ArticleScientific reports2017
Basal autophagy prevents autoactivation or enhancement of inflammatory signals by targeting monomeric MyD88.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Crosstalk Between Autophagy and Inflammation in Chronic Cerebral Ischaemia.Cellular and molecular neurobiology · 2023Review
- The STAT3-Regulated Autophagy Pathway in Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2023Review
- The emerging mechanisms and functions of microautophagy.Nature reviews. Molecular cell biology · 2023Review
- The Role and Mechanism of Metformin in Inflammatory Diseases.Journal of inflammation research · 2023Review
- Monitoring Autophagy in Neural Stem and Progenitor Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Signaling through polymerization and degradation: Analysis and simulations of T cell activation mediated by Bcl10.PLoS computational biology · 2021Article
- Use of Human Induced Pluripotent Stem Cells and Kidney Organoids To Develop a Cysteamine/mTOR Inhibition Combination Therapy for Cystinosis.Journal of the American Society of Nephrology : JASN · 2020Article
- Regulation of immune response byExperimental and therapeutic medicine · 2020Review
- [Mechanism of ulinastatin in reducing lung inflammatory injury in rats with hemorrhagic shock].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- MyD88 signaling causes autoimmune sialadenitis through formation of high endothelial venules and upregulation of LTβ receptor-mediated signaling.Scientific reports · 2018Article
- Anti-inflammatory action of cysteine derivative S-1-propenylcysteine by inducing MyD88 degradation.Scientific reports · 2018Article
- Small Molecule Analogues of the parasitic worm product ES-62 interact with the TIR domain of MyD88 to inhibit pro-inflammatory signalling.Scientific reports · 2018Article
- Checks and Balances between Autophagy and Inflammasomes during Infection.Journal of molecular biology · 2018Review
- Chloroquine Protects Human Corneal Epithelial Cells from Desiccation Stress Induced Inflammation without Altering the Autophagy Flux.BioMed research international · 2018Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy, the processes of delivery of intracellular components to lysosomes, regulates induction of inflammation. Inducible macroautophagy degrades inflammasomes and dysfunctional mitochondria to downregulate inflammatory signals. Nonetheless, the effects of constitutive basal autophagy on inflammatory signals are largely unknown. Here, we report a previously unknown effect of basal autophagy. Lysosomal inhibition induced weak inflammatory signals in the absence of a cellular stimulus and in the presence of a nutrient supply, and their induction was impaired by MyD88 deficiency. During lysosomal inhibition, MyD88 was accumulated, and overabundant MyD88 autoactivated downstream signaling or enhanced TLR/IL-1R-mediated signaling. MyD88 is probably degraded via basal microautophagy because macroautophagy inhibitors, ATG5 deficiency, and an activator of chaperone-mediated autophagy did not affect MyD88. Analysis using a chimeric protein whose monomerization/dimerization can be switched revealed that monomeric MyD88 is susceptible to degradation. Immunoprecipitation of monomeric MyD88 revealed its interaction with TRAF6. In TRAF6-deficient cells, degradation of basal MyD88 was enhanced, suggesting that TRAF6 participates in protection from basal autophagy. Thus, basal autophagy lowers monomeric MyD88 expression, and thereby autoactivation of inflammatory signals is prevented. Given that impairment of lysosomes occurs in various settings, our results provide novel insights into the etiology of inflammatory signals that affect consequences of inflammation.
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