PTPN14 aggravates inflammation through promoting proteasomal degradation of SOCS7 in acute liver failure

Fu, Binying; Yin, Shutao; Lin, Xiaoyuan; Shi, Lei; Wang, Yu; Zhang, Shanfu; Zhao, Qingting; Li, Zhifeng; Yang, Yanling; Wu, Haibo

doi:10.1038/s41419-020-03014-7

Cited by 16 publications

(12 citation statements)

References 30 publications

(32 reference statements)

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“…Immunoblot analysis was performed as previously described (Fu et␣al , 2020b). Cell lysates were fractionated by sodium dodecyl sulfate polyacrylamide gel electrophoresis and transferred to polyvinylidene fluoride membranes (Millipore, Bedford, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

MiR‐342 controls Mycobacterium tuberculosis susceptibility by modulating inflammation and cell death

Lin

Tan

et al. 2021

EMBO Reports

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Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis (Mtb) that places a heavy strain on public health. Host susceptibility to Mtb is modulated by macrophages, which regulate the balance between cell apoptosis and necrosis. However, the role of molecular switches that modulate apoptosis and necrosis during Mtb infection remains unclear. Here, we show that Mtb‐susceptible mice and TB patients have relatively low miR‐342‐3p expression, while mice with miR‐342‐3p overexpression are more resistant to Mtb. We demonstrate that the miR‐342‐3p/SOCS6 axis regulates anti‐Mtb immunity by increasing the production of inflammatory cytokines and chemokines. Most importantly, the miR‐342‐3p/SOCS6 axis participates in the switching between Mtb‐induced apoptosis and necrosis through A20‐mediated K48‐linked ubiquitination and RIPK3 degradation. Our findings reveal several strategies by which the host innate immune system controls intracellular Mtb growth via the miRNA‐mRNA network and pave the way for host‐directed therapies targeting these pathways.

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Section: Methodsmentioning

confidence: 99%

MiR‐342 controls Mycobacterium tuberculosis susceptibility by modulating inflammation and cell death

Lin

Tan

et al. 2021

EMBO Reports

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“… 196 In a mouse model of LPS- and D-GalN-induced acute liver failure, PTPN14 initiated a cytokine storm by promoting ubiquitination of a suppressor of cytokine signaling and its downstream NF-κB signaling. 197 In summary, the limited evidence in inflammation-related diseases indicates that PTPN14 may have an important role in the immune response and other inflammatory diseases.…”

Section: The Signaling Pathways Regulated By the Protein Phosphatases...mentioning

confidence: 99%

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

Pan

Zhou

Zhang

et al. 2022

Sig Transduct Target Ther

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Inflammation is the common pathological basis of autoimmune diseases, metabolic diseases, malignant tumors, and other major chronic diseases. Inflammation plays an important role in tissue homeostasis. On one hand, inflammation can sense changes in the tissue environment, induce imbalance of tissue homeostasis, and cause tissue damage. On the other hand, inflammation can also initiate tissue damage repair and maintain normal tissue function by resolving injury and restoring homeostasis. These opposing functions emphasize the significance of accurate regulation of inflammatory homeostasis to ameliorate inflammation-related diseases. Potential mechanisms involve protein phosphorylation modifications by kinases and phosphatases, which have a crucial role in inflammatory homeostasis. The mechanisms by which many kinases resolve inflammation have been well reviewed, whereas a systematic summary of the functions of protein phosphatases in regulating inflammatory homeostasis is lacking. The molecular knowledge of protein phosphatases, and especially the unique biochemical traits of each family member, will be of critical importance for developing drugs that target phosphatases. Here, we provide a comprehensive summary of the structure, the “double-edged sword” function, and the extensive signaling pathways of all protein phosphatases in inflammation-related diseases, as well as their potential inhibitors or activators that can be used in therapeutic interventions in preclinical or clinical trials. We provide an integrated perspective on the current understanding of all the protein phosphatases associated with inflammation-related diseases, with the aim of facilitating the development of drugs that target protein phosphatases for the treatment of inflammation-related diseases.

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“…A module of DEGs was also identified as upregulated in old PLX5622 microglia, downregulated in old AF hi , and mixed expression in young. The AF hi gene signature in old mice included up-regulation of Pvrig , an immune checkpoint receptor ( 19 ) and Alzheimer’s disease risk enhancer in macrophages ( 20 ), and Ptpn14 , a pro-inflammatory suppressor of SOCS7 ( 21 ), and down-regulation of Cd74 , Senp3, and Kynu . We tested whether transcriptional signatures could explain functional differences in old AF hi microglia by performing sample-level enrichment analysis (SLEA) on gene sets for phagocytosis, ROS biosynthesis, autophagy, and DAM/senescence pathways (Fig.…”

Section: Resultsmentioning

confidence: 99%

Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration

Ritzel

Jiao

et al. 2022

Preprint

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Lipofuscin is an autofluorescent (AF) pigment formed by lipids and misfolded proteins that accumulates in post-mitotic cells with advanced age. Here we immunophenotyped microglia in the brain of old C57BL/6 mice (>18 months-old) and demonstrate that in comparison to young mice, one third of old microglia are AF, characterized by profound changes in lipid and iron content, phagocytic activity, and oxidative stress. Pharmacological depletion of microglia in old mice eliminated the AF microglia following repopulation and reversed microglial dysfunction. Age-related neurological deficits and neurodegeneration after traumatic brain injury (TBI) were attenuated in old mice lacking AF microglia. Furthermore, hyperphagocytic activity and lipid accumulation in microglia persisted for up to one year after TBI, were modified by Apoe4 genotype, and chronically driven by phagocyte-mediated oxidative stress. Thus, AF may reflect a pathological state in aging microglia associated with hyperphagocytosis and inflammatory neurodegeneration that can be further accelerated by TBI.TeaserTraumatic brain injury accelerates age-related pathological phagocytosis and lipofuscin formation in microglia.

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PTPN14 aggravates inflammation through promoting proteasomal degradation of SOCS7 in acute liver failure

Cited by 16 publications

References 30 publications

MiR‐342 controls Mycobacterium tuberculosis susceptibility by modulating inflammation and cell death

MiR‐342 controls Mycobacterium tuberculosis susceptibility by modulating inflammation and cell death

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration

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