Regulation of Stress Granule Formation by Inflammation, Vascular Injury, and Atherosclerosis

Herman, Allison N.; Afonso, Milessa da Silva; Kelemen, Sheri E.; Ray, Mitali; Vrakas, Christine; Burke, Amy C.; Scalia, Rosario; Moore, Kathryn J.; Autieri, Michael V.

doi:10.1161/atvbaha.119.313034

Cited by 46 publications

(33 citation statements)

References 54 publications

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“…Overexpression of nucleating proteins ( e.g ., G3BP1, TIA1, TIA-1-related, TIAR) is sufficient to trigger SGs formation in absence of stress[ 19 ]. Moreover, the stressful conditions present within the tumor microenvironment ( e.g ., hypoxia, oxidative stress, nutrient deprivation, chronic inflammation)[ 20 ], as well as specific molecules present (prostaglandin J2 and A1), promote SGs assembly in cancer cells[ 19 ]. Other factors including oxidized-low density lipoprotein or high-fat diet are also contributing factors to SGs formation[ 21 ].…”

Section: Complexity Of Stress Granules Formation and Car-cinogenesismentioning

confidence: 99%

Stress granules in colorectal cancer: Current knowledge and potential therapeutic applications

Legrand¹,

Dixon²,

Sobolewski³

2020

WJG

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Stress granules (SGs) represent important non-membrane cytoplasmic compartments, involved in cellular adaptation to various stressful conditions ( e.g ., hypoxia, nutrient deprivation, oxidative stress). These granules contain several scaffold proteins and RNA-binding proteins, which bind to mRNAs and keep them translationally silent while protecting them from harmful conditions. Although the role of SGs in cancer development is still poorly known and vary between cancer types, increasing evidence indicate that the expression and/or the activity of several key SGs components are deregulated in colorectal tumors but also in pre-neoplastic conditions ( e.g ., inflammatory bowel disease), thus suggesting a potential role in the onset of colorectal cancer (CRC). It is therefore believed that SGs formation importantly contributes to various steps of colorectal tumorigenesis but also in chemoresistance. As CRC is the third most frequent cancer and one of the leading causes of cancer mortality worldwide, development of new therapeutic targets is needed to offset the development of chemoresistance and formation of metastasis. Abolishing SGs assembly may therefore represent an appealing therapeutic strategy to re-sensitize colon cancer cells to anti-cancer chemotherapies. In this review, we summarize the current knowledge on SGs in colorectal cancer and the potential therapeutic strategies that could be employed to target them.

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Section: Complexity Of Stress Granules Formation and Car-cinogenesismentioning

confidence: 99%

Stress granules in colorectal cancer: Current knowledge and potential therapeutic applications

Legrand¹,

Dixon²,

Sobolewski³

2020

WJG

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“…Atherosclerosis is touted as a leading cause of cardiovascular diseases, leading to a high rate of mortality [ 1 , 2 ]. Epidemiological studies and clinical examinations showed that obesity and metabolic disorders predispose individuals to atherosclerotic changes.…”

Section: Introductionmentioning

confidence: 99%

Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

et al. 2021

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Background Atherosclerosis is touted as one of the most critical consequences of diabetes mellitus indicated by local inflammation of endothelial cells. The Effect of Omega 3 fatty acids, mainly docosahexaenoic acid (DHA), has been investigated in cells after exposure to high doses of lipids. The current experiment aimed to address the modulatory effects of docosahexaenoic acid and insulin in palmitic-treated human endothelial cells. Methods Human umbilical vein endothelial cells were treated with 1 mM palmitic acid, 50 μM insulin, 50 μM docosahexaenoic acid, and their combination for 48 h. Cell survival rate and apoptosis were measured using MTT and flow cytometry assays. The Griess assay detected NO levels. Protein levels of TNF-α, IL-6, and NF-κB were studied using ELISA and immunofluorescence imaging. The expression of genes participating in atherosclerosis was monitored using PCR array analysis. Results Oil Red O staining showed the inhibitory effect of DHA and insulin to reduce the intracellular accumulation of palmitic acid. Both DHA and Insulin blunted palmitic acid detrimental effects on HUVECs indicated by an increased survival rate (p < 0.05). The percent of apoptotic cells was decreased in palmitic-treated cells received insulin and DHA compared to palmitic-treated group (p < 0.05). Based on our data, DHA and Insulin diminished the production of all inflammatory cytokines, TNF-α, IL-6, and NF-κB, in palmitic-treated cells (p < 0.05). Similar to these data, NO production was also decreased in all groups treated with insulin and DHA compared to the palmitic-treated cells (p < 0.05). PCR array analysis revealed the modulatory effect of DHA and insulin on the expression of atherosclerosis-related genes pre-treated with palmitic acid compared to the control group (p < 0.05). Conclusion DHA and Insulin could alter the dynamic growth and dysfunctional activity of human endothelial cells after treatment with palmitic acid. Taken together, Omega 3 fatty acids, along with insulin, could dictate specific cell behavior in endothelial cells in vitro.

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“…Vascular disease, such as atherosclerosis, is touted as one of the leading causes of death globally [1].…”

Section: Introductionmentioning

confidence: 99%

Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

Abriz

Rahbarghazi‬

Nourazarian

et al. 2020

Preprint

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Background: Atherosclerosis is touted as one of the most critical consequences of diabetes mellitus indicated by local inflammation of endothelial cells. The Effect of Omega 3 fatty acids, mainly docosahexaenoic acid (DHA), has been investigated in cells after exposure to high doses of lipids. The current experiment aimed to address the modulatory effects of docosahexaenoic acid and insulin in palmitic-treated human endothelial cells. Methods: Human umbilical vein endothelial cells were treated with 1mM palmitic acid, 50μM insulin, 50μM docosahexaenoic acid, and their combination for 48 hours. Cell survival rate and apoptosis were measured using MTT and flow cytometry assays. The Griess assay detected NO levels. Protein levels of TNF-α, IL-6, and NF-κB were studied using ELISA and immunofluorescence imaging. The expression of genes participating in atherosclerosis was monitored using PCR array analysis. Results: Oil Red O staining showed the inhibitory effect of DHA and insulin to reduce the intracellular accumulation of palmitic acid. Both DHA and Insulin increased the reduced cell survival rate of cells after exposure to palmitic acid (p<0.05). The percent of apoptotic cells was decreased in palmitic-treated cells received insulin and DHA compared to palmitic-treated group (p<0.05). Based on our data, DHA and Insulin diminished the production of all inflammatory cytokines, TNF-α, IL-6, and NF-κB, in palmitic-treated cells (p<0.05). Similar to these data, NO production was also decreased in all groups treated with insulin and DHA compared to the palmitic-treated cells (p<0.05). PCR array analysis revealed the modulatory Effect of DHA and insulin on the expression of atherosclerosis-related genes pre-treated with palmitic acid compared to the control group (p<0.05). Conclusion: DHA and Insulin could alter the dynamic growth and dysfunctional activity of human endothelial cells after treatment with palmitic acid. Taken together, Omega 3 fatty acids, along with insulin, could dictate specific cell behavior in endothelial cells in vitro.

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Regulation of Stress Granule Formation by Inflammation, Vascular Injury, and Atherosclerosis

Cited by 46 publications

References 54 publications

Stress granules in colorectal cancer: Current knowledge and potential therapeutic applications

Stress granules in colorectal cancer: Current knowledge and potential therapeutic applications

Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

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