Responses of multifunctional immune complement component 1q (C1q) and apoptosis-related genes in Macrophthalmus japonicus tissues and human cells following exposure to environmental pollutants.

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Kiyun Park, Byoung-San Moon, Ihn-Sil Kwak
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引用次数: 0

Abstract

Apoptosis is a key defense process for multiple immune system functions, playing a central role in maintaining homeostasis and cell development. The purpose of this study was to evaluate the effects of environmental pollutant exposure on immune-related apoptotic pathways in crab tissues and human cells. To do this, we characterized the multifunctional immune complement component 1q (C1q) gene and analyzed C1q expression in Macrophthalmus japonicus crabs after exposure to di(2-ethylhexyl) phthalate (DEHP) or hexabromocyclododecanes (HBCDs). Moreover, the responses of apoptotic signal-related genes were observed in M. japonicus tissues and human cell lines (HEK293T and HCT116). C1q gene expression was downregulated in the gills and hepatopancreas of M. japonicus after exposure to DEHP or HBCD. Pollutant exposure also increased antioxidant enzyme activities and altered transcription of 15 apoptotic signaling genes in M. japonicus. However, patterns in apoptotic signaling in response to these pollutants differed in human cells. HBCD exposure generated an apoptotic signal (cleaved caspase-3) and inhibited cell growth in both cell lines, whereas DEHP exposure did not produce such a response. These results suggest that exposure to environmental pollutants induced different levels of immune-related apoptosis depending on the cell or tissue type and that this induction of apoptotic signaling may trigger an initiation of carcinogenesis in M. japonicus and in humans as consumers.

暴露于环境污染物后日本鲣鱼组织和人体细胞中多功能免疫补体成分1q(C1q)和细胞凋亡相关基因的反应。
细胞凋亡是多种免疫系统功能的关键防御过程,在维持体内平衡和细胞发育方面发挥着核心作用。本研究的目的是评估环境污染物暴露对螃蟹组织和人类细胞中免疫相关凋亡途径的影响。为此,我们鉴定了多功能免疫补体成分1q(C1q)基因,并分析了接触邻苯二甲酸二(2-乙基己基)酯(DEHP)或六溴环十二烷(HBCDs)后日本梭子蟹体内C1q的表达情况。此外,在日本螃蟹组织和人类细胞系(HEK293T 和 HCT116)中观察到了凋亡信号相关基因的反应。接触 DEHP 或六溴环十二烷后,日本贻贝鳃和肝胰腺中的 C1q 基因表达下调。接触污染物还增加了日本贻贝的抗氧化酶活性,并改变了15个凋亡信号基因的转录。不过,人类细胞对这些污染物的凋亡信号转导模式有所不同。暴露于六溴环十二烷会产生凋亡信号(裂解的 Caspase-3)并抑制两种细胞系的细胞生长,而暴露于 DEHP 则不会产生这种反应。这些结果表明,暴露于环境污染物会诱导不同程度的免疫相关凋亡,这取决于细胞或组织类型,而这种凋亡信号的诱导可能会引发日本蝇和作为消费者的人类的癌变。
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来源期刊
Cell Stress & Chaperones
Cell Stress & Chaperones 生物-细胞生物学
CiteScore
7.60
自引率
2.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.
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