FASEB journal : official publication of the Federation of American Societies for Experimental Biology
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This study investigated the effects of exercise preconditioning-induced modification in gut microbiota composition and host responses to cecal ligation and puncture (CLP)-induced sepsis. Four-week-old C57BL/6N male mice were randomly assigned to either CLP ( n = 30) or CLP-exercise (CLP+Exe; n = 30) groups. Prior to CLP-induced sepsis, the CLP+Exe mice were subjected to 8 wk of treadmill running. ⋯ Compared with control mice, preconditioned mice had a higher survival rate and less organ damage during the acute phase of sepsis, secondary to attenuation of the host response to septic shock. The current findings suggest that exercise preconditioning-induced modification in gut microbiota composition may lead to an attenuated host response to CLP-induced sepsis in wild-type mice, as shown by increased survival and less organ damage, as well as the establishment of a balance between pro- and anti-inflammatory responses.-Kim, D., Kang, H. Exercise training modifies gut microbiota with attenuated host responses to sepsis in wild-type mice.
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Neuron-derived exosomes (NDEs) were enriched by anti-L1CAM antibody immunoabsorption from plasmas of subjects ages 18-26 yr within 1 wk after a sports-related mild traumatic brain injury (acute mTBI) ( n = 18), 3 mo or longer after the last of 2-4 mTBIs (chronic mTBI) ( n = 14) and with no recent history of TBI (controls) ( n = 21). Plasma concentrations of NDEs, assessed by counts and levels of extracted exosome marker CD81, were significantly depressed by a mean of 45% in acute mTBI ( P < 0.0001), but not chronic mTBI, compared with controls. Mean CD81-normalized NDE levels of a range of functional brain proteins were significantly abnormal relative to those of controls in acute but not chronic mTBI, including ras-related small GTPase 10, 73% decrease; annexin VII, 8.8-fold increase; ubiquitin C-terminal hydrolase L1, 2.5-fold increase; AII spectrin fragments, 1.9-fold increase; claudin-5, 2.7-fold increase; sodium-potassium-chloride cotransporter-1, 2.8-fold increase; aquaporin 4, 8.9-fold increase (3.6-fold increase in chronic mTBI); and synaptogyrin-3, 3.1-fold increase (1.3-fold increase in chronic mTBI) (all acute mTBI proteins P < 0.0001). ⋯ M., Mustapic, M., Kapogiannis, D., Pryhoda, M., Gilmore, A., Gorgens, K. A., Davidson, B., Granholm, A.-C., Ledreux, A. Altered levels of plasma neuron-derived exosomes and their cargo proteins characterize acute and chronic mild traumatic brain injury.
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Cartilage engineering strategies using mesenchymal stem cells (MSCs) could provide preferable solutions to resolve long-segment tracheal defects. However, the drawbacks of widely used chondrogenic protocols containing TGF-β3, such as inefficiency and unstable cellular phenotype, are problematic. In our research, to optimize the chondrogenic differentiation of human umbilical cord MSCs (hUCMSCs), kartogenin (KGN) preconditioning was performed prior to TGF-β3 induction. hUCMSCs were preconditioned with 1 μM of KGN for 3 d, sequentially pelleted, and incubated with TGF-β3 for 28 d. ⋯ In summary, KGN preconditioning likely improves the chondrogenic differentiation of hUCMSCs by committing them to a precartilaginous stage with enhanced JNK phosphorylation and suppressed β-catenin. This novel protocol consisting of KGN preconditioning and subsequent TGF-β3 induction might be preferable for cartilage engineering strategies using MSCs.-Jing, H., Zhang, X., Gao, M., Luo, K., Fu, W., Yin, M., Wang, W., Zhu, Z., Zheng, J., He, X. Kartogenin preconditioning commits mesenchymal stem cells to a precartilaginous stage with enhanced chondrogenic potential by modulating JNK and β-catenin-related pathways.