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Pornsiriwong, W., Estavillo, G.M., Chan, K.X., Tee, E.E., Ganguly, D., Crisp, P.A., Yong, M.T., et al. (2017) A Chloroplast Retrograde Signal, 3’-Phosphoadenosine 5’-Phosphate, Acts as a Secondary Messenger in Abscisic Acid Signaling in Stomatal Closure and Germination. Elife, 6, e23361. https://doi.org/10.7554/eLife.23361

has been cited by the following article:

• TITLE: Bone Marrow Cells Obtained from Old Animals Differ from the Young Animals Cells in Their Ability to Divide and in Response to the Presence of Liver Fibrosis in Primary Culture

  AUTHORS: S. L. Ohiienko, A. I. Bozhkov, A. Yu. Bondar, E. G. Ivanov, I. A. Ionov

  KEYWORDS: Bone Marrow, Aging, Proliferation, Lymphocyte, Intracellular Ca2+

  JOURNAL NAME: Advances in Aging Research, Vol.8 No.1, January 31, 2019

  ABSTRACT: Dynamics of bone marrow cells number (BMC) in the primary culture isolated from young (3 months) and old (20 months) Wistar rats was investigated. Proliferative activity of BMC of old animals was 2 times higher than that of young animals in the primary culture. Such superiority of the proliferative activity of BMC in the primary culture obtained from old animals is associated with the ability to actively divide lymphocytes and longer “lifespan” of segmented neutrophils obtained from old animals. It should be noted, that the lymphocytes of young animals did not proliferate in the primary culture. The content of intracellular calcium in BMC in the cells of old animals was 3 times higher compared with cells of young animals, which revealed the relationship of intracellular calcium and proliferative activity of BMC. Induction of liver fibrosis led to an increase in the lymphocyte content in young animals by 167%, and in old ones only by 26%, while the lymphocytes of young animals acquired the ability to proliferate in the primary culture. It has been suggested that such differences in the behavior of BMC in primary culture obtained in young and old animals reflect differences in the BMC microenvironment of young and old animals, which leads to changes in the epigenetic-metabolic characteristics of BMC.