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首页> 外文期刊>Journal of Cellular Physiology >Vitamin D Attenuates Cytokine-Induced Remodeling in Human Fetal Airway Smooth Muscle Cells
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Vitamin D Attenuates Cytokine-Induced Remodeling in Human Fetal Airway Smooth Muscle Cells

机译：维生素D变弱细胞因子诱导的重构在人类胎儿气管平滑肌细胞

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Asthma in the pediatric population remains a significant contributor to morbidity and increasing healthcare costs. Vitamin D-3 insufficiency and deficiency have been associated with development of asthma. Recent studies in models of adult airway diseases suggest that the bioactive Vitamin D-3 metabolite, calcitriol (1,25-dihydroxyvitamin D-3; 1,25(OH)(2)D-3), modulates responses to inflammation; however, this concept has not been explored in developing airways in the context of pediatric asthma. We used human fetal airway smooth muscle (ASM) cells as a model of the early postnatal airway to explore how calcitriol modulates remodeling induced by pro-inflammatory cytokines. Cells were pre-treated with calcitriol and then exposed to TNF or TGF for up to 72h. Matrix metalloproteinase (MMP) activity, production of extracellular matrix (ECM), and cell proliferation were assessed. Calcitriol attenuated TNF enhancement of MMP-9 expression and activity. Additionally, calcitriol attenuated TNF and TGF-induced collagen III expression and deposition, and separately, inhibited proliferation of fetal ASM cells induced by either inflammatory mediator. Analysis of signaling pathways suggested that calcitriol effects in fetal ASM involve ERK signaling, but not other major inflammatory pathways. Overall, our data demonstrate that calcitriol can blunt multiple effects of TNF and TGF in developing airway, and point to a potentially novel approach to alleviating structural changes in inflammatory airway diseases of childhood. J. Cell. Physiol. 230: 1189-1198, 2015. (c) 2014 Wiley Periodicals, Inc., A Wiley Company
机译：哮喘在儿科人口仍然是一个在发病率和重大的贡献增加医疗成本。不足和缺陷有关与哮喘的发展。模型表明,成人呼吸道疾病生物活性维生素d 3代谢物,骨化三醇(1、25-dihydroxyvitamin d 3;调节炎症反应;这一概念还没有探索发展中航空公司在小儿哮喘。使用人类胎儿气管平滑肌细胞(ASM)作为一个早期产后气道的模型探讨骨化三醇调节改造促炎细胞因子引起的。预处理与骨化三醇,然后接触到肿瘤坏死因子或TGF 72 h。金属蛋白酶(MMP)活动,生产细胞外基质(ECM)和细胞扩散进行了评估。减毒TNF MMP-9表达的增强和活动。肿瘤坏死因子和第三TGF-induced胶原蛋白表达和沉积,另外,抑制引起的胎儿ASM细胞扩散炎性介质。信号通路建议骨化三醇影响胎儿ASM涉及ERK信号,但是没有其他主要炎症通路。我们的数据表明,骨化三醇可以直言不讳多个肿瘤坏死因子的影响和TGF在发展中气道,指向一个潜在的新方法在炎症缓解结构性变化童年的呼吸道疾病。230: 1189 - 1198, 2015。Inc .威利公司

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