Tunicamycin induced endoplasmic reticulum changes in endothelial cells investigated <i>in vitro</i> by confocal Raman imaging

Bik, Ewelina; Mielniczek, Nikola; Jarosz, Magdalena; Denbigh, Joanna; Budzynska, Renata; Barańska, Małgorzata; Majzner, Katarzyna

doi:10.1039/c9an01456j

Cited by 13 publications

(8 citation statements)

References 49 publications

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“…Lipid profiling using 1 H nuclear magnetic resonance (NMR) showed that protein misfolding caused by acyclic retinoid significantly reduced unsaturated FA content in a human cancer cell line [120]. Imaging by scanning electron microscopy and Raman spectroscopy of individual, tunicamycin-treated endothelial cells showed a decrease in ER phospholipid content [121]. Furthermore, mass-spectrometry-based lipid analysis showed that a short cultivation of S. cerevisiae in DTT is sufficient to induce substantial lipidomic changes, including an increase in overall PA and a shift of PA lipids toward a higher average acyl chain length and a greater unsaturation [122].…”

Section: Crosstalk Between Proteotoxicity-and Lipotoxicity-induced Upr-ermentioning

confidence: 99%

Beyond Proteostasis: Lipid Metabolism as a New Player in ER Homeostasis

Taubert

2021

Metabolites

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Biological membranes are not only essential barriers that separate cellular and subcellular structures, but also perform other critical functions such as the initiation and propagation of intra- and intercellular signals. Each membrane-delineated organelle has a tightly regulated and custom-made membrane lipid composition that is critical for its normal function. The endoplasmic reticulum (ER) consists of a dynamic membrane network that is required for the synthesis and modification of proteins and lipids. The accumulation of unfolded proteins in the ER lumen activates an adaptive stress response known as the unfolded protein response (UPR-ER). Interestingly, recent findings show that lipid perturbation is also a direct activator of the UPR-ER, independent of protein misfolding. Here, we review proteostasis-independent UPR-ER activation in the genetically tractable model organism Caenorhabditis elegans. We review the current knowledge on the membrane lipid composition of the ER, its impact on organelle function and UPR-ER activation, and its potential role in human metabolic diseases. Further, we summarize the bi-directional interplay between lipid metabolism and the UPR-ER. We discuss recent progress identifying the different respective mechanisms by which disturbed proteostasis and lipid bilayer stress activate the UPR-ER. Finally, we consider how genetic and metabolic disturbances may disrupt ER homeostasis and activate the UPR and discuss how using -omics-type analyses will lead to more comprehensive insights into these processes.

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Section: Crosstalk Between Proteotoxicity-and Lipotoxicity-induced Upr-ermentioning

confidence: 99%

Beyond Proteostasis: Lipid Metabolism as a New Player in ER Homeostasis

Taubert

2021

Metabolites

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“…The intensities of the relevant Raman bands at 2840−2870, 1073, 1549, 1086, and 785 cm −1 were analyzed to determine the distribution positions of the components in the cells (Figure 3A). These bands were attributed to the CH 2 stretching of the lipid, the C−N stretching vibration of the lysosome (Lys), 35 the C−C stretching of the mitochondria (Mit), 35 and the PO 2 − stretching of the phospholipids, respecting the endoplasmic reticulum (ER) membrane, 36 and the O−P−O stretching of the DNA. 34 The center of the cells and the band at 1001 cm −1 of phenylalanine (yellow) were occupied by the cell nucleus (purple).…”

Section: ■ Results and Discussionmentioning

confidence: 99%

Phenotype Identification of HeLa Cells Knockout CDK6 Gene Based on Label-Free Raman Imaging

Hou

Zhu

et al. 2022

Anal. Chem.

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Identifying cell phenotypes is essential for understanding the function of biological macromolecules and molecular biology. We developed a noninvasive, label-free, single-cell Raman imaging analysis platform to distinguish between the cell phenotypes of the HeLa cell wild type (WT) and cyclin-dependent kinase 6 (CDK6) gene knockout (KO) type. Via large-scale Raman spectral and imaging analysis, two phenotypes of the HeLa cells were distinguished by their intrinsic biochemical profiles. A significant difference was found between the two cell lines: large lipid droplets formed in the knockout HeLa cells but were not observed in the WT cells, which was confirmed by Oil Red O staining. The band ratio of the Raman spectrum of saturated/unsaturated fatty acids was identified as the Raman spectral marker for HeLa cell WT or gene knockout type differentiation. The interaction between organelles involved in lipid metabolism was revealed by Raman imaging and Lorentz fitting, where the distribution intensity of the mitochondria and the endoplasmic reticulum membrane decreased. At the same time, lysosomes increased after the CDK6 gene knockout. The parameters obtained from Raman spectroscopy are based on hierarchical cluster analysis and one-way ANOVA, enabling highly accurate cell classification.

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“…The shift of vascular function to vasoconstriction, proinflammatory state, oxidative stress and NO deficiency may lead to endothelial dysfunction and injury. This shift is a key event in the pathophysiological process of cardiovascular diseases, including hypertension, diabetes, atherosclerosis, arterial hypertension and pulmonary hypertension ( 28 , 29 ). In the present study, HUVECs were treated with 1 µM AngII for 24 h to establish an AngII-induced endothelial cell model.…”

Section: Discussionmentioning

confidence: 99%

Bazedoxifene activates the angiotensin II‑induced HUVEC hypertension model by targeting SIRT1

Zhao

Liu

2021

Exp Ther Med

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The shift in vascular function to vasoconstriction, pro-inflammatory state, oxidative stress and carbon monoxide deficiency may to endothelial dysfunction and injury, which is the key event in hypertension. Estrogen receptor modulators play a protective role in blood vessels. The present study aimed to investigate the effect of bazedoxifene, a selective estrogen receptor modulator, on human umbilical vein endothelial cells (HUVECs) and its potential underlying mechanism of action. The present study treated endothelial cells with different concentrations of bazedoxifene and determined cell viability using Cell Counting Kit-8 to screen for the optimal working concentration of bazedoxifene. Subsequently, an angiotensin II (AngII)-induced vascular endothelial cell model was established to observe the effect of bazedoxifene on AngII-induced endothelial cells. The concentrations of nitric oxide (NO) and reactive oxygen species (ROS) were detected using NO and ROS kits, respectively. The protein expression of sirtuin 1 (SIRT1), oxidative stress-related proteins and apoptosis-related proteins was detected using western blotting, and apoptosis was detected using a TUNEL assay. The results demonstrated that bazedoxifene promoted AngII-induced HUVEC viability, reduced the expression of stress-related proteins and inhibited apoptosis. Furthermore, bazedoxifene activated SIRT1 to promote the proliferation and inhibit the oxidative stress and apoptosis of AngII-induced HUVECs. These findings suggested that bazedoxifene could effectively promote AngII-induced HUVEC proliferation and inhibit cell apoptosis and oxidative stress. In addition, bazedoxifene protected HUVEC dysfunction induced by AngII by targeting the activation of SIRT1. In summary, bazedoxifene could improve the protective role against hypertension induced by AngII.

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Tunicamycin induced endoplasmic reticulum changes in endothelial cells investigated in vitro by confocal Raman imaging

Abstract: This paper describes how tunicamycin (Tu), the most widely used pharmacological agent for inducing endoplasmic reticulum (ER) stress, interacts with endothelial cells.

Cited by 13 publications

References 49 publications

Beyond Proteostasis: Lipid Metabolism as a New Player in ER Homeostasis

Beyond Proteostasis: Lipid Metabolism as a New Player in ER Homeostasis

Phenotype Identification of HeLa Cells Knockout CDK6 Gene Based on Label-Free Raman Imaging

Bazedoxifene activates the angiotensin II‑induced HUVEC hypertension model by targeting SIRT1

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