Endoplasmic Reticulum Stress Is Associated with the Mesencephalic Dopaminergic Neuron Injury in Stressed Rats

Niu, Shiba; Shi, Wanying; Li, Yingmin; Yi, Shanyong; Yang, Li; Liu, Xia; Cong, Bin; He, Ge

doi:10.1155/2021/7852710

Cited by 2 publications

(2 citation statements)

References 36 publications

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“…Western blot assay was fulfilled as formerly depicted [ 11 ]. Total protein (50 μg of protein/lane) was put into SDS–PAGE gels, then incubated by electrophoresis and delivered to PVDF membranes.…”

Section: Methodsmentioning

confidence: 99%

miR-96-5p is involved in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73

Yang

Wang

et al. 2023

PLoS ONE

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Objective The present study opted for the adrenal phaeochromocytoma (PC12) cell line to frame a neuronal injury model induced by alcohol exposure in vitro, aiming to probe whether TAp73 and miR-96-5p are involved in the neuronal injury process induced by alcohol and elucidate the regulatory relationship between miR-96-5p and TAp73. Methods Immunofluorescence staining was used to observe the structural features of PC12 cells after culturing in medium with nerve growth factor (NGF). After different doses and different durations of alcohol treatment, CCK-8 assay was performed to detect the viability of PC12 cells, flow cytometry assay was carried out to detect the apoptosis rate of PC12 cells, dual-luciferase reporter assay was used to definitude the regulatory relationship between miR-96-5p and Tp73, and western blot was used to detect the protein expression of TAp73. Results The result of immunofluorescence staining demonstrated that PC12 cells abundantly expressed Map2, CCK-8 assay illustrated alcohol exposure significantly downregulated the cell viability of PC12 cells, Treatment with miR-96-5p inhibitor induced apoptosis and upregulated the expression of TAp73 in PC12 cells. Contrastingly, miR-96-5p mimic reversed the above effects and downregulation of TAp73 inhibited the apoptosis of PC12 cells. Conclusion The present study demonstrated that miR-96-5p participates in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73.

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Section: Methodsmentioning

confidence: 99%

miR-96-5p is involved in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73

Yang

Wang

et al. 2023

PLoS ONE

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“…When the stressor is too intense and persistent, although the various responses of the organism still have some adaptive defensive significance [2], the main mechanisms of stress are those that lead to an increase in homeostatic load, hypoglycemia, ischemia, and hypoxia, imbalance of Ca 2+ levels in the body or disturbance of regulatory factors and hormone levels. These deregulate the redox balance of the endoplasmic reticulum (ER), leading to the accumulation of unfolded or misfolded proteins in the ER, triggering ER stress, and activating the body's unfolded protein reaction (UPR) [3][4][5]. UPR can transmit unfolded protein signals through the ER membrane by activating three ER transmembrane proteins in vivo: the type I transmembrane protein kinase R-like ER kinase (PERK), Analytical Cellular Pathology inositol requiring enzyme 1 (IRE1), and active transcription factor 6 (ATF6), which mediate distinct signaling pathways at the transcriptional and translational levels [5,6].…”

Section: Introductionmentioning

confidence: 99%

Bioinformatics Analysis of Molecular Interactions between Endoplasmic Reticulum Stress and Ferroptosis under Stress Exposure

Zhu

et al. 2023

Analytical Cellular Pathology

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Stress has become a universal biological phenomenon in the body, which leads to pathophysiological changes. However, the molecular network interactions between endoplasmic reticulum (ER) stress and ferroptosis under stressful conditions are not clear. For this purpose, we screened the gene expression profile of GSE173795 for intersection with ferroptosis genes and screened 68 differentially expressed genes (DEGs) (63 up-regulated, 5 down-regulated), mainly related to lipid and atherosclerosis, autophagy—animal, mitophagy—animal, focal adhesion, DNA replication, proteasome, oocyte meiosis, toll-like receptor signaling pathway, cell cycle, etc. Immune infiltration analysis revealed that stress resulted in decreased B cells memory, T cells CD8 and T cells CD4 memory resting, monocytes, macrophages M2, and increased B cells naive, T cells follicular helper, and macrophages M1. 19 core-DEGs (ASNS, TRIB3, ATF4, EIF2S1, CEBPG, RELA, HSPA5, DDIT3, STAT3, MAP3K5, HIF1A, HNF4A, MAPK14, HMOX1, CDKN1A, KRAS, SP1, SIRT1, EGFR) were screened, all of which were up-regulated DEGs. These biological processes and pathways were mainly involved in responding to ER stress, lipid and atherosclerosis, cellular response to stress, cellular response to chemical stress, and regulation of DNA-templated transcription in response to stress, etc. Spearman analysis did not find MAPK14 to be significantly associated with immune cells. Other core-DEGs were associated with immune cells, including B cells naive, T cells follicular helper, and monocytes. Based on core-DEGs, 283 miRNAs were predicted. Among the 22 miRNAs with highly cross-linked DEGs, 11 had upstream lncRNA, mainly targeting STAT3, SP1, CDKN1A, and SIRT1, and a total of 39 lncRNA were obtained. 85 potential drugs targeting 11 core-DEGs were identified and were expected to be potential immunotherapeutic agents for stress injury. Our experiments also confirmed that Liproxstatin-1 alleviates common cross-linked proteins between ER stress and ferroptosis. In conclusion, our study explored the molecular mechanisms and network interactions among stress—ER stress—ferroptosis from a novel perspective, which provides new research ideas for studying stressful injury.

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Endoplasmic Reticulum Stress Is Associated with the Mesencephalic Dopaminergic Neuron Injury in Stressed Rats

Cited by 2 publications

References 36 publications

miR-96-5p is involved in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73

miR-96-5p is involved in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73

Bioinformatics Analysis of Molecular Interactions between Endoplasmic Reticulum Stress and Ferroptosis under Stress Exposure

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