) -
Moya Claudia E,
Jacobs Robert S
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.729.7
Subject(s) - agonist , wound healing , chemistry , receptor , pertussis toxin , degranulation , pharmacology , microbiology and biotechnology , in vivo , adenosine receptor , inflammation , adenosine , biochemistry , g protein , immunology , biology
Pseudopterosins are marine natural products that inhibit phorbol ester (PMA) induced inflammation, inhibit the release of prostaglandins and leukotrienes from macrophages, and also inhibit degranulation of human PMNs. Pseudopterosins exhibit anti‐inflammatory and wound healing properties in several animal models and have shown significant activity in promoting wound healing at donor sites of patients undergoing autologous tissue transplants. At the cellular level, pseudopterosin activity is blocked by pertussis toxin (PTX) pretreatment, indicating that pseudopterosins act upon a G protein or G protein coupled receptor. One of the pseudopterosins, Iso‐pseudopterosin‐E (Iso‐PsE), has recently been shown to bind the adenosine A2 A and A3 receptors expressed in HEK‐293 cells with ED 50 values of 13 and 6.6 μM, respectively. In these binding experiments the potency of iso‐PsE is low when compared to the specific adenosine A2 A agonist (NECA, ED 50 = 49 nM) and A3 agonist (IB‐MECA ED 50 = 1.2 nM), but in physiological and in vivo experiments, iso‐PsE is equipotent, and in some cases more potent than NECA and IB‐MECA. In this report we propose the mechanisms by which iso‐PsE binds to these receptors and contributes to the wound healing process. This research is supported by ARMY grant # W81XWH‐06‐1‐0089.