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.
Original language | English (US) |
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Pages (from-to) | 4708-4719 |
Number of pages | 12 |
Journal | FEBS Letters |
Volume | 588 |
Issue number | 24 |
DOIs | |
State | Published - Dec 20 2014 |
Externally published | Yes |
Keywords
- Ghrelin
- Glucocorticoid
- Proliferation
- Signaling
- Stress
- T-cell
- Thymus
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Cell Biology
- Genetics
- Molecular Biology
- Structural Biology