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Fig. 1 | Cell & Bioscience

Fig. 1

From: Role of metastasis-induced protein S100A4 in human non-tumor pathophysiologies

Fig. 1

Extra-S100A4 can be released into the extracellular space by fibroblasts, macrophages, lymphocytes, neutrophils, vascular cells, and other bone marrow derived cells. The S100A4 interacted with IL-10R exerts a neuron pro-survival effect under various injuries via JAK/STAT pathway partially. Besides, the expression of extra-S100A4 leads to increasing phosphorylation of Pyk-2, MAPKs, and activating NF-κB through the RAGE-dependent regulation associated with cell migratory abilities and chemotaxis. On the other hand, the intracellular S100A4 can combine with numerous target molecules, such as NMIIA, tropomyosin, P53, and actin, to form the complexes, facilitating the remodeling of microtubes and microfilaments to enhance cell motility and chemotaxis, contributing to the infiltration of fibroblasts, immune and vascular cells into the affected region releasing inflammatory factors. In addition, S100A4 colocalizes with P53 promoting cell proliferation and collagen expression via MAPK activation and phosphorylation of ERK. The TGF-β-mediated process induces the up-regulation of S100A4 promoting the generation of extracellular matrix, collagen, elastin and others underlying the basis for the course of inflammation tissue fibrosis. Moreover, the intracellular S100A4 regulates its upstream and/or downstream gene expression involved in proteolytic activity, angiogenesis and cell survival by modulating signal pathways of MAPKs, ERK, p38, JNK, NF-κB, and p53

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