Journal
FEBS LETTERS
Volume 588, Issue 24, Pages 4708-4719Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2014.10.044
Keywords
Ghrelin; T-cell; Stress; Glucocorticoid; Proliferation; Signaling; Thymus
Funding
- Intramural Research Program of the National Institute on Aging, National Institutes of Health
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Thymic atrophy occurs during normal aging, and is accelerated by exposure to chronic stressors that elevate glucocorticoid levels and impair the naive 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. Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
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