ArticleInflammation2019
MerTK Downregulates Lipopolysaccharide-Induced Inflammation Through SOCS1 Protein but Does Not Affect Phagocytosis of Escherichia coli in Macrophages.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
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Who cites it
7 citing papers in PubMed, 26 citations in OpenAlex.
- Macrophage efferocytosis promotes inflammation resolution and accelerates wound healing.Communications biology · 2026Review
- Mer activation ameliorates nerve injury-induced neuropathic pain by regulating microglial polarization and neuroinflammation via SOCS3 in male rats.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Axl and Mertk Receptors Cooperate to Promote Breast Cancer Progression by Combined Oncogenic Signaling and Evasion of Host Antitumor Immunity.Cancer research · 2021Article
- Mer regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following traumatic brain injury.Journal of neuroinflammation · 2021Article
- Dual Effect of Soloxolone Methyl on LPS-Induced Inflammation In Vitro and In Vivo.International journal of molecular sciences · 2020Article
- MERTK in cancer therapy: Targeting the receptor tyrosine kinase in tumor cells and the immune system.Pharmacology & therapeutics · 2020Review
- Expression of TAM-R in Human Immune Cells and Unique Regulatory Function of MerTK in IL-10 Production by Tolerogenic DC.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial lipopolysaccharide (LPS) induces inflammatory response via toll-like receptor 4 (TLR4). However, this response must be strictly regulated because unbalanced overproduction of pro-inflammatory cytokines can lead to tissue damage and even be fatal. Herein, we explore whether Mer receptor tyrosine kinase (MerTK) regulates Escherichia coli (E. coli) LPS-induced inflammation and mediates phagocytosis of E. coli by macrophages. The results showed that LPS activated TLR4 signaling pathway and induced MerTK pathway in RAW264.7 macrophages, including suppressor of cytokine signaling1 (SOCS1). Preincubation with MerTK-specific blocking antibody (MerTK-Ab) markedly suppressed LPS-induced expression of phosphorylated MerTK, while further promoted LPS-induced production of TNF-α, IL-6, and IL-1β as well as phosphorylation of IκB-α and p65. Likewise, MerTK-Ab prevented LPS-induced SOCS1 expression. Furthermore, LPS-induced production of pro-inflammatory cytokines and activation of NF-κB were increased by transfection with SOCS1 siRNA. Additionally, we demonstrated that MerTK was dispensable in phagocytosis of E. coli by RAW264.7 or peritoneal macrophages. Collectively, these results indicate that MerTK downregulates LPS-induced inflammation through SOCS1 protein without affecting phagocytosis of E. coli in macrophages.
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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.