Ghrelin augments murine T-cell proliferation by activation of the phosphatidylinositol-3-kinase,extracellular signal-regulated kinase and protein kinase C signaling pathways |
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Institution: | 1. Laboratory of Molecular Biology and Immunology, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, United States;2. Department of Biochemistry and Division of Brain Korea 21 Plus Program for Biomedical Science, Korea University College of Medicine, Seoul 136-701, Republic of Korea;3. Laboratory of Cardiovascular Science, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, United States;4. Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, United States;5. Center of Translational Studies, Medical Services, Veteran Affairs Medical Center, Washington, DC 20422, United States |
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Abstract: | Thymic atrophy occurs during normal aging, and is accelerated by exposure to chronic stressors that elevate glucocorticoid levels and impair the naïve T cell output. The orexigenic hormone ghrelin was recently shown to attenuate age-associated thymic atrophy. Here, we report that ghrelin enhances the proliferation of murine CD4+ primary T cells and a CD4+ T-cell line. Ghrelin induced activation of the ERK1/2 and Akt signaling pathways, via upstream activation of phosphatidylinositol-3-kinase and protein kinase C, to enhance T-cell proliferation. Moreover, ghrelin induced expression of the cell cycle proteins cyclin D1, cyclin E, cyclin-dependent kinase 2 (CDK2) and retinoblastoma phosphorylation. Finally, ghrelin activated the above-mentioned signaling pathways and stimulated thymocyte proliferation in young and older mice in vivo. |
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Keywords: | Ghrelin T-cell Stress Glucocorticoid Proliferation Signaling Thymus |
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