Silkworm Hemolymph Down-Regulates the Expression of Endoplasmic Reticulum Chaperones under Radiation-Irradiation

Lee, Kyeong Ryong; Kim, Seung Whan; Kim, Young Kook; Kwon, Kisang; Choi, Jong-Soon; Yu, Kweon; Kwon, O‐Yu

doi:10.3390/ijms12074456

Cited by 3 publications

(3 citation statements)

References 25 publications

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“…The reason for this may be contention of the transcriptional factors biding to the ubiquitous enhancer occurring at the beginning of ER stress for ERp29. These results have been shown in other ERp29 experiments (7,17). Under the same experimental conditions, naloxone dose dependently increased the gene expression of ER stress sensors (ATF6, IRE1 and PERK).…”

Section: A B Csupporting

confidence: 84%

Naloxone induces endoplasmic reticulum stress in PC12 cells

Seo

Kwon

et al. 2014

Molecular Medicine Reports

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Naloxone is an opioid inverse agonist used in the treatment of opiate overdose, with well known pharmacology. In the present study, we determined the effects of naloxone on the unfolded protein response (UPR) in PC12 cells. Data from a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay indicated that naloxone may accelerate PC12 cell apoptosis in a dose-dependent manner. We also demonstrated that naloxone upregulated gene expression of endoplasmic reticulum (ER) chaperones, including binding immunoglobulin protein (Bip), calnexin, ER protein 29 (ERp29) and protein disulfide isomerase (PDI), and ER stress sensors, including activating transcription factor 6 (ATF6), inositol-requiring enzyme 1 (IRE1) and protein kinase-like ER kinase (PERK). In addition, naloxone also induced typical ER stress phenomena, including ART6 proteolytic cleavage, eIF2α phosphorylation and XBP1 mRNA splicing. Furthermore, naloxone upregulated gene expression of ER chaperones and ER stress sensors in in vivo experiments. To the best of our knowledge, these results are the first to indicate that naloxone induces ER stress in vitro and in vivo.

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Section: A B Csupporting

confidence: 84%

Naloxone induces endoplasmic reticulum stress in PC12 cells

Seo

Kwon

et al. 2014

Molecular Medicine Reports

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“…Orthologs of malectins have been identified in D. melanogaster and A. aegypti, but have not been studied yet [27,28]. Calnexin/calreticulin chaperones have been identified in B. mori [29,30] and D. melanogaster [31,32]. In Drosophila, calnexin was reported to be related to neuron functions and sodium channel regulation [31,32].…”

Section: Insect Lectinsmentioning

confidence: 99%

Can Plant Lectins Help to Elucidate Insect Lectin-Mediated Immune Response?

Chen

Schutter

Damme

et al. 2021

Insects

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Lectins are carbohydrate-binding proteins that recognize and selectively bind to specific sugar structures. This group of proteins is widespread in plants, animals, and microorganisms, and exerts a broad range of functions. Many plant lectins were identified as exogenous stimuli of vertebrate immunity. Despite being the largest and most diverse taxon on earth, the study of lectins and their functions in insects is lagging behind. In insects, research on lectins and their biological importance has mainly focused on the C-type lectin (CTL) family, limiting our global understanding of the function of insect lectins and their role in insect immunity. In contrast, plant lectins have been well characterized and the immunomodulatory effects of several plant lectins have been documented extensively in vertebrates. This information could complement the missing knowledge on endogenous insect lectins and contribute to understanding of the processes and mechanisms by which lectins participate in insect immunity. This review summarizes existing studies of immune responses stimulated by endogenous or exogenous lectins. Understanding how lectins modulate insect immune responses can provide insight which, in turn, can help to elaborate novel ideas applicable for the protection of beneficial insects and the development of novel pest control strategies.

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“…IR has been shown to induce ER stress in rat intestinal epithelial cells, IEC-6, and neuronal PC12 cells (32,33) at a dose of 10 Gy, indicating that ER may be a cytoplasmic target of IR. However, in the current study, FTC-133 cells treated with 1, 2, and 4 Gy of radiation was not found to result in an increase in the mRNA expression of GRP78 and EDEM or XBP1 mRNA splicing.…”

mentioning

confidence: 99%

Endoplasmic reticulum stress protects human thyroid carcinoma cell lines against ionizing radiation-induced apoptosis

Fan

Cui

et al. 2014

Molecular Medicine Reports

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Abstract. Radiotherapy is one of the most effective forms of cancer treatment, used in the treatment of a number of malignant tumors. However, the resistance of tumor cells to ionizing radiation remains a major therapeutic problem and the critical mechanisms determining radiation resistance are poorly defined. In the present study, a cellular endoplasmic reticulum (ER) stress microenvironment was established through the pretreatment of cultured thyroid cancer cells with tunicamycin (TM) and thapsigargin (TG), in order to mimic the ER stress response in a tumor microenvironment. This microenviroment was confirmed through the X-box binding protein 1 splice process, glucose-regulated protein 78 kD and ER degradation-enhancing α-mannosidase-like mRNA expression. A clonogenic assay was used to measure cancer cell resistance to 60 Co-γ following TM pretreatment; in addition, human C/EBP homologous protein (CHOP) mRNA expression was determined and apoptosis assays were performed. The results showed that TM or TG pretreatment inhibited CHOP expression and reduced the apoptotic rate of cells. Furthermore, the results demonstrated that the induced ER stress response rendered cancer cells more resistant to ionizing radiation-induced apoptosis. Therefore, the ER stress pathway may be a potential therapeutic target in order to improve the clinical efficiency of radiotherapy.

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Silkworm Hemolymph Down-Regulates the Expression of Endoplasmic Reticulum Chaperones under Radiation-Irradiation

Cited by 3 publications

References 25 publications

Naloxone induces endoplasmic reticulum stress in PC12 cells

Naloxone induces endoplasmic reticulum stress in PC12 cells

Can Plant Lectins Help to Elucidate Insect Lectin-Mediated Immune Response?

Endoplasmic reticulum stress protects human thyroid carcinoma cell lines against ionizing radiation-induced apoptosis

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