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转录组学揭示人类细胞系中热休克诱导的经典和非经典途径

Transcriptomics Unveil Canonical and Non-Canonical Heat Shock-Induced Pathways in Human Cell Lines.

作者信息

Reinschmidt Andrew, Solano Luis, Chavez Yonny, Hulsy William Drew, Nikolaidis Nikolas

机构信息

Department of Biological Science, Center for Applied Biotechnology Studies, and Center for Computational and Applied Mathematics, California State University Fullerton, Fullerton, CA, USA.

出版信息

bioRxiv. 2024 Dec 23:2024.12.22.629972. doi: 10.1101/2024.12.22.629972.

DOI:10.1101/2024.12.22.629972
PMID:39763846
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11703194/
Abstract

The cellular stress response (CSR) is a conserved mechanism that protects cells from environmental and physiological stressors. The heat shock response (HSR), a critical component of the CSR, utilizes molecular chaperones to mitigate proteotoxic stress caused by elevated temperatures. We hypothesized that while the canonical HSR pathways are conserved across cell types, specific cell lines may exhibit unique transcriptional responses to heat shock. To test this, we compared the transcriptomic responses of HEK293, HepG2, and HeLa cells under control conditions immediately following heat shock and after an 8-hour recovery period. RNA sequencing revealed conserved activation of canonical HSR pathways, including the unfolded protein response, alongside enrichment of the non-canonical "Receptor Ligand Activity" pathway across all cell lines. Cell line-specific variations were also observed, with HepG2 cells displaying more uniquely expressed genes and elevated expression levels (fold changes) of shared genes under stress conditions. Validation by qPCR confirmed the activation of key genes within the "Receptor Ligand Activity" pathway across time points. These findings provide insights into conserved and context-specific aspects of the HSR, contributing to a more comprehensive understanding of stress response mechanisms across mammalian cells.

摘要

细胞应激反应(CSR)是一种保守机制,可保护细胞免受环境和生理应激源的影响。热休克反应(HSR)是CSR的一个关键组成部分,它利用分子伴侣来减轻高温引起的蛋白质毒性应激。我们假设,虽然经典的HSR途径在不同细胞类型中是保守的,但特定的细胞系可能对热休克表现出独特的转录反应。为了验证这一点,我们比较了热休克后立即以及8小时恢复期后,HEK293、HepG2和HeLa细胞在对照条件下的转录组反应。RNA测序揭示了经典HSR途径的保守激活,包括未折叠蛋白反应,以及所有细胞系中非经典的“受体配体活性”途径的富集。还观察到细胞系特异性差异,HepG2细胞在应激条件下显示出更多独特表达的基因和共享基因的表达水平升高(倍数变化)。通过qPCR验证证实了“受体配体活性”途径中关键基因在各个时间点的激活。这些发现为HSR的保守和背景特异性方面提供了见解,有助于更全面地了解哺乳动物细胞的应激反应机制。

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