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Reactive oxygen species and neuroepithelial interactions during wound healing
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
The ability of cutaneous sensory axons to regenerate after injury is critical, since their regeneration contributes to the restoration of somatosensation and tissue repair (Table 2.2). Classical experiments in the chick model demonstrate that denervated skin is impaired in healing. When a piece of neural tube that normally gives rise to DRG neurons innervating the wing bud skin was UV-irradiated to prevent sensory nerve innervation, wounds healed at a much slower rate compared with innervated skin (Harsum et al. 2001). Similar observations have been made in a rat injury model, where partial denervation of the skin with capsaicin treatment significantly delayed the re-epithelialization process after skin injury (Smith and Liu 2002). Using an artificial skin graft model constructed from human and mouse cells, it was shown that the lack of re-epithelialization is due to a defect in keratinocyte migration. In this model, type I and type III collagen sponges were co-cultured with fibroblasts, keratinocytes, and endothelial cells, either in the absence or in the presence of sensory neurons. Skin grafts without innervation showed defects in keratinocyte migration. These defects were attributed to reduced levels of the neuropeptide Substance P in the wound (Blais et al. 2014), which is secreted by unmyelinated cutaneous nerve endings after tissue injury. Substance P promotes vasodilatation and local immune functions by binding to its receptor, tachykinin 1 (Holzer 1988; Antezana et al. 2002). The same mechanism seems to be responsible for impaired wound healing in human patients with diabetic peripheral neuropathy, where reduced Substance P levels have been found. Diabetic wounds also show increased expression levels of neutral endopeptidase, a Substance P−degrading enzyme, indicating that additional feedback mechanisms between nerve endings and skin exist to regulate Substance P levels (Antezana et al. 2002).
Irritable bowel syndrome and the gut microbiota
Published in Journal of the Royal Society of New Zealand, 2020
Phoebe E. Heenan, Jacqueline I. Keenan, Simone Bayer, Myrthe Simon, Richard B. Gearry
Antibiotic use has long been associated with short-term GI symptoms that may become chronic, despite the cessation of treatment (Goldin and Gorbach 1984). Clostridium difficile infection is most commonly associated with antibiotic use and has become a major cause for morbidity and mortality in hospitalised patients (Ambrose et al. 1985). These observations support to the idea that antibiotic-mediated disruption of the normal gut microbiota has the potential to facilitate the growth of opportunistic pathogenic bacteria in at least a subset of patients with IBS. This is illustrated by the increased incidence of IBS in women given (Balsari et al. 1982) peri-operative metronidazole before undergoing hysterectomy (Alun Jones et al. 1984), and in Italians (Mendall and Kumar 1998) who received antibiotics for an outbreak of Salmonella enteritis (Barbara et al. 2000). A recent study confirmed the association between antibiotic use and IBS incidence in a Danish population (Krogsgaard et al. 2018). Mechanistic information is still lacking but animal studies suggest transient alterations in the gut microbiota triggered by the antibiotics are associated with altered GI motility (Corinaldesi et al. 1999; Barbara et al. 2005), increased inflammatory activity, and increased release of Substance P, a neurotransmitter associated with increased visceral hypersensitivity to colonic distension (Verdu et al. 2006).
Exaggerated post exercise hypotension following concentric but not eccentric resistance exercise: Implications for metabolism
Published in European Journal of Sport Science, 2019
Jon Stavres, Stephen M Fischer, John McDaniel
Baroreflex resetting is another mechanism that likely contributes to the augmentation of PEH following metabolically active concentric work. As exercise ceases, sympathetic withdraw and increased parasympathetic control reduce heart rate, muscle sympathetic nerve activity, and ultimately blood pressure. Additionally, GABAergic buffering of the baroreflex is diminished following the cessation of exercise due to a temporary internalisation of neurokinin-1 receptors (Chen, Bechtold, Tabor, & Bonham, 2009; Kajekar, Chen, Mutoh, & Bonham, 2002). The internalisation of neurokinin-1 receptors is suggested to be mediated by substance P release via group III and IV muscle afferent feedback, which would likely be greater during concentric exercise compared to eccentric exercise due to differences in metabolite accumulation. Therefore, GABAergic buffering of the baroreflex may be less affected following eccentric exercise compared to concentric exercise, which would result in more sympathoinhibition following concentric exercise. For a more in depth review on this topic, see Halliwill, Buck, Lacewell, and Romero (2013). Future research may consider exploring the influence of muscle afferent mediated resetting of the baroreflex on PEH between positive and negative work.
Design of a RADA16-based self-assembling peptide nanofiber scaffold for biomedical applications
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Rongrong Wang, Zhaoyue Wang, Yayuan Guo, Hongmin Li, Zhuoyue Chen
Apart from its application in the study of nerve defect repair, the RADA16 3D cell culture scaffold also plays a part in studying vascular and skin defect repair. For example, human umbilical vein endothelial cells can form an interconnected capillary-like network similar to capillaries on RADA16 hydrogel scaffolds to promote the formation of blood vessels in vivo [60]. Im et al. [49] combined the self-assembling peptide hydrogel RADA16 with substance P to form RADA16-SP. Then, they transplanted the PLCL scaffolds containing RADA16-SP subcutaneously into immunodeficient mice. They found that a PLCL-containing RADA16-SP scaffold can promote angiogenesis and induce tissue regeneration by mesenchymal stem cells (MSCs). Thus, the combination of RADA16-SP hydrogel and a porous PLCL scaffold is expected to be applied to the repair of skin defects [49]. Bradshaw et al. used RADA16 self-assembling peptide to study cellular responses to biological stimulation [38]. They demonstrated that, relative to unmodified RADA16 [38], the collagen I motif-modified RADA16 significantly promoted keratinocyte and dermal fibroblast migration, which may be more suitable for tissue engineering scaffolds for skin defect repair.