Solano Luis, Keshet Uri, Reinschmidt Andrew, Chavez Yonny, Hulsy William Drew, Fiehn Oliver, Nikolaidis Nikolas
Department of Biological Science, Center for Applied Biotechnology Studies, and Center for Computational and Applied Mathematics, California State University Fullerton, Fullerton, CA, USA.
West Coast Metabolomics Center, University of California Davis, Davis, CA 95616, USA.
bioRxiv. 2025 Feb 23:2025.02.18.638884. doi: 10.1101/2025.02.18.638884.
The heat shock response (HSR) is a conserved cellular mechanism critical for adaptation to environmental and physiological stressors, with broad implications for cell survival, immune responses, and cancer biology. While the HSR has been extensively studied at the proteomic and transcriptomic levels, the role of lipid metabolism and membrane reorganization remains underexplored. Here, we integrate mass spectrometry-based lipidomics with RNA sequencing to characterize global lipidomic and transcriptomic changes in HeLa cells exposed to three conditions: control, heat shock (HS), and HS with eight hours of recovery. Heat shock-induced extensive lipid remodeling, including significant increases in fatty acids, glycerophospholipids, and sphingolipids, with partial normalization during recovery. Transcriptomic analysis identified over 2,700 upregulated and 2,300 downregulated genes under heat shock, with GO enrichment suggesting potential transcriptional contributions to lipid metabolism. However, transcriptional changes alone did not fully explain the observed lipidomic shifts, suggesting additional layers of regulation. Joint pathway analysis revealed enrichment in glycerophospholipid and sphingolipid metabolism, while network analysis identified lipid transport regulators (STAB2, APOB), stress-linked metabolic nodes (KNG1), and persistent sphingolipid enrichment during recovery. These findings provide a comprehensive framework for understanding lipid-mediated mechanisms of the HSR and highlight the importance of multi-omics integration in stress adaptation and disease biology.
热休克反应(HSR)是一种保守的细胞机制,对适应环境和生理应激源至关重要,对细胞存活、免疫反应和癌症生物学具有广泛影响。虽然已经在蛋白质组学和转录组学水平上对HSR进行了广泛研究,但脂质代谢和膜重组的作用仍未得到充分探索。在这里,我们将基于质谱的脂质组学与RNA测序相结合,以表征HeLa细胞在三种条件下的全局脂质组学和转录组学变化:对照、热休克(HS)以及热休克后恢复8小时。热休克诱导了广泛的脂质重塑,包括脂肪酸、甘油磷脂和鞘脂显著增加,恢复过程中部分恢复正常。转录组分析确定在热休克下有超过2700个基因上调和2300个基因下调,基因本体富集表明对脂质代谢有潜在的转录贡献。然而,仅转录变化并不能完全解释观察到的脂质组变化,这表明存在额外的调控层面。联合通路分析显示甘油磷脂和鞘脂代谢富集,而网络分析确定了脂质转运调节因子(STAB2、APOB)、应激相关代谢节点(KNG1)以及恢复过程中持续的鞘脂富集。这些发现为理解HSR的脂质介导机制提供了一个全面的框架,并突出了多组学整合在应激适应和疾病生物学中的重要性。