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吸烟对端粒长度、致癌应激诱导和导致衰老的慢性炎症反应的影响。

The Effects of Smoking on Telomere Length, Induction of Oncogenic Stress, and Chronic Inflammatory Responses Leading to Aging.

机构信息

Department of Biomedical Sciences, University of Illinois College of Medicine at Rockford, Rockford, IL 61107, USA.

Department of Pathology, UW Health SwedishAmerican Hospital, Rockford, IL 61107, USA.

出版信息

Cells. 2024 May 21;13(11):884. doi: 10.3390/cells13110884.

DOI:10.3390/cells13110884
PMID:38891017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11172003/
Abstract

Telomeres, potential biomarkers of aging, are known to shorten with continued cigarette smoke exposure. In order to further investigate this process and its impact on cellular stress and inflammation, we used an in vitro model with cigarette smoke extract (CSE) and observed the downregulation of telomere stabilizing and genes after CSE treatment. is a subunit of telomerase and a well-known oncogenic marker, which is overexpressed in over 85% of cancers and may contribute to lung cancer development in smokers. We also observed an increase in and expression levels after CSE treatment, as well as increased protein levels revealed by immunohistochemical staining in smokers' lung tissue samples compared to non-smokers. The effects of overexpression were further studied by quantifying , an inflammatory protein induced by , which showed greater upregulation in smokers compared to non-smokers. Similar changes in gene expression patterns for , , , and were observed in blood and buccal swab samples from smokers compared to non-smokers. The results from this study provide insight into the mechanisms behind smoking causing telomere shortening and how this may contribute to the induction of inflammation and/or tumorigenesis, which may lead to comorbidities in smokers.

摘要

端粒是衰老的潜在生物标志物，已知随着持续的香烟烟雾暴露而缩短。为了进一步研究这个过程及其对细胞应激和炎症的影响，我们使用了香烟烟雾提取物（CSE）的体外模型，并观察到 CSE 处理后端粒稳定和基因的下调。 是端粒酶的亚基，是一种众所周知的致癌标志物，在超过 85%的癌症中过度表达，可能导致吸烟者肺癌的发生。我们还观察到 CSE 处理后 和 表达水平增加，与非吸烟者相比，吸烟者肺组织样本中的免疫组织化学染色显示蛋白质水平也增加。通过定量分析 ，进一步研究了 过表达的影响， 是由 诱导的一种炎症蛋白，吸烟者中的上调幅度大于非吸烟者。与非吸烟者相比，吸烟者的血液和口腔拭子样本中也观察到 、 、 和 的基因表达模式发生类似变化。这项研究的结果深入了解了吸烟导致端粒缩短的机制，以及这如何导致炎症和/或肿瘤发生的诱导，这可能导致吸烟者出现合并症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/11172003/9dcb24c26cd9/cells-13-00884-g011.jpg
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