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Exercise protects against PCB-induced inflammation and associated cardiovascular risk factors.

ABSTRACT: Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that contribute to the initiation of cardiovascular disease. Exercise has been shown to reduce the risk of cardiovascular disease; however, whether exercise can modulate PCB-induced vascular endothelial dysfunction and associated cardiovascular risk factors is unknown. We examined the effects of exercise on coplanar PCB-induced cardiovascular risk factors including oxidative stress, inflammation, impaired glucose tolerance, hypercholesteremia, and endothelium-dependent relaxation. Male ApoE(-/-) mice were divided into sedentary and exercise groups (voluntary wheel running) over a 12-week period. Half of each group was exposed to vehicle or PCB 77 at weeks 1, 2, 9, and 10. For ex vivo studies, male C57BL/6 mice exercised via voluntary wheel training for 5 weeks and then were administered with vehicle or PCB 77 24 h before vascular reactivity studies were performed. Exposure to coplanar PCB increased risk factors associated with cardiovascular disease, including oxidative stress and systemic inflammation, glucose intolerance, and hypercholesteremia. The 12-week exercise intervention significantly reduced these proatherogenic parameters. Exercise also upregulated antioxidant enzymes including phase II detoxification enzymes. Sedentary animals exposed to PCB 77 exhibited endothelial dysfunction as demonstrated by significant impairment of endothelium-dependent relaxation, which was prevented by exercise. Lifestyle modifications such as aerobic exercise could be utilized as a therapeutic approach for the prevention of adverse cardiovascular health effects induced by environmental pollutants such as PCBs.

SUBMITTER: Murphy MO

PROVIDER: S-EPMC4503535 | biostudies-literature | 2016 Feb

REPOSITORIES: biostudies-literature

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Exercise protects against PCB-induced inflammation and associated cardiovascular risk factors.

Murphy Margaret O MO Petriello Michael C MC Han Sung Gu SG Sunkara Manjula M Morris Andrew J AJ Esser Karyn K Hennig Bernhard B

Environmental science and pollution research international 20150115 3

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that contribute to the initiation of cardiovascular disease. Exercise has been shown to reduce the risk of cardiovascular disease; however, whether exercise can modulate PCB-induced vascular endothelial dysfunction and associated cardiovascular risk factors is unknown. We examined the effects of exercise on coplanar PCB-induced cardiovascular risk factors including oxidative stress, inflammation, impaired glucose tolerance, ...[more]

PMID: 25586614

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Project description:AimsTransient Receptor Potential Melastatin 7 (TRPM7) cation channel is a chanzyme (channel + kinase) that influences cellular Mg2+ homeostasis and vascular signalling. However, the pathophysiological significance of TRPM7 in the cardiovascular system is unclear. The aim of this study was to investigate the role of this chanzyme in the cardiovascular system focusing on inflammation and fibrosis.Methods and resultsTRPM7-deficient mice with deletion of the kinase domain (TRPM7+/?kinase) were studied and molecular mechanisms investigated in TRPM7+/?kinase bone marrow-derived macrophages (BMDM) and co-culture systems with cardiac fibroblasts. TRPM7-deficient mice had significant cardiac hypertrophy, fibrosis, and inflammation. Cardiac collagen and fibronectin content, expression of pro-inflammatory mediators (SMAD3, TGF?) and cytokines [interleukin (IL)-6, IL-10, IL-12, tumour necrosis factor-?] and phosphorylation of the pro-inflammatory signalling molecule Stat1, were increased in TRPM7+/?kinase mice. These processes were associated with infiltration of inflammatory cells (F4/80+CD206+ cardiac macrophages) and increased galectin-3 expression. Cardiac [Mg2+]i, but not [Ca2+]i, was reduced in TRPM7+/?kinase mice. Calpain, a downstream TRPM7 target, was upregulated (increased expression and activation) in TRPM7+/?kinase hearts. Vascular functional and inflammatory responses, assessed in vivo by intra-vital microscopy, demonstrated impaired neutrophil rolling, increased neutrophil: endothelial attachment and transmigration of leucocytes in TRPM7+/?kinase mice. TRPM7+/?kinase BMDMs had increased levels of galectin-3, IL-10, and IL-6. In co-culture systems, TRPM7+/?kinase macrophages increased expression of fibronectin, proliferating cell nuclear antigen, and TGF? in cardiac fibroblasts from wild-type mice, effects ameliorated by MgCl2 treatment.ConclusionsWe identify a novel anti-inflammatory and anti-fibrotic role for TRPM7 and suggest that its protective effects are mediated, in part, through Mg2+-sensitive processes.

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Exercise protects against PCB-induced inflammation and associated cardiovascular risk factors.

Publications

Exercise protects against PCB-induced inflammation and associated cardiovascular risk factors.

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