ArticleJournal of cellular physiology2018
Mig6 reduces inflammatory mediators production by regulating the activation of EGFR in LPS-induced endotoxemia.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- ERRFI1 exacerbates hepatic ischemia reperfusion injury by promoting hepatocyte apoptosis and ferroptosis in a GRB2-dependent manner.Molecular medicine (Cambridge, Mass.) · 2024Article
- Tissue-resident macrophages exacerbate lung injury after remote sterile damage.Cellular & molecular immunology · 2024Article
- Exploring shared pathways and the shared biomarker ERRFI1 in Obstructive sleep apnoea and atherosclerosis using integrated bioinformatics analysis.Scientific reports · 2023Article
- EGFR tyrosine kinase activity and Rab GTPases coordinate EGFR trafficking to regulate macrophage activation in sepsis.Cell death & disease · 2022Article
- Macrophage ICAM-1 functions as a regulator of phagocytosis in LPS induced endotoxemia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Mig6 reduces inflammatory mediators production by regulating the activation of EGFR in LPS-induced endotoxemia.Journal of cellular physiology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial growth factor receptor (EGFR), a tyrosine kinase receptor, plays a critical role in lipopolysaccharide (LPS)-induced endotoxemia. Meanwhile, EGFR signaling is regulated by multiple feedback regulators, including mitogen-inducible gene 6 protein (Mig6). However, as an EGFR regulator, the role of Mig6 in endotoxemia is still remained unknown. Here, we reported for the first time that LPS treatment increased the expression of Mig6 and this effect could be inhibited by EGFR inhibitor, PD168393 or erlotinib. Furthermore, knocking down of Mig6 expression led to increased EGFR activation and inflammatory mediators (TNF-α, il-1β) production in response to LPS treatment. On the other hand, the increased EGFR activation and TNF-α or il-1β production in LPS treatment could be inhibited by Mig6 overexpression. Besides, in LPS-induced endotoxemia, ERK1/2 and p-38 activation required Mig6. All these results indicated that Mig6 regulates the production of inflammatory mediators (TNF-α, il-1β) through inhibiting the over activation of EGFR, which in turn inhibit MAPKs signaling (ERK1/2, p-38). These finding suggested that Mig6 may be a novel potential target for controlling the over inflammatory response in endotoxemia.
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