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- Title
Excessive Accumulation of Intracellular Ca<sup>2+</sup> After Acute Exercise Potentiated Impairment of T-cell Function.
- Authors
Liu, Renyi; Krüger, Karsten; Pilat, Christian; Fan, Wei; Xiao, Yu; Seimetz, Michael; Ringseis, Robert; Baumgart-Vogt, Eveline; Eder, Klaus; Weissmann, Norbert; Mooren, Frank Christoph
- Abstract
Ca2+ is an important intracellular second messenger known to regulate several cellular functions. This research aimed to investigate the mechanisms of exercise-induced immunosuppression by measuring intracellular calcium levels, Ca2+-regulating gene expression, and agonist-evoked proliferation of murine splenic T lymphocytes. Mice were randomly assigned to the control, sedentary group (C), and three experimental groups, which performed a single bout of intensive and exhaustive treadmill exercise. Murine splenic lymphocytes were separated by density-gradient centrifugation immediately (E0), 3h (E3), and 24h after exercise (E24). Fura-2/AM was used to monitor cytoplasmic free Ca2+ concentration in living cells. The combined method of carboxyfluorescein diacetate succinimidyl ester (CFSE) labeling and flow cytometry was used for the detection of T cell proliferation. The transcriptional level of Ca2+-regulating genes was quantified by using qPCR. Both basal intracellular Ca2+ levels and agonist (ConA, OKT3, or thapsigargin)-induced Ca2+ transients were significantly elevated at E3 group (p <0.05 vs. control). However, mitogen-induced cell proliferation was significantly decreased at E3 group (p <0.05 vs. control). In parallel, the transcriptional level of plasma membrane Ca2+-ATPases (PMCA), sarco/endoplasmic reticulum Ca2+-ATPases (SERCA), TRPC1, and P2X7 was significantly downregulated, and the transcriptional level of IP3R2 and RyR2 was significantly upregulated in E3 (p <0.01 vs. control). In summary, this study demonstrated that acute exercise affected intracellular calcium homeostasis, most likely by enhancing transmembrane Ca2+ influx into cells and by reducing expression of Ca2+-ATPases such as PMCA and SERCA. However, altered Ca2+ signals were not transduced into an enhanced T cell proliferation suggesting other pathways to be responsible for the transient exercise-associated immunosuppression.
- Subjects
CELL physiology; T cells; MOLECULAR mechanisms of immunosuppression; CELL membranes; HOMEOSTASIS; INTRACELLULAR calcium
- Publication
Frontiers in Physiology, 2021, Vol 12, p1
- ISSN
1664-042X
- Publication type
Article
- DOI
10.3389/fphys.2021.728625