Age-related disruption of autophagy in dermal fibroblasts modulates extracellular matrix components

自噬 ATG5型 成纤维细胞 真皮成纤维细胞 细胞生物学 自噬体 细胞外基质 化学 脂褐素 免疫印迹 细胞内 生物 生物化学 细胞凋亡 体外 基因
作者
Kanae Tashiro,Mayumi Shishido,Keiko Fujimoto,Yuko Hirota,Kazuyuki Yo,Takamasa Gomi,Yoshitaka Tanaka
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier BV]
卷期号:443 (1): 167-172 被引量:49
标识
DOI:10.1016/j.bbrc.2013.11.066
摘要

Autophagy is an intracellular degradative system that is believed to be involved in the aging process. The contribution of autophagy to age-related changes in the human skin is unclear. In this study, we examined the relationship between autophagy and skin aging. Transmission electron microscopy and immunofluorescence microscopy analyses of skin tissue and cultured dermal fibroblasts derived from women of different ages revealed an increase in the number of nascent double-membrane autophagosomes with age. Western blot analysis showed that the amount of LC3-II, a form associated with autophagic vacuolar membranes, was significantly increased in aged dermal fibroblasts compared with that in young dermal fibroblasts. Aged dermal fibroblasts were minimally affected by inhibition of autophagic activity. Although lipofuscin autofluorescence was elevated in aged dermal fibroblasts, the expression of Beclin-1 and Atg5—genes essential for autophagosome formation—was similar between young and aged dermal fibroblasts, suggesting that the increase of autophagosomes in aged dermal fibroblasts was due to impaired autophagic flux rather than an increase in autophagosome formation. Treatment of young dermal fibroblasts with lysosomal protease inhibitors, which mimic the condition of aged dermal fibroblasts with reduced autophagic activity, altered the fibroblast content of type I procollagen, hyaluronan and elastin, and caused a breakdown of collagen fibrils. Collectively, these findings suggest that the autophagy pathway is impaired in aged dermal fibroblasts, which leads to deterioration of dermal integrity and skin fragility.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
大翟完成签到,获得积分10
1秒前
不远完成签到,获得积分10
2秒前
冯珂完成签到 ,获得积分10
4秒前
Graham完成签到,获得积分10
4秒前
稳重乌冬面完成签到 ,获得积分10
6秒前
一苇以航完成签到 ,获得积分10
7秒前
戚雅柔完成签到 ,获得积分10
7秒前
vsvsgo完成签到,获得积分10
8秒前
米奇完成签到 ,获得积分10
8秒前
加一点荒谬完成签到,获得积分10
8秒前
8秒前
一一一给轻松白桃的求助进行了留言
10秒前
zz2905完成签到,获得积分10
10秒前
小超人完成签到 ,获得积分10
11秒前
香蕉初瑶完成签到,获得积分10
11秒前
meimei完成签到 ,获得积分10
11秒前
儒雅的菠萝吹雪完成签到,获得积分10
12秒前
12秒前
13秒前
水寒完成签到,获得积分10
13秒前
拉长的念珍完成签到,获得积分10
14秒前
大气夜山完成签到 ,获得积分10
14秒前
Tristan完成签到 ,获得积分10
16秒前
我思故我在完成签到,获得积分10
16秒前
17秒前
何浏亮完成签到,获得积分10
18秒前
阿成完成签到,获得积分10
18秒前
Pauline完成签到 ,获得积分10
18秒前
19秒前
微笑的语芙完成签到,获得积分10
19秒前
19秒前
小背包完成签到 ,获得积分10
19秒前
水寒发布了新的文献求助10
21秒前
希望天下0贩的0应助17采纳,获得10
21秒前
yu完成签到 ,获得积分10
21秒前
钟瑞乾完成签到,获得积分10
21秒前
花痴的电灯泡完成签到,获得积分10
22秒前
虚心念桃完成签到,获得积分10
23秒前
jiaolulu发布了新的文献求助10
24秒前
zyw完成签到 ,获得积分10
24秒前
高分求助中
【提示信息,请勿应助】关于scihub 10000
Les Mantodea de Guyane: Insecta, Polyneoptera [The Mantids of French Guiana] 3000
徐淮辽南地区新元古代叠层石及生物地层 3000
The Mother of All Tableaux: Order, Equivalence, and Geometry in the Large-scale Structure of Optimality Theory 3000
Handbook of Industrial Diamonds.Vol2 1100
Global Eyelash Assessment scale (GEA) 1000
Picture Books with Same-sex Parented Families: Unintentional Censorship 550
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 4038235
求助须知:如何正确求助?哪些是违规求助? 3575992
关于积分的说明 11374009
捐赠科研通 3305760
什么是DOI,文献DOI怎么找? 1819276
邀请新用户注册赠送积分活动 892662
科研通“疑难数据库(出版商)”最低求助积分说明 815022