细胞外基质
血小板源性生长因子受体
生长因子
化学
Ⅰ型胶原
成纤维细胞
伤口愈合
转化生长因子
趋化因子
血小板衍生生长因子
促炎细胞因子
真皮成纤维细胞
纤维化
表皮生长因子
胶原受体
免疫学
细胞生物学
细胞因子
医学
炎症
内分泌学
生物
内科学
细胞
受体
生物化学
整合素
体外
作者
Mi‐Sun Kim,Hye Jin Song,Sang Hwa Lee,Cheon Koo Lee
摘要
Summary Background Dermal fibroblast is a primary cell type responsible for synthesis and remodeling of extracellular matrix in human skin. Type I collagen and hyaluronan are main components that have roles in skin fibrosis, wound healing, tissue remodeling as well as skin aging. Several studies have reported cytokine‐dependent changes in collagen expression or hyaluronan production; however, the cytokines’ effect was controversial in human dermal fibroblasts. Aims To clarify the role of various growth factors, cytokines or chemokines on the production of interstitial type I collagen and hyaluronan in dermal fibroblasts. Methods We confirmed the presence of various corresponding receptors and assessed the effects of 33 human recombinants on the production of type I collagen and hyaluronan using the assay system in dermal fibroblasts. Results Platelet‐derived growth factor ( PDGF )‐ AA , PDGF ‐ BB , epidermal growth factor ( EGF ), transforming growth factor ( TGF )‐β1, MCP ‐1, IP ‐10, interleukin ( IL )‐1α, IL ‐1β, and IL ‐15 were effective on both type I collagen and hyaluronan production, as compared with no stimulated control. On the other hand, IL ‐10 and IFN ‐ α caused a significant decrease in type I collagen production, and IL ‐8 and GM ‐ CSF caused a decrease in hyaluronan production compared with no cytokine‐treated control. Interestingly, some chemokines, such as MCP ‐1 ( CCL 2), RANTES ( CCL 5), eotaxin‐2 ( CCL 24), IP ‐10 ( CXCL 10), or fractalkine ( CX 3 CL 1) significantly induced the type I collagen or hyaluronan production. Conclusions Various growth factors and cytokines on the regulation of type I collagen and hyaluronan in human dermal skin probably function as key factors in skin remodeling and skin aging. Our profile may help to apply to cosmeceutical area maintaining as young skin through the increase in extracellular matrix.
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