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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 second messenger functions of H2O2 are largely achieved via oxidation of specific cysteine thiols in signaling proteins, which are often found in catalytic domains of signaling enzymes (Claiborne et al. 1999). Oxidation of cysteine thiols stimulates the formation of sulfenic acid (sulfenylation), a highly unstable metabolite that can rapidly convert to other metabolites, such as sulfinic acid and sulfonic acid, or nitrosothiol (Leonard et al. 2009). However, a more common metabolic process in which sulfenic acid participates is to promote disulfide bond formation. It was found that this can lead to a conformational change in signaling proteins, which modulates their enzymatic activity, either activating or inactivating the enzyme (Stone and Yang 2006; Leonard and Carroll 2011; Truong and Carroll 2012). This has been shown to lead to the modulation of phosphorylation cascades within cells, often by activating kinases and deactivating phosphatases (Claiborne et al. 1999; Gough and Cotter 2011). In zebrafish, oxidative activation of the kinase, Lyn, a member of the Src-family kinase (SFK), recruits neutrophils toward the wound site (Niethammer et al. 2009; Yoo et al. 2011). Hydrogen peroxide oxidizes a specific cysteine residue (C466) in the kinase domain, which promotes autophosphorylation and Lyn activation (Yoo et al. 2011). A homolog of Lyn in Drosophila is Src42A, which also harbors this oxidation-sensitive cysteine residue 466, indicating the conservation of this signaling mechanism in fruit flies. It was demonstrated that Src42A similarly stimulates immune cell migration through interactions with two downstream targets, Draper/CED1 and Shark, which have been implicated in the vertebrate adaptive immune response (Underhill and Goodridge 2007). Oxidative regulation of wound repair is also conserved in the nematode Caenorhabditis elegans. However, mitochondrial superoxide rather than H2O2 mediates this process. The skin in nematodes, the hypodermis, is an epithelium that consists of large syncytial cells. Puncture or laser wounding of the hypodermis leads to a calcium-dependent repair mechanism by which an actin purse string contracts around the wound to seal the injury (Xu and Chisholm 2014). Injuries rapidly trigger the formation of calcium flashes emanating from the wound site. The calcium enters the mitochondria via the mitochondrial calcium uniporter (MCU-1). Once in the mitochondria, calcium stimulates the production of superoxide (mtROS) and subsequent local inhibition of Rho-1 GTPase activity via a redox-sensitive motif and oxidation of Cys16, leading to actin reorganization and closure.
Serum from differently exercised subjects induces myogenic differentiation in LHCN-M2 human myoblasts
Published in Journal of Sports Sciences, 2018
D. Vitucci, E. Imperlini, R. Arcone, A. Alfieri, A. Canciello, L. Russomando, D. Martone, A. Cola, G. Labruna, S. Orrù, D. Tafuri, A. Mancini, P. Buono
In this study we also examined the effects of human serum factors, such as IGF-1, on myogenic differentiation. We found that serum from differently exercised subjects, containing high levels of IGF-1, induces myogenic differentiation in LHCN-M2 cells, differently from untrained subject’s serum, containing low IGF-1 levels. This finding prompts us to speculate that IGF-1 plays a crucial role in the myogenic differentiation process in LHCN-M2 cells. A series of previously reported results are consistent with this concept. In particular, it has been demonstrated that IGF-1, together with myogenic regulatory factors, is involved in the progression of satellite cell activation during myogenesis and muscle regeneration (Shi & Garry, 2006; Zanou & Gailly, 2013). More recently, it was found that blood factors mediate tissue adaptation in response to exercise in sedentary rats (Goutianos et al., 2016). Notably, serum from exercised subjects was found to affect mitochondrial calcium uniporter expression levels, which in turn conteracts age-related muscle loss in sarcopenia and also reduces the oxidative stress that cause many different dysmetabolic and cardiovascular diseases (Conti et al., 2012; Zampieri et al., 2016). Furthermore, other studies demonstrated that circulating blood factors favour synaptic plasticity in the brain of elderly mice, and reduce age-related cardiac hypertrophy (Loffredo et al., 2013; Villeda et al., 2014).