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1. NLRP3 Phosphorylation Is an Essential Priming Event for Inflammasome Activation.

Author

Song N, Liu ZS, Xue W, Bai ZF, Wang QY, Dai J, Liu X, Huang YJ, Cai H, Zhan XY, Han QY, Wang H, Chen Y, Li HY, Li AL, Zhang XM, Zhou T, and Li T

Subjects
Amino Acid Sequence, Animals, Deubiquitinating Enzymes genetics, Deubiquitinating Enzymes immunology, Escherichia coli chemistry, Female, Gene Expression Regulation, HEK293 Cells, Humans, Inflammasomes immunology, Lipopolysaccharides pharmacology, Macrophages pathology, Male, Mice, Mice, Transgenic, Mitogen-Activated Protein Kinase 8 immunology, NLR Family, Pyrin Domain-Containing 3 Protein deficiency, NLR Family, Pyrin Domain-Containing 3 Protein immunology, Phosphorylation, Sequence Alignment, Sequence Homology, Amino Acid, Shock, Septic chemically induced, Shock, Septic mortality, Shock, Septic pathology, Signal Transduction, Survival Analysis, Inflammasomes genetics, Macrophages immunology, Mitogen-Activated Protein Kinase 8 genetics, NLR Family, Pyrin Domain-Containing 3 Protein genetics, Shock, Septic genetics
Abstract

Many infections and stress signals can rapidly activate the NLRP3 inflammasome to elicit robust inflammatory responses. This activation requires a priming step, which is thought to be mainly for upregulating NLRP3 transcription. However, recent studies report that the NLRP3 inflammasome can be activated independently of transcription, suggesting that the priming process has unknown essential regulatory steps. Here, we report that JNK1-mediated NLRP3 phosphorylation at S194 is a critical priming event and is essential for NLRP3 inflammasome activation. We show that NLRP3 inflammasome activation is disrupted in NLRP3-S194A knockin mice. JNK1-mediated NLRP3 S194 phosphorylation is critical for NLRP3 deubiquitination and facilitates its self-association and the subsequent inflammasome assembly. Importantly, we demonstrate that blocking S194 phosphorylation prevents NLRP3 inflammasome activation in cryopyrin-associated periodic syndromes (CAPS). Thus, our study reveals a key priming molecular event that is a prerequisite for NLRP3 inflammasome activation. Inhibiting NLRP3 phosphorylation could be an effective treatment for NLRP3-related diseases., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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2. Dysregulation of the miR-324-5p-CUEDC2 axis leads to macrophage dysfunction and is associated with colon cancer.

Author

Chen Y, Wang SX, Mu R, Luo X, Liu ZS, Liang B, Zhuo HL, Hao XP, Wang Q, Fang DF, Bai ZF, Wang QY, Wang HM, Jin BF, Gong WL, Zhou T, Zhang XM, Xia Q, and Li T

Subjects
Adaptor Proteins, Signal Transducing, Animals, Carrier Proteins biosynthesis, Carrier Proteins genetics, Carrier Proteins immunology, Colitis genetics, Colitis immunology, Colitis metabolism, Colitis pathology, Colonic Neoplasms genetics, Colonic Neoplasms immunology, Female, Gene Expression Regulation, HeLa Cells, Humans, Macrophage Activation, Macrophages immunology, Macrophages pathology, Membrane Proteins biosynthesis, Membrane Proteins genetics, Membrane Proteins immunology, Mice, Mice, Transgenic, MicroRNAs genetics, Repressor Proteins biosynthesis, Repressor Proteins genetics, Repressor Proteins immunology, Signal Transduction, Carrier Proteins metabolism, Colonic Neoplasms metabolism, Macrophages metabolism, Membrane Proteins metabolism, MicroRNAs metabolism, Repressor Proteins metabolism
Abstract

CUEDC2, a CUE-domain-containing protein, modulates inflammation, but its involvement in tumorigenesis is still poorly understood. Here, we report that CUEDC2 is a key regulator of macrophage function and critical for protection against colitis-associated tumorigenesis. CUEDC2 expression is dramatically upregulated during macrophage differentiation, and CUEDC2 deficiency results in excessive production of proinflammatory cytokines. The level of CUEDC2 in macrophages is modulated by miR- 324-5p. We find that Cuedc2 KO mice are more susceptible to dextran-sodium-sulfate-induced colitis, and macrophage transplantation results suggest that the increased susceptibility results from the dysfunction of macrophages lacking CUEDC2. Furthermore, we find that Cuedc2 KO mice are more prone to colitis-associated cancer. Importantly, CUEDC2 expression is almost undetectable in macrophages in human colon cancer, and this decreased CUEDC2 expression is associated with high levels of interleukin-4 and miR-324-5p. Thus, CUEDC2 plays a crucial role in modulating macrophage function and is associated with both colitis and colon tumorigenesis., (Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2014
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