Abstract
Aging-associated inflammation is characterized by senescent cell-mediated secretion of high levels of inflammatory mediators, such as microRNA (miR)-146a. Moreover, a rise of circulating cell-free DNA (cfDNA) is also related to systemic inflammation and frailty in the elderly. Exosome-mediated cell-to-cell communication is fundamental in cellular senescence and aging. The plasma changes in exercise-promoted miR-146a-5p, cfDNA, and exosome release could be the key to facilitate intercellular communication and systemic adaptations to exercise in aging. Thirty-eight elderly subjects (28 trained and 10 controls) volunteered in an 8-week resistance training protocol. The levels of plasma miR-146a-5p, cfDNA, and exosome markers (CD9, CD14, CD63, CD81, Flotillin [Flot]-1, and VDAC1) were measured prior to and following training. Results showed no changes in plasma miR-146a-5p and cfDNA levels with training. The levels of exosome markers (Flot-1, CD9, and CD81) as well as exosome-carried proteins (CD14 and VDAC1) remained unchanged, whereas an attenuated CD63 response was found in the trained group compared to the controls. These findings might partially support the anti-inflammatory effect of resistance training in the elderly as evidenced by the diminishment of exosome CD63 protein expression, without modification of plasma miR-146a-5p and cfDNA.
Highlights
The aging process is characterized by the accumulation of failures at the molecular and cellular level, which leads to functional decline of tissues and organs [1] and deterioration of physiological functions [2]
Taking into consideration all aforementioned observations, this study aimed to examine the effects of both aging and an 8-week resistance training on the levels of plasma miR-146a-5p, cell-free DNA (cfDNA), and exosome cargo (CD9, CD14, CD63, CD81, Flot-1, and VDAC1) in elderly subjects
Unlike the studies demonstrating an upregulation of miR-146a-5p in senescent human umbilical vein endothelial cells (HUVECs) [6] and fibroblasts [41], our results did not show any difference in the baseline level of plasma miR-146a-5p between young and elderly subjects
Summary
The aging process is characterized by the accumulation of failures at the molecular and cellular level, which leads to functional decline of tissues and organs [1] and deterioration of physiological functions [2]. The age-related changes in the immune system, known as immunosenescence, result in a low-grade pro-inflammatory condition referred as inflammaging This inflammaging is mainly attributed to a somatic cellular senescenceassociated secretory phenotype (SASP) [3], in which senescent cells secrete high levels of inflammatory mediators, such as cytokines and microRNAs (miRNAs or miRs) [4,5]. MiR-146a-5p has been identified as an important regulator of DNA damage response (DDR)—senescence—inflammation crosstalk [7] In this regard, cell-free DNA (cfDNA) has been recognized as a damage-associated molecular pattern (DAMP), inducing NF-κB inflammatory response [8], and elevated levels of circulating cfDNA have been found to reflect systemic inflammation and frailty in the elderly [9,10]. Eitan and colleagues [15] have discovered a lower level of plasma EVs in the elderly compared to young individuals, possibly due to increased internalization of peripheral blood mononuclear cells (PBMCs)
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