ArticleInternational journal of molecular sciences2022
E3 Ubiquitin Ligase Midline 1 Regulates Endothelial Cell ICAM-1 Expression and Neutrophil Adhesion in Abdominal Sepsis.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Identification and Co-expression Analysis of Differentially Expressed LncRNAs and mRNAs Regulate Intramuscular Fat Deposition in Yaks at Two Developmental Stages.Biochemical genetics · 2026Article
- Bufalin inhibits immune escape in metastatic colorectal cancer by regulating M2 macrophage polarization.Apoptosis : an international journal on programmed cell death · 2025Article
- Mac-1 blockade impedes adhesion-dependent neutrophil extracellular trap formation and ameliorates lung injury in LPS-induced sepsis.Frontiers in immunology · 2025Article
- Midline 1 associated with Fas signaling enhances murine antigen-induced arthritis.Frontiers in cell and developmental biology · 2025Article
- Article
- The role of reactive oxygen species in plant-virus interactions.Plant cell reports · 2024Review
- Communications between Neutrophil-Endothelial Interaction in Immune Defense against Bacterial Infection.Biology · 2024Review
- Midline-1 regulates effector T cell motility in experimental autoimmune encephalomyelitis via mTOR/microtubule pathway.Theranostics · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Septic lung damage is associated with endothelial cell and neutrophil activation. This study examines the role of the E3 ubiquitin ligase midline 1 (Mid1) in abdominal sepsis. Mid1 expression was increased in endothelial cells derived from post-capillary venules in septic mice and TNF-α challenge increased Mid1 levels in endothelial cells in vitro. The siRNA-mediated knockdown of Mid1 decreased TNF-α-induced upregulation of ICAM-1 and neutrophil adhesion to endothelial cells. Moreover, Mid1 silencing reduced leukocyte adhesion in post-capillary venules in septic lungs in vivo. The silencing of Mid1 not only decreased Mid1 expression but also attenuated expression of ICAM-1 in lungs from septic mice. Lastly, TNF-α stimulation decreased PP2Ac levels in endothelial cells in vitro, which was reversed in endothelial cells pretreated with siRNA directed against Mid1. Thus, our novel data show that Mid1 is an important regulator of ICAM-1 expression and neutrophil adhesion in vitro and septic lung injury in vivo. A possible target of Mid1 is PP2Ac in endothelial cells. Targeting the Mid1-PP2Ac axis may be a useful way to reduce pathological lung inflammation in abdominal sepsis.
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Registered trials
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