Selenium deficiency caused hepatitis in chickens <i>via</i> the miR-138-5p/SelM/ROS/Ca<sup>2+</sup> overload pathway induced by hepatocyte necroptosis

Sun, Xinyue; Zhang, Wenyue; Shi, Xu; Wang, Yuqi; Zhang, Yilei; Liu, Xiaojing; Xu, Shiwen; Zhang, Jiuli

doi:10.1039/d3fo00683b

Cited by 1 publication

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“…Se deficiency destroys the body's REDOX homeostasis, and ROS accumulation promotes the occurrence of oxidative stress in mastitis [37]. Previous studies have confirmed that Se deficiency causes inflammatory damage through oxidative stress in chickens [38], mice [39], carps [40], and cattle [41]. The present study established the Se-deficient MAC-T cell model in vitro by continuous delivery culture using FBS with very low Se concentrations.…”

Section: Discussionmentioning

confidence: 59%

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

Chen,

Zhang,

Yang

et al. 2023

Antioxidants

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Selenium (Se) deficiency disrupts intracellular REDOX homeostasis and severely deteriorates immune and anti-inflammatory function in high-yielding periparturient dairy cattle. To investigate the damage of extracellular vesicles derived from Se-deficient MAC-T cells (SeD-EV) on normal mammary epithelial cells, an in vitro model of Se deficiency was established. Se-deficient MAC-T cells produced many ROS, promoting apoptosis and the release of inflammatory factors. Extracellular vesicles were successfully isolated by ultrahigh-speed centrifugation and identified by transmission electron microscopy, particle size analysis, and surface markers (CD63, CD81, HSP70, and TSG101). RNA sequencing was performed on exosomal RNA. A total of 9393 lncRNAs and 63,155 mRNAs transcripts were identified in the SeC and SeD groups, respectively, of which 126 lncRNAs and 955 mRNAs were differentially expressed. Furthermore, SeD-EV promoted apoptosis of normal MAC-T cells by TUNEL analysis. SeD-EV significantly inhibited Bcl-2, while Bax and Cleaved Caspase3 were greatly increased. Antioxidant capacity (CAT, T-AOC, SOD, and GSH-Px) was inhibited in SeD-EV-treated MAC-T cells. Additionally, p-PERK, p-eIF2α, ATF4, CHOP, and XBP1 were all elevated in MAC-T cells supplemented with SeD-EV. In addition, p-PI3K, p-Akt, and p-mTOR were decreased strikingly by SeD-EV. In conclusion, SeD-EV caused oxidative stress, thus triggering apoptosis and inflammation through endoplasmic reticulum stress and the PI3K-Akt-mTOR signaling pathway, which contributed to explaining the mechanism of Se deficiency causing mastitis.

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Section: Discussionmentioning

confidence: 59%

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

Chen,

Zhang,

Yang

et al. 2023

Antioxidants

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Selenium deficiency caused hepatitis in chickens via the miR-138-5p/SelM/ROS/Ca²⁺ overload pathway induced by hepatocyte necroptosis

Abstract: Selenium deficiency cause oxidative stress through upregulation of miR-138-5p targeting SelM, which disrupted Ca2+ and energy metabolic homeostasis allowing hepatocyte necroptosis leading to hepatitis in chickens.

Cited by 1 publication

References 63 publications

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

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Selenium deficiency caused hepatitis in chickens via the miR-138-5p/SelM/ROS/Ca2+ overload pathway induced by hepatocyte necroptosis

Abstract: Selenium deficiency cause oxidative stress through upregulation of miR-138-5p targeting SelM, which disrupted Ca2+ and energy metabolic homeostasis allowing hepatocyte necroptosis leading to hepatitis in chickens.

Cited by 1 publication

References 63 publications

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

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Selenium deficiency caused hepatitis in chickens via the miR-138-5p/SelM/ROS/Ca²⁺ overload pathway induced by hepatocyte necroptosis