ArticleInflammation2019
Phosphorylated Heat Shock Protein 27 Inhibits Lipopolysaccharide-Induced Inflammation in Thp1 Cells by Promoting TLR4 Endocytosis, Ubiquitination, and Degradation.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- RNF152-mediated, ubiquitin-dependent degradation of HSP27 activates the PI3K/AKT pathway, driving synovial inflammatory cascades in TMJOA.Arthritis research & therapy · 2025Article
- Heat shock proteins at the crossroads of endosomal trafficking pathways.Cell biology and toxicology · 2025Review
- Linoleic acid inhibits lipopolysaccharide-induced inflammation by promoting TLR4 regulated autophagy in murine RAW264.7 macrophages.Journal of applied biomedicine · 2024Article
- Tropomodulin1 exacerbates inflammatory response in macrophages by negatively regulating LPS-induced TLR4 endocytosis.Cellular and molecular life sciences : CMLS · 2024Article
- First-trimester plasma extracellular heat shock proteins levels and risk of preeclampsia.Journal of cellular and molecular medicine · 2023Article
- HSP27 Interacts with Nonstructural Proteins of Porcine Reproductive and Respiratory Syndrome Virus and Promotes Viral Replication.Pathogens (Basel, Switzerland) · 2023Article
- Noncoding RNAs: Novel Targets for Opioid Tolerance.Current neuropharmacology · 2023Review
- Selenium-Alleviated Testicular Toxicity by Modulating Inflammation, Heat Shock Response, and Autophagy Under Oxidative Stress in Lead-Treated Chickens.Biological trace element research · 2021Article
- Hypoxia-Inducible Ubiquitin Specific Peptidase 13 Contributes to Tumor Growth and Metastasis via Enhancing the Toll-Like Receptor 4/Myeloid Differentiation Primary Response Gene 88/Nuclear Factor-κB Pathway in Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The aims of this study were to investigate the effect of Hsp27 on LPS-induced inflammation and identify the precise mechanisms about how Hsp27 regulates LPS-induced TLR4 signaling in Thp1 cells. Thp1 cells were transfected with Flag-Hsp27 or pcDNA3.1, and then treated with LPS for indicated time. TNF-α, IL-1β, and IL-6 were determined by ELISA. The protein levels of Hsp27, p-Hsp27 (Ser15, Ser78, and Ser82), and TLR4 were measured by Western blotting. In vitro study showed that over-expression of Hsp27 downregulated the release of TNF-α, IL-1β, and IL-6 and suppressed the activation of TLR4 signals after stimulated by LPS. The location of TLR4 and RAB5 was detected by confocal microscopy. Immunoprecipitation was used to determine the ubiquitination and degradation of TLR4 and interaction between Hsp27 and TLR4. Results showed that Hsp27 could promote TLR4 endocytosis and ubiquitination and degradation. Further research revealed that Hsp27 was phosphorylated after LPS, only phosphorylated Hsp27 can interact with TLR4 and inhibit the activation of TLR4 signaling, which was demonstrated by inhibition of Hsp27 phosphorylation with inhibitors or transfection of Hsp27 mutants into Thp1 cells. Phosphorylated Hsp27 reduced the release of TNF-α, IL-1β, and IL-6, and suppressed the activation of TLR4 signaling by promoting TLR4 endocytosis, ubiquitination, and degradation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.