Regulation of cellular immunity by activating transcription factor 4

Dk, Mukherjee; Bercz, Lena; Torok, Molly; Mace, Thomas A.

doi:10.1016/j.imlet.2020.09.006

Cited by 27 publications

(18 citation statements)

References 93 publications

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“…Similarly, Smad7, a negative regulator of TGF-β1, is suppressed by miR-182-5p which is induced by TGF-β1, resulting in the development of IPF ( 46 ). TGF-β1 activates Semaphorin (SEMA) 7A and its receptors through a Smad3-independent and Smad 2/3-independent mechanism, respectively, promoting pulmonary fibrosis ( 47 ) Activating transcription factor 4 (ATF4) was a pivotal transcriptional regulator for the metabolism of amino acid ( 48 ). TGF-β1/Smad3 signaling could increase the expression of the ATF4 through initiating the mechanistic target of rapamycin complex 1 (mTORC1) and its downstream translation initiation factor 4E binding protein 1 (4E-BP1), promoting collagen biosynthesis ( 49 ).…”

Section: Tgf-β1-involved Pathway In Ipfmentioning

confidence: 99%

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

2021

Int J Mol Med

121

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Idiopathic pulmonary fibrosis (IPF) is a worldwide disease characterized by the chronic and irreversible decline of lung function. Currently, there is no drug to successfully treat the disease except for lung transplantation. Numerous studies have been devoted to the study of the fibrotic process of IPF and findings showed that transforming growth factor-β1 (TGF-β1) plays a central role in the development of IPF. TGF-β1 promotes the fibrotic process of IPF through various signaling pathways, including the Smad, MAPK, and ERK signaling pathways. There are intersections between these signaling pathways, which provide new targets for researchers to study new drugs. In addition, TGF-β1 can affect the fibrosis process of IPF by affecting oxidative stress, epigenetics and other aspects. Most of the processes involved in TGF-β1 promote IPF, but TGF-β1 can also inhibit it. This review discusses the role of TGF-β1 in IPF. Contents1. Introduction 2. TGF-β1-involved pathway in IPF 3. Discussion 4. Conclusion

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Section: Tgf-β1-involved Pathway In Ipfmentioning

confidence: 99%

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

2021

Int J Mol Med

121

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“…Once the alpha cells reprogrammed into insulin-producing cells, they maintained glucagon production, which may confuse the immune system of NOD/ShiLt mice. In addition, the GCG promoter is signi cantly different from the insulin promoter; for example, the transcription factor ATF4 binds to the insulin promoter, causing beta cell dysfunction and apoptosis (37,38), and activated ATF4 regulates cell immunity (39), which may play an attractive role in immune cell homing to islets. The mechanisms by which Pdx1 and MafA reprogram alpha cells into insulin-producing cells with protective action on transgenic islets or after AAV8-GCG-Pdx1 and MafA-mediated gene delivery have not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Specific Reprogramming of Alpha Cells to Insulin-Producing Cells by Short Glucagon Promoter-Driven Pdx1 and MafA

Guo

Zhang

et al. 2021

Preprint

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Endogenous reprogramming of pancreas-derived non-beta cells into insulin-producing cells is a promising approach to treat type 1 diabetes (T1D). One strategy that has yet to be explored is the specific delivery of insulin-producing essential genes, Pdx1 and MafA, to pancreatic alpha cells to reprogram the cells into insulin-producing cells in an adult pancreas. In this study, we utilized an alpha cell-specific glucagon (GCG) promoter to drive Pdx1 and MafA transcription factors to reprogram alpha cells to insulin-producing cells in chemically induced and autoimmune diabetic mice. Our results showed that a combination of a short glucagon-specific promoter with AAV serotype 8 can be used to successfully deliver Pdx1 and MafA into alpha cells in the mouse pancreas. Pdx1 and MafA expression specifically in alpha cells was also able to correct hyperglycemia in both induced and autoimmune diabetic mice. With this technology, targeted gene specificity and reprogramming were accomplished with an alpha-specific promotor combined with an AAV-specific serotype and provide an initial basis to develop a novel therapy for the treatment of T1D.

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“…The regulation of immunity via ATF4 can be indirect by initiating inflammation that will secrete a series of cytokine directed immune responses. In contrast, ATF4 can also directly interfere with maturation, development, or polarization states of different immune cells such as macrophages, T cell, B cells, NK cells and dendritic cells contributing to progression of disease (39). Interestingly, ATF4 can act together with ATF6 to transactivate the transcription factor C/EBP homologous protein (CHOP), which was found to regulate mediators of apoptosis such as B-cell lymphoma 2 (BCL2) and BCL2 interacting mediator of cell death (40,41).…”

Section: Discussionmentioning

confidence: 99%

The bZIP Transcription Factor ZIP-11 Is Required for the Innate Immune Regulation in Caenorhabditis elegans

et al. 2021

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Innate immunity is the first line of host defense against pathogen infection in metazoans. However, the molecular mechanisms of the complex immune regulatory network are not fully understood. Based on a transcriptome profiling of the nematode Caenorhabditis elegans, we found that a bZIP transcription factor ZIP-11 was up-regulated upon Pseudomonas aeruginosa PA14 infection. The tissue specific RNAi knock-down and rescue data revealed that ZIP-11 acts in intestine to promote host resistance against P. aeruginosa PA14 infection. We further showed that intestinal ZIP-11 regulates innate immune response through constituting a feedback loop with the conserved PMK-1/p38 mitogen-activated protein signaling pathway. Intriguingly, ZIP-11 interacts with a CCAAT/enhancer-binding protein, CEBP-2, to mediate the transcriptional response to P. aeruginosa PA14 infection independently of PMK-1/p38 pathway. In addition, human homolog ATF4 can functionally substitute for ZIP-11 in innate immune regulation of C. elegans. Our findings indicate that the ZIP-11/ATF4 genetic program activates local innate immune response through conserved PMK-1/p38 and CEBP-2/C/EBPγ immune signals in C. elegans, raising the possibility that a similar process may occur in other organisms.

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Regulation of cellular immunity by activating transcription factor 4

Cited by 27 publications

References 93 publications

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

Specific Reprogramming of Alpha Cells to Insulin-Producing Cells by Short Glucagon Promoter-Driven Pdx1 and MafA

The bZIP Transcription Factor ZIP-11 Is Required for the Innate Immune Regulation in Caenorhabditis elegans

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