title: Autocrine abscisic acid mediates the UV-B-induced inflammatory response in human granulocytes and keratinocytes.
abstract: UV-B is an abiotic environmental stress in both plants and animals. Abscisic acid (ABA) is a phytohormone regulating fundamental physiological functions in plants, including response to abiotic stress. We previously demonstrated that ABA is an endogenous stress hormone also in animal cells. Here, we investigated whether autocrine ABA regulates the response to UV-B of human granulocytes and keratinocytes, the cells involved in UV-triggered skin inflammation. The intracellular ABA concentration increased in UV-B-exposed granulocytes and keratinocytes and ABA was released into the supernatant. The UV-B-induced production of NO and of reactive oxygen species (ROS), phagocytosis, and cell migration were strongly inhibited in granulocytes irradiated in the presence of a monoclonal antibody against ABA. Moreover, presence of the same antibody strongly inhibited release of NO, prostaglandin E2 (PGE(2)), and tumor necrosis factor-α (TNF-α) by UV-B irradiated keratinocytes. Lanthionine synthetase C-like protein 2 (LANCL2) is required for the activation of the ABA signaling pathway in human granulocytes. Silencing of LANCL2 in human keratinocytes by siRNA was accompanied by abrogation of the UV-B-triggered release of PGE(2), TNF-α, and NO and ROS production. These results indicate that UV-B irradiation induces ABA release from human granulocytes and keratinocytes and that autocrine ABA stimulates cell functions involved in skin inflammation.
authors: Department of Experimental Medicine and CEBR, University of Genova, Genova, Italy.
authors: Santina
authors: S
authors: Bruzzone
authors: Giovanna
authors: G
authors: Basile
authors: Elena
authors: E
authors: Mannino
authors: Laura
authors: L
authors: Sturla
authors: Mirko
authors: M
authors: Magnone
authors: Alessia
authors: A
authors: Grozio
authors: Annalisa
authors: A
authors: Salis
authors: Chiara
authors: C
authors: Fresia
authors: Tiziana
authors: T
authors: Vigliarolo
authors: Lucrezia
authors: L
authors: Guida
authors: Antonio
authors: A
authors: De Flora
authors: Vanesa
authors: V
authors: Tossi
authors: Raul
authors: R
authors: Cassia
authors: Lorenzo
authors: L
authors: Lamattina
authors: Elena
authors: E
authors: Zocchi
mesh_terms: D000040:Abscisic Acid / Q000378:metabolism*; D019898:Autocrine Communication; D002460:Cell Line; D002634:Chemotaxis, Leukocyte; D017077:Culture Media, Conditioned / Q000378:metabolism; D003872:Dermatitis / Q000209:etiology* / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004307:Dose-Response Relationship, Radiation; D006098:Granulocytes / Q000378:metabolism / Q000528:radiation effects*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D015603:Keratinocytes / Q000378:metabolism / Q000528:radiation effects*; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D010587:Phagocytosis; D028044:Phosphate-Binding Proteins; D034622:RNA Interference; D017382:Reactive Oxygen Species / Q000378:metabolism; D013997:Time Factors; D014162:Transfection; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014466:Ultraviolet Rays; D015854:Up-Regulation
chemical_list: D017077:Culture Media, Conditioned; D018836:Inflammation Mediators; C471704:LANCL2 protein, human; D008565:Membrane Proteins; D009687:Nuclear Proteins; D028044:Phosphate-Binding Proteins; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D000040:Abscisic Acid; D015232:Dinoprostone