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

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Year: 2008 Volume: 151 Issue: 2

Year: 2008 Volume: 151 Issue: 1

Year: 2007 Volume: 150

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fernández-Riejos, P. Goberna, R. Sánchez-Margalet, V.
Description	Country affiliation: Spain Author Affiliation: Fernández-Riejos P ( Department of Clinical Biochemistry, Virgen Macarena University Hospital, Medical School University of Seville, Seville, Spain.)
Abstract	Leptin (Ob) is a non-glycosylated peptide hormone that regulates energy homeostasis centrally, but also has systemic effects including the regulation of the immune function. We have reported previously that leptin activates human peripheral blood lymphocytes co-stimulated with phytohaemagglutinin (PHA) (4 microg/ml), which prevented the employment of pharmacological inhibitors of signalling pathways. In the present study, we used Jurkat T cells that responded to leptin with minimal PHA co-stimulation (0.25 microg/ml). The long isoform of leptin receptor is expressed on Jurkat T cells and upon leptin stimulation, the expression of early activation marker CD69 increases in a dose-dependent manner (0.1-10 nM). We have also found that leptin activates receptor-associated kinases of the Janus family-signal transucers and activators of transcription (JAK-STAT), mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3 kinase (PI3K) signalling pathways. Moreover, we sought to study the possible effect of leptin on cell survival and apoptosis of Jurkat T cells by culture in serum-free conditions. We have assayed the early phases of apoptosis by flow cytometric detection of fluorescein isothiocyanate (FITC)-labelled annexin V simultaneously with dye exclusion of propidium iodide (PI). As well, we have assayed the activation level of caspase-3 by inmunoblot with a specific antibody that recognizes active caspase-3. We have found that leptin inhibits the apoptotic process dose-dependently. By using pharmacological inhibitors, we have found that the stimulatory and anti-apoptotic effects of leptin in Jurkat T cells are dependent on MAPK activation, rather than the PI3K pathway, providing new data regarding the mechanism of action of leptin in T cells, which may be useful to understand more clearly the association between nutritional status and the immune function.
File Format	HTM / HTML
ISSN	00099104
e-ISSN	13652249
DOI	10.1111/j.1365-2249.2007.03563.x
Journal	Clinical & Experimental Immunology
Issue Number	3
Volume Number	151
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2008-03-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Immunology Leptin Immunology Lymphocyte Activation Mitogen-activated Protein Kinases Metabolism T-lymphocytes Cell Survival Dose-response Relationship, Immunologic Enzyme Activation Jurkat Cells Map Kinase Signaling System Neoplasm Proteins Phosphatidylinositol 3-kinases Phosphorylation Receptors, Leptin Recombinant Proteins Reverse Transcriptase Polymerase Chain Reaction Stat3 Transcription Factor Tyrosine
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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

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