Zinc supplementation augments TGF‐β1‐dependent regulatory T cell induction

Maywald, Martina; Meurer, Steffen K.; Weiskirchen, Ralf; Rink, Lothar

doi:10.1002/mnfr.201600493

Cited by 38 publications

(36 citation statements)

References 79 publications

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“…Szuster-Ciesielska et al previously reported that Zn supplementation decreases ethanol- and acetaldehyde-induced activation of liver stellate cells and inhibit liver fibrosis changes though inhibiting TGF-β/Smad signaling [30]. Maywald et al have very recently demonstrated that zinc supplementation increased TGF-β1-dependent regulatory T cell induction in allogeneic reaction due to a triggered intracellular zinc signal, which in association with an increased Smad 2/3 activation [31]. Data from the present study suggested that TGF-β/Smad signaling activation might also occur through this process in NRK-52E cells with HG treatment, and also implicated that ZnT7 protect HG-induced EMT in NRK-52E cells partly by inhibiting TGF-β/Smad signaling.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Znt7 on High Glucose-Induced Epithelial-to-Mesenchymal Transition in Renal Tubular Epithelial Cells

Zhang

Liang³

et al. 2018

Kidney Blood Press Res

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Background/Aims: Evidence from our and other groups has demonstrated that zinc transporter 7 in SLC30 family (ZnT7) inhibited epithelial-to-mesenchymal transition (EMT) and apoptosis in rat peritoneal mesothelial cells (RPMCs) under high glucose (HG) concentration. In the present study, we investigated the effect of ZnT7 on EMT of renal tubular epithelial cells (RTECs) in an in vitro model of diabetic nephropathy (DN). Methods: A dual-fluorescent staining protocol was used for detection of ZnT7 in a normal rat kidney tubular epithelial cell line (NRK-52E cells). EMT was induced with HG (30 mM). NRK-52E cells were transfected with plasmids codifying for hZnT7-EGFP and interfering RNA for determination of the effect of ZnT7 over-expression and silencing, respectively. Expression of ZnT7, activation of the MAPK/ERK and TGF-β/Smad pathways were analyzed with by means of Western blot. Results: ZnT7 was localized in the perinuclear region and Golgi apparatus. In HG-induced EMT of NRK-52E cells, ZnT7 was up-regulated. Over-expression of ZnT7 led to inhibition of HG-induced EMT, while knock-down of ZnT7 increased EMT. Furthermore, knock-down of ZnT7 and increased HG-induced EMT was accompanied by activation of the MAPK/ERK and TGF-β/Smad pathways. Conclusion: The present study provides evidence that ZnT7 has a protective effect over EMT of RTECs in DN and suggests that the inhibition of HG-induced EMT may be achieved through the MAPK/ERK and TGF-β/Smad pathways. Thereby, ZnT7 could be a potential target for translation medicine and prevention program in DN.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Znt7 on High Glucose-Induced Epithelial-to-Mesenchymal Transition in Renal Tubular Epithelial Cells

Zhang

Liang³

et al. 2018

Kidney Blood Press Res

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“…Additionally, regulatory T cells (Treg) are induced and stabilized in zinc-supplemented mixed lymphocyte culture (MLC), in lymphocytes from patients allergic to pollen [88] and in experimental autoimmune encephalomyelitis (EAE) [89]. Furthermore, zinc enhances the capacity of TGFβ1 to induce Treg cells [90,91]. However, the capacity of zinc to induce Tregs is dependent on the activation status of the cells.…”

Section: Zinc In Inflammationmentioning

confidence: 99%

Zinc in Infection and Inflammation

2017

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Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps (NET) formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors of differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B (NF-κB), a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.

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“…Additionally, regulatory T cells (Treg) are induced and stabilized in zinc-supplemented lymphocyte culture (MLC), in lymphocytes from patients allergic to pollen [83] and in experimental autoimmune encephalomyelitis (EAE) [84]. Furthermore, zinc enhances the capacity of TGFβ1 to induce Treg cells [85,86]. However, the capacity of zinc to induce Tregs is dependent on the activation status of the cells.…”

Section: Zinc Status and Inflammatory Cytokinesmentioning

confidence: 99%

Zinc in Infection and Inflammation

Gammoh¹,

Rink²

2017

Preprint

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126

139

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Abstract:Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors or differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B, a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.

show abstract

Zinc supplementation augments TGF‐β1‐dependent regulatory T cell induction

Cited by 38 publications

References 79 publications

Protective Effect of Znt7 on High Glucose-Induced Epithelial-to-Mesenchymal Transition in Renal Tubular Epithelial Cells

Protective Effect of Znt7 on High Glucose-Induced Epithelial-to-Mesenchymal Transition in Renal Tubular Epithelial Cells

Zinc in Infection and Inflammation

Zinc in Infection and Inflammation

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