The Function of Thioredoxin‐Binding Protein‐2 (TBP‐2) in Different Diseases

Hu, Jianghua; Yu, Yibo

doi:10.1155/2018/4582130

Cited by 37 publications

(34 citation statements)

References 74 publications

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“…In the present study, we used the autophagic inhibitor ba lomycin A1 to block the its last stage which is the fusion of autophagosomes and lysosomes and autophagic inhibitor wortmannin to inhibit autophagy at the initiation stage. Our data indicated that Trx-1 mainly regulates autophagy in the initiation stage and facilitates autophagic induction, which consistent with our previous nding on the autophagic ux induction by TBP-2 in the initiation stage [18].…”

Section: Discussionsupporting

confidence: 93%

“…Our previous study showed oxidative stress induced autophagic response of LECs with increased LC3-II, p62, and GFP/mCherry-LC3 puncta. Overexpression of TBP-2 further strengthens autophagic response in the initiation stage, which is mTOR-independent and probably caused by the dephosphorylation of Akt under oxidative stress [18]. In the present study, we used the autophagic inhibitor ba lomycin A1 to block the its last stage which is the fusion of autophagosomes and lysosomes and autophagic inhibitor wortmannin to inhibit autophagy at the initiation stage.…”

Section: Discussionmentioning

confidence: 96%

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The role of Trx/TBP-2 in oxidative stress induced autophagy in human lens epithelial cells

Hu¹,

Shen²,

Zhang³

et al. 2019

Preprint

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Background: Oxidative stress plays an important role in age-related cataract development. The cellular antioxidant protein thioredoxin (Trx) and its negative regulator, thioredoxin binding protein-2 (TBP-2), maintain the intracellular redox balance upon oxidative stress. The aim of this study is to investigate role of Trx and TBP-2 in human lens epithelial cells (LECs) under oxidative stress.Methods: LECs were treated with 50 μM of H2O2 serum-free medium for different duration, and the mRNA and protein levels of Trx-1, Trx-2 and TBP-2 were measured by reverse transcriptionpolymerase chain reaction and Western blot. Trx-1 activity was evaluated by Thioredoxin Activity Fluorescent Assay. The subcellular localization of Trx-1, Trx-2 and TBP-2 was evaluated by cellular immunofluorescence. The cell viability was detected by Cell Counting Kit-8 (CCK-8) and the LC3-II protein level was detected to evaluate the autophagy level. The interaction between Trx-2 and TBP-2 was examined by Co-Immunoprecipitation (Co-IP). Results: The results showed that the mRNA levels of the Trx-1, Trx-2 and TBP-2 were kinetically changed after treatment with 50 μM of H2O2 for different duration. Exposure to H2O2 increased the expression of Trx-2 and TBP-2 but not Trx-1, while the exposure inhibited Trx-1 activity. TBP-2 was co-localized with Trx-1 and Trx-2, exposure to H2O2 enriched co-localization of TBP-2 to Trx-1 but not Trx-2, and increased the interaction between TBP-2 and Trx-1. Under normal circumstances, Trx-1 over-expression enhanced autophagic response and mainly regulates autophagy in the initiation. Conclusions: This study demonstrates differential roles of Trx-1 and Trx-2 in cellular response to oxidative stress, and oxidative stress increased Trx-1 interacting to TBP-2 and Trx-1 regulating autophagic response. BackgroundBlindness because of cataracts afflicts millions of people worldwide, and continues to be the major cause of blindness globally [1]. Generally, cataracts can be classified as age-related cataracts, paediatric cataracts, and cataracts secondary to other causes. Age-related cataract is the most common type in adults, with the onset between age 45 years and 50 years, and is a multifactorial disease caused by interactions between genes (e.g., genetic polymorphisms susceptibility to agerelated cataract) and environmental factors including aging, gender, ultraviolet rays, ionizing

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 96%

The role of Trx/TBP-2 in oxidative stress induced autophagy in human lens epithelial cells

Hu¹,

Shen²,

Zhang³

et al. 2019

Preprint

Self Cite

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“…Indeed, VDUP1 has been originally identified in HL-60 cells as one of the proteins, the gene of which is strongly induced by vitamin D ( Figure 5 ) [ 397 , 398 ]. In turn, VDUP1 has been isolated in studies aimed to characterize the endogenous inhibitor of the reactive oxygen species (ROS) scavenger system of Thioredoxin (Trx) and for this, it was also called TXNIP [ 399 ] or Thioredoxin Binding Protein 2 (TBP2) [ 400 ].…”

Section: Vitamin D and Neurofibromatosismentioning

confidence: 99%

Understanding the Biological Activities of Vitamin D in Type 1 Neurofibromatosis: New Insights into Disease Pathogenesis and Therapeutic Design

Riccardi

Perrone

Napolitano

et al. 2020

Cancers

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Vitamin D is a fat-soluble steroid hormone playing a pivotal role in calcium and phosphate homeostasis as well as in bone health. Vitamin D levels are not exclusively dependent on food intake. Indeed, the endogenous production—occurring in the skin and dependent on sun exposure—contributes to the majority amount of vitamin D present in the body. Since vitamin D receptors (VDRs) are ubiquitous and drive the expression of hundreds of genes, the interest in vitamin D has tremendously grown and its role in different diseases has been extensively studied. Several investigations indicated that vitamin D action extends far beyond bone health and calcium metabolism, showing broad effects on a variety of critical illnesses, including cancer, infections, cardiovascular and autoimmune diseases. Epidemiological studies indicated that low circulating vitamin D levels inversely correlate with cutaneous manifestations and bone abnormalities, clinical hallmarks of neurofibromatosis type 1 (NF1). NF1 is an autosomal dominant tumour predisposition syndrome causing significant pain and morbidity, for which limited treatment options are available. In this context, vitamin D or its analogues have been used to treat both skin and bone lesions in NF1 patients, alone or combined with other therapeutic agents. Here we provide an overview of vitamin D, its characteristic nutritional properties relevant for health benefits and its role in NF1 disorder. We focus on preclinical and clinical studies that demonstrated the clinical correlation between vitamin D status and NF1 disease, thus providing important insights into disease pathogenesis and new opportunities for targeted therapy.

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“…Furthermore, TBP-2 inhibits Akt/Bcl-xL signaling, independent of mTOR, to facilitate the initial stage of autophagy [80]. ese findings will inspire more studies to explore target therapies for preventing autophagy induced by ROS in LECs and prevent cataract formation in elderly people [83].…”

Section: Cataractmentioning

confidence: 99%

Autophagy and Age-Related Eye Diseases

Yang

Pan

Zhao

et al. 2019

BioMed Research International

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Background. Autophagy is a catabolic process that depends on the lysosome. It is usually used to maintain cellular homeostasis, survival and development by degrading abnormal substances and dysfunctional organelles, especially when the cell is exposed to starvation or other stresses. Increasing studies have reported that autophagy is associated with various eye diseases, of which aging is one of the important factors. Objective. To summarize the functional and regulatory role of autophagy in ocular diseases with aging, and discuss the possibility of autophagy-targeted therapy in age-related diseases. Methods. PubMed searches were performed to identify relevant articles published mostly in the last 5 years. The key words were used to retrieve including “autophagy”, “aging”, “oxidative stress AND autophagy”, “dry eye AND autophagy”, “corneal disease AND autophagy”, “glaucoma AND autophagy”, “cataract AND autophagy”, “AMD AND autophagy”, “cardiovascular diseases AND autophagy”, “diabetes AND autophagy”. After being classified and assessed, the most relevant full texts in English were chosen. Results. Apart from review articles, more than two research articles for each age-related eye diseases related to autophagy were retrieved. We only included the most relevant and recent studies for summary and discussion. Conclusion. Autophagy has both protective and detrimental effects on the progress of age-related eye diseases. Different types of studies based on certain situations in vitro showed distinct results, which do not necessarily coincide with the actual situation in human bodies completely. It means the exact role and regulatory function of autophagy in ocular diseases remains largely unknown. Although autophagy as a potential therapeutic target has been proposed, many problems still need to be solved before it applies to clinical practice.

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The Function of Thioredoxin‐Binding Protein‐2 (TBP‐2) in Different Diseases

Cited by 37 publications

References 74 publications

The role of Trx/TBP-2 in oxidative stress induced autophagy in human lens epithelial cells

The role of Trx/TBP-2 in oxidative stress induced autophagy in human lens epithelial cells

Understanding the Biological Activities of Vitamin D in Type 1 Neurofibromatosis: New Insights into Disease Pathogenesis and Therapeutic Design

Autophagy and Age-Related Eye Diseases

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