ArticleDrug design, development and therapy2018
MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1.
Article in Drug design, development and therapy, 2018. 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, 8 citations in OpenAlex.
- Exploring the Mechanism of Action of Xuebijing Injection in Treating Acute Respiratory Distress Syndrome Based on Network Pharmacology and Animal Experiments.Journal of inflammation research · 2025Article
- Mechanisms of pulmonary endothelial barrier dysfunction in acute lung injury and acute respiratory distress syndrome.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Advances in Biomarkers for Diagnosis and Treatment of ARDS.Diagnostics (Basel, Switzerland) · 2023Review
- Focus on long non-coding RNA MALAT1: Insights into acute and chronic lung diseases.Frontiers in genetics · 2022Review
- Vitamin D Inhibits Lipopolysaccharide (LPS)-Induced Inflammation in A549 Cells by Downregulating Inflammatory Cytokines.Medical science monitor basic research · 2021Article
- The role and mechanism of the annexin A1 peptide Ac2-26 in rats with cardiopulmonary bypass lung injury.Basic & clinical pharmacology & toxicology · 2021Article
- Endothelial Damage in Acute Respiratory Distress Syndrome.International journal of molecular sciences · 2020Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeICAM-1 plays a critical role in the development of acute respiratory distress syndrome (ARDS). MK2 regulates the expression of ICAM-1 in human pulmonary microvascular endothelial cells. To explore whether the inhibition of MK2 activation has the same effect in experimental animals, MMI-0100, a peptide-mediated inhibitor of MK2, was used to verify whether MMI-0100 can ameliorate lung inflammation in a mouse model of ARDS by reducing endothelial expression of ICAM-1.
methodsIn this study, C57BL/6 mice were randomly divided into three groups: a control group, an lipopolysaccharides (LPS) group, and an LPS plus MMI-0100 group. Mice were killed 24 hours after the administration of LPS and MMI-0100. The mouse lung tissue histopathology, wet/dry weight ratio (W/D), and the neutrophil count were used to measure the severity of lung inflammation in mice. The pulmonary microvascular endothelial cells (PMVECs) of the mice were isolated. The mRNA expression of ICAM-1 in mouse PMVECs was determined using RT-PCR, and the protein expression of MK2 and ICAM-1 in mouse PMVECs was analyzed using Western blotting and immunohistochemistry.
resultsWe found that the level of phosphorylated MK2 in the LPS plus MMI-0100 group was reduced. Compared with the LPS group, the LPS plus MMI-0100 group of mice showed less severe inflammation, including a lower W/D and neutrophil count. The mRNA and protein expression of ICAM-1 in the LPS group was significantly higher than in the control group in mouse PMVECs, and the ICAM-1 level was reduced after the administration of MMI-0100.
conclusionThese data indicate that MMI-0100 ameliorates lung inflammation in a mouse model of ARDS by reducing endothelial expression of ICAM-1.
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