Thioredoxin-interacting protein: a critical link between autophagy disorders and pancreatic β-cell dysfunction

Deng, Wenzhen; Li, Yang; Ren, Zhijian; He, Qirui; Jia, Yanjun; Liu, Yongjian; Zhang, Weiwei; Gan, Xianfeng; Liu, Dongfang

doi:10.1007/s12020-020-02471-6

Cited by 9 publications

(5 citation statements)

References 49 publications

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“…Work by Sun et al [ 4 ] reported that activation of autophagy alleviated H 2 O 2 -induced oxidative stress in bovine mammary epithelial cells. In non-ruminants, Rap, an activator of autophagy, can enhance autophagy through upregulation of LC3-II and downregulation of p62, and promotion of fusion between the autophagosomes and lysosomes [ 34 , 35 ]. In this study, the increased protein abundance of LC3-II and the decreased protein abundance of p62 confirmed the role of Rap on autophagy in mammary epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting nuclear factor erythroid 2 related factor 2-mediated autophagy in bovine mammary epithelial cells induces oxidative stress in response to exogenous fatty acids

Chang

Sun

Jia

et al. 2022

J Animal Sci Biotechnol

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Background In early lactation, bovine mammary epithelial cells undergo serious metabolic challenges and oxidative stress both of which could be alleviated by activation of autophagy. Nuclear factor erythroid 2 related factor 2 (NFE2L2), a master regulator of cellular redox homeostasis, plays an important role in the regulation of autophagy and oxidative stress. Thus, the objective of this study was to investigate the role of NFE2L2-mediated autophagy on oxidative stress of bovine mammary epithelial cells in response to exogenous free fatty acids (FFA). Results Exogenous FFA induced linear and quadratic decreases in activities of glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD), and increases in the contents of reactive oxygen species (ROS) and malondialdehyde (MDA). Protein abundance of LC3-phosphatidylethanolamine conjugate (LC3-II) and the number of autophagosomes and autolysosomes decreased in a dose-dependent manner, while protein abundance of p62 increased in cells challenged with FFA. Activation of autophagy via pre-treatment with Rap attenuated the FFA-induced ROS accumulation. Importantly, FFA inhibited protein abundance of NFE2L2 and the translocation of NFE2L2 into the nucleus. Knockdown of NFE2L2 by siRNA decreased protein abundance of LC3-II, while it increased protein abundance of p62. Furthermore, sulforaphane (SFN) pre-treatment attenuated the FFA-induced oxidative stress by activating NFE2L2-mediated autophagy. Conclusions The data suggested that NFE2L2-mediated autophagy is an important antioxidant mechanism in bovine mammary epithelial cells experiencing increased FFA loads.

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Section: Discussionmentioning

confidence: 99%

Inhibiting nuclear factor erythroid 2 related factor 2-mediated autophagy in bovine mammary epithelial cells induces oxidative stress in response to exogenous fatty acids

Chang

Sun

Jia

et al. 2022

J Animal Sci Biotechnol

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“…We attempt to elucidate the effect of HCG on autophagy in GCTB stromal cells. LC3 and P62 are widely used as autophagy marker proteins [ 25 ]. Immunofluorescence and immunoblotting showed that the expression levels of LC3 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Human Chorionic Gonadotropin Regulates the Smad Signaling Pathway by Antagonizing TGF-β in Giant Cell Tumor of Bone

et al. 2024

PRA

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Background: Giant cell tumor of bone (GCTB) is a locally aggressive bone tumour aggravated by stromal cell proliferation and metastasis. Objective: We investigated the mechanism of action of human chorionic gonadotropin (HCG) in mediating GCTB proliferation and invasion. Methods: The expression of HCG was quantified using quantitative real-time PCR. After the primary stromal cells were isolated and identified, the function of HCG in GCTB was estimated using the cell counting kit-8, flow cytometry, scratch experiment, transwell assay, Western blot, and immunofluorescence. Moreover, the mechanism of HCG was assessed through western blotting. Results: HCG expression was decreased in clinical tissue samples from patients with GCTB. We validated that HCG repressed stromal cell proliferation, migration, invasion, autophagy, and epithelial-mesenchymal transition (EMT) and promoted cell apoptosis in GCTB. We also verified that HCG repressed the autophagy and EMT of stromal cells through the Smad signaling axis in GCTB. HCG inhibited the transduction of the Smad signaling pathway by restraining the binding of the TGF-β II receptor to ligand Activin A. Conclusion: HCG restrained the Smad signaling pathway by antagonizing TGF-β signaling in GCTB. HCG may serve as a useful patent to treat GCTB.

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“…45,46 Besides, inhibition of TrxR activity can block autophagy by impairing lysosomal activity due to excessive oxidative stress. 47 Overexpression of Trx-interacting protein (TXNIP), an endogenous inhibitor of Trx, also contributes to impaired autophagic flux, 48 while silencing TXNIP alleviates CQ-induced autophagy inhibition, 49 indicating that Trx system inhibition mediated the autophagy inhibition.…”

Section: Cq@mos Induces Inhibition Of Autophagymentioning

confidence: 99%

Inhibition of thioredoxin reductase and upregulation of apoptosis genes for effective anti-tumor sono-chemotherapy using a meso-organosilica nanomedicine

Li,

Tian,

Wen

et al. 2024

Biomater. Sci.

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Thioredoxin-interacting protein: a critical link between autophagy disorders and pancreatic β-cell dysfunction

Cited by 9 publications

References 49 publications

Inhibiting nuclear factor erythroid 2 related factor 2-mediated autophagy in bovine mammary epithelial cells induces oxidative stress in response to exogenous fatty acids

Inhibiting nuclear factor erythroid 2 related factor 2-mediated autophagy in bovine mammary epithelial cells induces oxidative stress in response to exogenous fatty acids

Human Chorionic Gonadotropin Regulates the Smad Signaling Pathway by Antagonizing TGF-β in Giant Cell Tumor of Bone

Inhibition of thioredoxin reductase and upregulation of apoptosis genes for effective anti-tumor sono-chemotherapy using a meso-organosilica nanomedicine

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