多功能免疫补体组分1q(C1q)和凋亡相关基因在日本大蠊组织和人类细胞暴露于环境污染物后的反应。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2023-11-01 Epub Date: 2023-10-26 DOI:10.1007/s12192-023-01389-y
Kiyun Park, Byoung-San Moon, Ihn-Sil Kwak
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引用次数: 0

摘要

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中发挥着核心作用。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免疫相关凋亡途径的影响。为此,我们对多功能免疫补体组分1q(C1q)基因进行了表征,并分析了暴露于邻苯二甲酸二(2-乙基己基)酯(DEHP)或六溴环十二烷(HBCDs)后日本巨眼蟹C1q的表达。此外,在日本血吸虫组织和人细胞系(HEK293T和HCT116)中观察到凋亡信号相关基因的反应。暴露于DEHP或HBCD后,日本血吸虫鳃和肝胰腺中C1q基因表达下调。污染物暴露还增加了刺参的抗氧化酶活性,并改变了15个凋亡信号基因的转录。然而,人类细胞对这些污染物的凋亡信号传导模式不同。六溴环十二烷暴露在两种细胞系中都产生凋亡信号(裂解的胱天蛋白酶-3)并抑制细胞生长,而DEHP暴露没有产生这种反应。这些结果表明,暴露于环境污染物诱导了不同水平的免疫相关细胞凋亡,这取决于细胞或组织类型,并且这种凋亡信号的诱导可能引发日本血吸虫和作为消费者的人类的致癌作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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

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.

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4.30%
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567
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