Abstract
Wound repair is controlled temporally and spatially to restore tissue homeostasis. Previously we reported that thermal damage of the larval zebrafish fin disrupts collagen organization and wound healing compared to tail transection (LeBert et al., 2018). Here we characterize different injury models in larval zebrafish to dissect temporal and spatial dynamics of repair in complex damage. We found that each damage model triggers distinct inflammatory and tissue responses, with Stat3 and TGFβ playing key roles in the regulation of mesenchymal cells during simple repair. While thermal injury disrupts collagen fibers initially, healing is recovered as inflammation resolves, and mesenchymal cells and collagen fibers align. By contrast, infected wounds lead to persistent inflammation and loss of mesenchymal cells, resulting in minimal tissue repair. These wound models have broad physiological relevance, thereby providing a valuable advance in our toolkit to probe the dynamics of inflammation and wound repair in complex tissue damage.
Highlights
Wound repair requires the integration of complex cellular networks and extracellular matrix remodeling to mediate resolution of damage
Unlike the simple transection, thermal injury at the caudal fin led to a dramatic loss of collagen fibers in the wound region, accompanied by a marked impact on healing progression at 48 hr post wound
The healing dynamics following burn wound or L. monocytogenes (Lm)infected transection were different from simple transection (Figure 1)
Summary
Wound repair requires the integration of complex cellular networks and extracellular matrix remodeling to mediate resolution of damage. Caudal fin transection or sterile needle wounding of larval zebrafish have become invaluable in vivo models of inflammation and wound repair (LeBert and Huttenlocher, 2014; Renshaw et al, 2006) These models have led to key insights into early wound signals (Niethammer et al, 2009; Yoo et al, 2012; Yoo et al, 2011) and mechanisms of resolution of inflammation (Mathias et al, 2006; Tauzin et al, 2014) due, in part, to the unique capability for monitoring the wound response over a long duration. Thermal injury and infected transection elicited different responses compared to the simple transection in all aspects that we characterized, allowing for new insights into the mechanisms of wound repair
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