Abstract
Skin is highly accessible and evaluable organ, which accelerate the understanding of novel medical innovation in association with organ transplantation, engineering, and wound healing, as well as the stage-specific adaptability of transplanted Bone Marrow (BM) cells. In skin transplantation biology, multi-stage/-angle damages occur in both grafted donor and perilesional host skin, and need to be repaired properly for the engraftment and later maintenance of the local homeostasis and characteristic skin architecture, such as stratified squamoid epithelium and dermal components. These local events are more unlikely to be regulated by the host immunity, because the donor (allogenic) skin engraftment mostly accomplishes onto the immunocompromised or immunosuppressive animals. Accumulating evidences have emerged the importance of alpha-Smooth Muscle Actin (SMA)-positive myofibroblasts, via stage- and cell type specific contribution of TGF-beta, PDGF, ET-1, CCN-2 signaling pathways and/or mastocyte-derived mediators (e.g. histamine and tryptase), for the functional reorganization of the grafted skin. Moreover, particular cell lineages from BM cells have been shown to harbor the differentiation capacity into multiple skin cell phenotypes, including epidermal keratinocytes, and dermal endothelial cells and pericytes, under controlled by chemokines or cytokines, but the trans-differentiation into alpha-SMA+ myofibroblasts is possibly reversed by inactivation of MEK/ERK signal cascade. We review the recent update of the myofibroblast biology in association with the reconstitution of the engrafted skin, and also work on translating this attractive action into the application of BM transplantation medicine in genetic skin diseases.
Highlights
Skin represents a substantial part of mammalian ectoderm, which is normally exposed by various exogenous stimuli, for example, UV irradiation, infection, temperature, moisture, and mechanical stimuli [1]
From a dermatological view point, this review focuses on these attractive points in association with the cell type-specific reorganization in the skin transplantation, dynamic action of myofibloblasts, as well as the relevant molecular profiles
The grafted skin sites need to repair some inevitable minor trauma and inflammation, for example, occasional hemorrhage caused by microvascular damage, exudative stress, later excess micro-fibrosis, or even focal necrotic changes, in order to adapt to the host skin circumstance
Summary
Skin represents a substantial part of mammalian ectoderm, which is normally exposed by various exogenous stimuli, for example, UV irradiation, infection, temperature, moisture, and mechanical stimuli [1]. The predominant cell populations in mammalian skin comprise dermal fibroblasts and epidermal keratinocytes. Both cells show different morphology and function, and are separated structurally by basement membrane. Ours and other studies have utilized two-/three-dimensional co-culture or complex “organotopic” culture systems, allowing to address the importance of paracrine interaction between fibroblasts and keratinocytes [3,4]. Upon these in vitro skin equivalent assays, little is known about how these two cell types are reorganized properly in the grafted skin. These advanced evidences may help to ask how we can establish and refine the better medical approaches for the persistent skin wound condition, in genetic skin diseases
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