Heat acclimation increases inflammatory and apoptotic responses to subsequent LPS challenge in C2C12 myotubes

Patton, Meghan G.; Gillum, Trevor; Szymanski, Mandy C.; Gould, Lacey M.; Lauterbach, Claire J.; Vaughan, Roger A.; Kuennen, Matthew R.

doi:10.1007/s12192-018-0923-0

Cited by 3 publications

(1 citation statement)

References 51 publications

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“…To culture the cells for a suitable duration for cellular HA, the cells were seeded in 25 cm 2 T-flasks (3 × 10 6 cells/flask) and 24-well plates (1 × 10 5 cells/well) at 37 • C in a humidified 5% CO 2 atmosphere. For HA, we exposed the cells to intermittent temperatures between 37 • C and 39.5 • C, mimicking the repeated thermal exposure to acquiring HA that has been previously reported (Patton et al, 2018). The cells were maintained in two incubators under a 20/4-h cycle of 37 • C/39.5 • C for 72 h. The culture medium was replaced with fresh preheated medium every 2 days.…”

Section: Cellular Heat Acclimationmentioning

confidence: 99%

TREM2 Regulates Heat Acclimation-Induced Microglial M2 Polarization Involving the PI3K-Akt Pathway Following EMF Exposure

Luo

Shen

et al. 2020

Front. Cell. Neurosci.

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The function of triggering receptor expressed on myeloid cells-2 (TREM2) has been described within microglia with a beneficial activated phenotype. However, the role of TREM2 underlying microglial phenotypic alterations in the cross-tolerance protection of heat acclimation (HA) against the inflammatory stimuli electromagnetic field (EMF) exposure is less well known. Here, we investigated the TREM2-related signaling mechanism induced by HA in EMF-stimulated N9 microglial cells (N9 cells). We found that EMF exposure significantly increased the production of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α, IL-1β, and IL-6), and the expression of M1 markers (CD11b and CD86); meanwhile, decreased the levels of anti-inflammatory cytokines (IL-4 and IL-10) and the expression of M2 markers (CD206 and Arg1) in N9 cells. Clearly, HA treatment decreased the secretion of TNF-α, IL-1β and IL-6 and the expression of CD11b and CD86, and enhanced the production of IL-4 and IL-10 and the expression of CD206 and Arg1. Moreover, TREM2 esiRNA and selective inhibitor of PI3K clearly decreased anti-inflammatory cytokines production, M2 markers expression, and phosphorylation of PI3K and Akt following HA plus EMF stimulation. These results indicate that TREM2 and PI3K-Akt pathway are involved in the cross-tolerance protective effect of HA in microglial polarization towards the EMF exposure. This finding inspires future studies that aim to explore the non-drug approaches underlying EMF stimulation and other central nervous system (CNS) inflammatory diseases.

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Section: Cellular Heat Acclimationmentioning

confidence: 99%

TREM2 Regulates Heat Acclimation-Induced Microglial M2 Polarization Involving the PI3K-Akt Pathway Following EMF Exposure

Luo

Shen

et al. 2020

Front. Cell. Neurosci.

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Dietary curcumin supplementation does not alter peripheral blood mononuclear cell responses to exertional heat stress

et al. 2018

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Nanoparticle drug delivery characterization for fluticasone propionate and in vitro testing

Sutariya

Kelly

Weigel

et al. 2019

Can. J. Physiol. Pharmacol.

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Glucocorticoids, such as fluticasone propionate (FP), are used for the treatment of inflammation and alleviation of nasal symptoms and allergies, and as an antipruritic. However, both short- and long-term therapeutic use of glucocorticoids can lead to muscle weakness and atrophy. In the present study, we evaluated the feasibility of the nanodelivery of FP with poly(dl-lactide-co-glycolide) (PLGA) and tested in vitro function. FP-loaded PLGA nanoparticles were prepared via nanoprecipitation and morphological characteristics were studied via scanning electron microscopy. FP-loaded nanoparticles demonstrated an encapsulation efficiency of 68.6% ± 0.5% with a drug loading capacity of 4.6% ± 0.04%, were 128.8 ± 0.6 nm in diameter with a polydispersity index of 0.07 ± 0.008, and displayed a zeta potential of –19.4 ± 0.7. A sustained in vitro drug release pattern was observed for up to 7 days. The use of fluticasone nanoparticle decreased lipopolysaccharide (LPS)-induced lactate dehydrogenase release compared with LPS alone in C2C12 treated cells. FP also decreased expression of LPS-induced inflammatory genes in C2C12 treated cells as compared with LPS alone. Taken together, the present study demonstrates in vitro feasibility of PLGA-FP nanoparticle delivery to the skeletal muscle cells, which may be beneficial for treating inflammation.

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Heat acclimation increases inflammatory and apoptotic responses to subsequent LPS challenge in C2C12 myotubes

Cited by 3 publications

References 51 publications

TREM2 Regulates Heat Acclimation-Induced Microglial M2 Polarization Involving the PI3K-Akt Pathway Following EMF Exposure

TREM2 Regulates Heat Acclimation-Induced Microglial M2 Polarization Involving the PI3K-Akt Pathway Following EMF Exposure

Dietary curcumin supplementation does not alter peripheral blood mononuclear cell responses to exertional heat stress

Nanoparticle drug delivery characterization for fluticasone propionate and in vitro testing

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