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Ghrelin augments murine T‐cell proliferation by activation of the phosphatidylinositol‐3‐kinase, extracellular signal‐regulated kinase and protein kinase C signaling pathways
Author(s) -
Lee Jun Ho,
Patel Kalpesh,
Tae Hyun Jin,
Lustig Ana,
Kim Jie Wan,
Mattson Mark P.,
Taub Dennis D.
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.10.044
Subject(s) - ghrelin , protein kinase b , microbiology and biotechnology , cyclin dependent kinase 2 , kinase , cyclin dependent kinase 4 , signal transduction , endocrinology , cell growth , biology , ask1 , medicine , protein kinase a , chemistry , cancer research , hormone , biochemistry
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.