Ghrelin augments murine T-cell proliferation by activation of the phosphatidylinositol-3-kinase, extracellular signal-regulated kinase and protein kinase C signaling pathways

Jun Ho Lee, Kalpesh Patel, Hyun Jin Tae, Ana Lustig, Jie Wan Kim, Mark P. Mattson, Dennis D. Taub

Research output: Contribution to journalArticlepeer-review

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 languageEnglish (US)
Pages (from-to)4708-4719
Number of pages12
JournalFEBS Letters
Volume588
Issue number24
DOIs
StatePublished - Dec 20 2014
Externally publishedYes

Keywords

  • Ghrelin
  • Glucocorticoid
  • Proliferation
  • Signaling
  • Stress
  • T-cell
  • Thymus

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology

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