Leptin promotes cell survival and activates Jurkat T lymphocytes by stimulation of mitogen-activated protein kinase.

作者: P. Fernández-Riejos , R. Goberna , V. Sánchez-Margalet

DOI: 10.1111/J.1365-2249.2007.03563.X

关键词: Jurkat cellsSignal transductionImmunologyLeptinMAPK/ERK pathwayPropidium iodideProtein kinase ALeptin receptorBiologyKinase

摘要: Leptin (Ob) is a non-glycosylated peptide hormone that regulates energy homeostasis centrally, but also has systemic effects including the regulation of immune function. We have reported previously leptin activates human peripheral blood lymphocytes co-stimulated with phytohaemagglutinin (PHA) (4 μg/ml), which prevented employment pharmacological inhibitors signalling pathways. In present study, we used Jurkat T cells responded to minimal PHA co-stimulation (0·25 μg/ml). The long isoform receptor expressed on and upon stimulation, expression early activation marker CD69 increases in dose-dependent manner (0·1–10 nM). found receptor-associated kinases Janus family-signal transucers activators transcription (JAK-STAT), mitogen-activated protein kinase (MAPK) phosphatidylinositol 3 (PI3K) Moreover, sought study possible effect cell survival apoptosis by culture serum-free conditions. assayed phases flow cytometric detection fluorescein isothiocyanate (FITC)-labelled annexin V simultaneously dye exclusion propidium iodide (PI). As well, level caspase-3 inmunoblot specific antibody recognizes active caspase-3. inhibits apoptotic process dose-dependently. By using inhibitors, stimulatory anti-apoptotic are dependent MAPK activation, rather than PI3K pathway, providing new data regarding mechanism action cells, may be useful understand more clearly association between nutritional status

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