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Fig. 2 | Respiratory Research

Fig. 2

From: Regulation of human airway smooth muscle cell migration and relevance to asthma

Fig. 2

Airway remodeling is an important feature of asthma pathogenesis. An important contribution to airway remodeling is increased ASM mass, which is thought to be brought on by ASMC migration, thereby adding to the local cellular hyperplasia. The source of these ASMCs has been thought to be due to local infiltration of myfibroblasts, neighbouring ASMCs, and circulating HPCs. Various mediators have been identified that influence ASMC migration, which are outlined in this figure. Local pro-inflammatory mediators produced by airway epithelial cells, including TGF-β, PDGF, EGF, PGD2, CXCL2, CXCL3, IL-8, eotaxin, TSLP, and CCL19 have been shown to induce ASMC migration, whereas PGE2 and Lipoxin A2 inhibit ASMC migration. In addition, inflammatory cytokines produced by Th17 and Th2 cells, as well as CysLTs produced by basophils and mast cells, further contribute to ASMC migration. Conversely, systemically circulating leptin inhibits ASMC migration. Abbreviations: EP- epithelium; LP- lamina propria; ASM- Airway Smooth Muscle; ASMCs- Airway Smooth Muscle Cells; HPCs- hemopoetic progenitor cells; CysLTs- cysteinyl leukotrienes

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