Frontiers in physiology
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Frontiers in physiology · Jan 2020
IL-1β Induced Cytokine Expression by Spinal Astrocytes Can Play a Role in the Maintenance of Chronic Inflammatory Pain.
It is now widely accepted that the glial cells of the central nervous system (CNS) are key players in many processes, especially when they are activated via neuron-glia or glia-glia interactions. In turn, many of the glia-derived pro-inflammatory cytokines contribute to central sensitization during inflammation or nerve injury-evoked pathological pain conditions. The prototype of pro-inflammatory cytokines is interleukin-1beta (IL-1β) which has widespread functions in inflammatory processes. ⋯ We also observed that the secretion of the three cytokines is mediated by the NFkB signaling pathway. Our data completes the picture of the IL-1β-triggered cytokine cascade in spinal astrocytes, which may lead to enhanced activation of the local cells (neurons and glia as well) and can lead to the prolonged maintenance of chronic pain. All these cytokines and the NFkB pathway can be possible targets of pain therapy.
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Sarcopenic obesity has been observed in people with neuromuscular impairment, and is linked to adverse health outcomes. It is unclear, however, if sarcopenic obesity develops in adults with facioscapulohumeral muscular dystrophy (FSHD). ⋯ Findings from this study suggest that people with FSHD, although similar in BMI and total body mass compared with controls, commonly meet the definition of sarcopenic obesity. Adults with co-existing FSHD and sarcopenic obesity may be at risk for significant impairments in quality of life, and encounter additional challenges in the management of FSHD manifestations.
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Lung diseases constitute a global health concern causing disability. According to WHO in 2016, respiratory diseases accounted for 24% of world population mortality, the second cause of death after cardiovascular diseases. The Kv7 channels family is a group of voltage-dependent K+ channels (Kv) encoded by KCNQ genes that are involved in various physiological functions in numerous cell types, especially, cardiac myocytes, smooth muscle cells, neurons, and epithelial cells. ⋯ Kv7 channels are now recognized as playing relevant physiological roles in many tissues, which have encouraged the search for Kv7 channel modulators with potential therapeutic use in many diseases including those affecting the lung. Modulation of Kv7 channels has been proposed to provide beneficial effects in a number of lung conditions. Therefore, Kv7 channel openers/enhancers or drugs acting partly through these channels have been proposed as bronchodilators, expectorants, antitussives, chemotherapeutics and pulmonary vasodilators.
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Frontiers in physiology · Jan 2020
Histone Deacetylase 3-Mediated Inhibition of microRNA-19a-3p Facilitates the Development of Rheumatoid Arthritis-Associated Interstitial Lung Disease.
Histone deacetylase (HDAC) has been implicated in rheumatoid arthritis (RA) progression. We investigated the roles of histone deacetylase 3 (HDAC3) involved in RA-associated interstitial lung disease (ILD) fibrosis. Firstly, we measured the expression of HDAC3 and interleukin 17 receptor A (IL17RA) in lung tissue samples from normal controls, idiopathic pulmonary fibrosis (IPF) patients, and RA-ILD patients. ⋯ In the mouse model, HDAC3 downregulated miR-19a-3p in lung fibroblasts to promote the progression of RA-ILD fibrosis. In lung fibroblasts of RA-ILD mice, IL17RA was a target gene of miR-19a-3p. miR-19a-3p negatively regulated IL17RA, thereby increasing the expression of fibrosis markers, COL1A1, COL3A1, and FN, in lung fibroblasts of mice. Taken together, HDAC3 upregulated IL17RA expression by targeting miR-19a-3p to facilitate the RA-ILD fibrosis development, which sheds light on a new HDAC3/miR-19a-3p/IL17RA axis functioning in RA-ILD fibrosis.
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Frontiers in physiology · Jan 2020
Exercising Caution Upon Waking-Can Exercise Reduce Sleep Inertia?
Sleep inertia, the transitional state of reduced alertness and impaired cognitive performance upon waking, is a safety risk for on-call personnel who can be required to perform critical tasks soon after waking. Sleep inertia countermeasures have previously been investigated; however, none have successfully dissipated sleep inertia within the first 15 min following waking. During this time, on-call personnel could already be driving, providing advice, or performing other safety-critical tasks. ⋯ Here, we examine these physiological processes and hypothesize how exercise can stimulate them, positioning exercise as an effective sleep inertia countermeasure. We then propose key considerations for research investigating the efficacy of exercise as a sleep inertia countermeasure, including the need to determine the intensity and duration of exercise required to reduce sleep inertia, as well as testing the effectiveness of exercise across a range of conditions in which the severity of sleep inertia may vary. Finally, practical considerations are identified, including the recommendation that qualitative field-based research be conducted with on-call personnel to determine the potential constraints in utilizing exercise as a sleep inertia countermeasure in real-world scenarios.