Selenium deficiency causes apoptosis through endoplasmic reticulum stress in swine small intestine

Zheng, Yingying; Zhang, Bo; Guan, Haoyue; Xing, Jinchun; Yang, Jie; Cai, Jingzeng; Liu, Qi

doi:10.1002/biof.1762

Cited by 19 publications

(6 citation statements)

References 57 publications

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“…33 The Se deficiency reduces the synthesis of intracellular glutathione (GSH) in mammalian cells, 34 further triggering the mitochondrial dysfunctions. The mitochondrial dysfunctions caused by the Se deficiency subsequently cause the abnormal accumulation of ROS and elevated oxidative stress, resulting in complex diseases including renal dysfunction, 35 heart failure, 36 intestinal damage 37 and thyroid disorders. 38 Moreover, maternal Se deficiencies alter the fetal development and predispose the adult offspring to thyroid dysfunction and fetal growth restriction via the alterations of mitochondrial protein expression.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effect of Selenium Doped Carbon Quantum Dots Supplementation on the in vitro Development Competence of Ovine Oocytes

Wang¹,

Ren²,

Liu³

et al. 2022

IJN

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Background: After the synthesis of selenium doped carbon quantum dots (Se/CDs) via a step-by-step hydrothermal synthesis method with diphenyl diselenide (DPDSe) as precursor, the beneficial effects of Se/CDs' supplementation on the in vitro development competence of ovine oocytes were firstly investigated in this study by the assay of maturation rate, cortical granules' (CGs) dynamics, mitochondrial activity, reactive oxygen species (ROS) production, epigenetic modification, transcript profile, and embryonic development competence. Results:The results showed that the Se/CDs' supplementation during the in vitro maturation (IVM) process not only enhanced the maturation rate, CGs' dynamics, mitochondrial activity and embryonic developmental competence of ovine oocytes, but remarkably decreased the ROS production level of ovine oocytes. In addition, the expression levels of H3K9me3 and H3K27me3 in the ovine oocytes were significantly up-regulated after the Se/CDs' supplementation, in consistent with the expression levels of 5mC and 5hmC. Moreover, 2994 up-regulated differentially expressed genes (DEGs) and 846 repressed DEGs were found in the oocytes after the Se/ CDs' supplementation. According to the analyses of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), these DEGs induced by the Se/CDs' supplementation were positively related to the progesterone mediated oocyte maturation and mitochondrial functions. And these remarkably up-regulated expression levels of DEGs related to oocyte maturation, mitochondrial function, and epigenetic modification induced by the Se/CDs' supplementation further confirmed the beneficial effect of Se/CDs' supplementation on the in vitro development competence of ovine oocytes. Conclusion:The Se/CDs prepared in our study significantly promoted the in vitro development competence of ovine oocytes, benefiting the extended research about the potential applications of Se/CDs in mammalian breeding technologies.

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Section: Discussionmentioning

confidence: 99%

Beneficial Effect of Selenium Doped Carbon Quantum Dots Supplementation on the in vitro Development Competence of Ovine Oocytes

Wang¹,

Ren²,

Liu³

et al. 2022

IJN

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“…Pterostilbene restores the intestinal barrier function by inhibiting ER stress in piglets [ 64 ]. It was reported that selenium deficiency leads to apoptosis by inducing ER stress in the swine small intestine and IPEC-J2 cells, indicating that selenium has a protective effect on porcine intestinal health through modulating ER stress [ 65 ]. A previous study showed that ER stress and oxidative stress showed a high correlation, and the lack of selenium triggers ER stress and oxidative stress, and apoptosis in chicken hepatocytes [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells

Pan

Huang

et al. 2023

IJMS

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Bisphenol A (BPA) is widely used to harden plastics and polycarbonates and causes serious toxic effects in multiple organs, including the intestines. Selenium, as an essential nutrient element for humans and animals, exhibits a predominant effect in various physiological processes. Selenium nanoparticles have attracted more and more attention due to their outstanding biological activity and biosafety. We prepared chitosan-coated selenium nanoparticles (SeNPs) and further compared the protective effects, and investigated the underlying mechanism of SeNPs and inorganic selenium (Na2SeO3) on BPA-induced toxicity in porcine intestinal epithelial cells (IPEC-J2). The particle size, zeta potential, and microstructure of SeNPs were detected by using a nano-selenium particle size meter and a transmission electron microscope. IPEC-J2 cells were exposed to BPA alone or simultaneously exposed to BPA and SeNPs or Na2SeO3. The CCK8 assay was performed to screen the optimal concentration of BPA exposure and the optimal concentration of SeNPs and Na2SeO3 treatment. The apoptosis rate was detected by flow cytometry. Real-time PCR and Western blot methods were used to analyze the mRNA and protein expression of factors related to tight junctions, apoptosis, inflammatory responses and endoplasmic reticulum stress. Increased death and morphological damage were observed after BPA exposure, and these increases were attenuated by SeNPs and Na2SeO3 treatment. BPA exposure disturbed the tight junction function involved with decreased expression of tight junction protein Zonula occludens 1 (ZO-1), occludin, and claudin-1 proteins. Proinflammatory response mediated by the transcription factor nuclear factor-k-gene binding (NF-κB), such as elevated levels of interleukin-1β(IL-1β), interleukin-6 (IL-6), interferon-γ (IFN-γ), interleukin-17 (IL-17), and tumor necrosis factor-α (TNF-α) expression was induced at 6 and 24 h after BPA exposure. BPA exposure also disturbed the oxidant/antioxidant status and led to oxidative stress. IPEC-J2 cell apoptosis was induced by BPA exposure, as indicated by increased BCL-2-associated X protein (Bax), caspase 3, caspase 8, and caspase 9 expression and decreased B-cell lymphoma-2 (Bcl-2) and Bcl-xl expression. BPA exposure activated the endoplasmic reticulum stress (ERS) mediated by the receptor protein kinase receptor-like endoplasmic reticulum kinase (PERK), Inositol requiring enzyme 1 (IRE1α), and activating transcription factor 6 (ATF6). We found that treatment with SeNPs and Na2SeO3 can alleviate the intestinal damage caused by BPA. SeNPs were superior to Na2SeO3 and counteracted BPA-induced tight junction function injury, proinflammatory response, oxidative stress, apoptosis, and ERS stress. Our findings suggest that SeNPs protect intestinal epithelial cells from BPA-induced damage, partly through inhibiting ER stress activation and subsequently attenuating proinflammatory responses and oxidative stress and suppressing apoptosis, thus enhancing the intestinal epithelial barrier function. Our data indicate that selenium nanoparticles may represent an effective and reliable tool for preventing BPA toxicity in animals and humans.

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“…It can also cause damage to the reproductive system function of male rats through mitochondrial mediated spermatogenic cell apoptosis (P. Wang, Luo, et al, 2014). Se deficiency has been shown to cause damage to a wide range of tissues and cells, including breast (Gao et al, 2016), liver (Tang et al, 2020), and intestinal epithelial cells (Zheng et al, 2021). The researchers found that BPA exposure and Se deficiency may lead to oxidative stress and eventually lead to apoptosis (H. Chen et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A aggravate selenium deficiency‐induced apoptosis via miR‐215‐3p/Dio1 to activate ROS/PI3K/AKT pathway in chicken arterial

Fan

et al. 2023

Journal Cellular Physiology

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Both bisphenol A (BPA) and selenium (Se) deficiency can affect the expression of microRNAs (miRNAs), which can specifically regulate its target mRNA and induce apoptosis, and play a significant role in cardiovascular injury diseases. To explore the mechanism of apoptosis induced by BPA and Se deficiency in chicken arterial endothelial tissue and the role of miRNAs in this process, the model of BPA exposure/Se deficiency in chicken and PAEC cells have been employed. The targeting relationship between miR‐215‐3p and iodothyronine deiodinase 1 (Dio1) in PAEC was verified by double luciferase gene report. The level of miR‐215‐3p was detected by qRT‐PCR. The oxidative stress level of arterial endothelial cells was detected by oxidative stress kit and DCFH‐DA probe method. The PI3K/AKT pathway, mitochondrial dynamics, and apoptosis‐related genes were detected by qRT‐PCR and western blot. The mitochondrial ATP level and nitric oxide synthases (NOSs) level were detected with the kit. TUNEL, acridine orange/ethidium bromide, and flow cytometry were used to detect the level of apoptosis. The results showed that BPA exposure and Se deficiency led to overexpression of miR‐215‐3p, aggravated oxidative stress, inhibited activation of PI3K/AKT pathway, promoted mitochondrial division, increased expression of apoptosis related genes, and finally led to apoptosis of chicken arterial endothelial cells. We also established knockdown/overexpression models of miR‐215‐3p and Dio1 in vitro, and found that overexpression of miR‐215‐3p and knockout of Dio1 can induce apoptosis. Interestingly, miR‐215‐3p‐Inhibitor and N‐acetyl‐ l‐cysteine (NAC) partially prevented apoptosis caused by BPA exposure and Se deficiency, and LY294002 aggravated apoptosis. These results suggest that BPA exposure aggravates the apoptosis of Se deficient arterial endothelial cells in chickens by regulating the ROS/PI3K/AKT pathway activated by miR‐215‐3p/Dio1. The miR‐215‐3p/Dio1 axis provides a new way to understand the toxic mechanism of BPA exposure and Se deficiency, and reveals a new regulatory model of apoptosis damage in vascular diseases.

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Selenium deficiency causes apoptosis through endoplasmic reticulum stress in swine small intestine

Cited by 19 publications

References 57 publications

Beneficial Effect of Selenium Doped Carbon Quantum Dots Supplementation on the in vitro Development Competence of Ovine Oocytes

Beneficial Effect of Selenium Doped Carbon Quantum Dots Supplementation on the in vitro Development Competence of Ovine Oocytes

Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells

Bisphenol A aggravate selenium deficiency‐induced apoptosis via miR‐215‐3p/Dio1 to activate ROS/PI3K/AKT pathway in chicken arterial

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