Adaptive responses to air pollution in human dermal fibroblasts and their potential roles in aging.

Adaptive responses to air pollution in human dermal fibroblasts and their potential roles in aging.
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DOI:
10.1096/fba.2021-00056
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发表时间:
2021-10
期刊:
影响因子:
2.7
通讯作者:
Birch-Machin MA
Birch-Machin MA
中科院分区:
其他
文献类型:
--
作者:
Reynolds WJ;Bowman A;Hanson PS;Critchley A;Griffiths B;Chavan B;Birch-Machin MA

文献摘要

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空气污染对皮肤的损害效应正得到越来越多的研究,这项研究的结果现在对护肤品配方的保护成分的选择和开发具有重大影响。然而,还没有对暴露在这些污染物中后受到影响的特定细胞防御系统进行广泛的研究。调查受影响系统的研究是制定适当干预措施的不可或缺的一部分,这些干预措施能够扩大受空气污染物暴露影响最大的系统。以下研究包括将原代人皮肤成纤维细胞暴露于不同浓度的颗粒物中,分析其对线粒体复合体活性的影响,用免疫细胞化学方法定位核因子红系相关因子2,并用免疫印迹法检测电子传递链复合体蛋白sirtuin-1(sirtuin-1)和过氧化物酶体增殖物激活受体γ共激活因子-1α(pgc-1α)的蛋白表达。颗粒物诱导线粒体复合体蛋白和活性的变化,表明氧化应激,这也与抗氧化蛋白GSTP1/2和SOD2表达增加有关。颗粒物似乎也改变了SIRT1和PGC-1α的表达,这两个蛋白在线粒体生物发生和能量代谢的调节中发挥着重要作用。鉴于已报道的结果表明,颗粒物通过氧化应激导致损伤,并对线粒体动态平衡产生深远影响,涉及靶向线粒体抗氧化剂的干预措施可能有助于将污染物诱导的氧化应激对下游的损害降至最低,这些影响源于线粒体。
The damaging effects of air pollution on the skin are becoming increasingly researched and the outcomes of this research are now a major influence in the selection and development of protective ingredients for skincare formulations. However, extensive research has not yet been conducted into the specific cellular defense systems that are being affected after exposure to such pollutants. Research investigating the affected systems is integral to the development of suitable interventions that are capable of augmenting the systems most impacted by air pollutant exposure. The following studies involved exposing primary human dermal fibroblasts to different concentrations of particulate matter and analyzing its effects on mitochondrial complex activity, nuclear factor erythroid 2‐related factor 2 localization using immunocytochemistry and protein expression of electron transport chain complex proteins, sirtuin‐1 (SIRT1), and peroxisome proliferator‐activated receptor gamma coactivator‐1α (PGC‐1α) using western blotting. Particulate matter‐induced alterations in both mitochondrial complex protein and activity, indicating oxidative stress, which was also complimented by increased expression of antioxidant proteins GSTP1/2 and SOD2. Particulate matter also seemed to modify expression of the proteins SIRT1 and PGC‐1α which are heavily involved in the regulation of mitochondrial biogenesis and energy metabolism. Given the reported results indicating that particulate matter induces damage through oxidative stress and has a profound effect on mitochondrial homeostasis, interventions involving targeted mitochondrial antioxidants may help to minimize the damaging downstream effects of pollutant‐induced oxidative stress originating from the mitochondria.