ArticleAmerican journal of respiratory cell and molecular biology2011
Non-muscle myosin light chain kinase isoform is a viable molecular target in acute inflammatory lung injury.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Gene Expression Analysis to Assess the Relevance of Rodent Models to Human Lung Injury.American journal of respiratory cell and molecular biology · 2017Pooled it
- The emerging regulatory roles of non-coding RNA in Ventilator-induced Lung Injury.Non-coding RNA research · 2026Review
- Article
- Vascular Endothelium at the Molecular Level: From Fundamental Knowledge Toward Medical Implementation.Biomedicines · 2024Article
- A Razor's Edge: Vascular Responses to Acute Inflammatory Lung Injury/Acute Respiratory Distress Syndrome.Annual review of physiology · 2024Review
- A cortactin CTTN coding SNP contributes to lung vascular permeability and inflammatory disease severity in African descent subjects.Translational research : the journal of laboratory and clinical medicine · 2022Article
- PI3Kγ stimulates a high molecular weight form of myosin light chain kinase to promote myeloid cell adhesion and tumor inflammation.Nature communications · 2022Article
- Critical role for the lung endothelial nonmuscle myosin light-chain kinase isoform in the severity of inflammatory murine lung injury.Pulmonary circulation · 2022Article
- ITRAQ-based quantitative proteomics analysis of forest musk deer with pneumonia.Frontiers in veterinary science · 2022Article
- CHD1L prevents lipopolysaccharide-induced hepatocellular carcinomar cell death by activating hnRNP A2/B1-nmMYLK axis.Cell death & disease · 2021Article
- Group V Phospholipase ACells · 2021Article
- Strategies to DAMPen COVID-19-mediated lung and systemic inflammation and vascular injury.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Genetic and epigenetic regulation of the non-muscle myosin light chain kinase isoform by lung inflammatory factors and mechanical stress.Clinical science (London, England : 1979) · 2021Article
- Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation.Cell transplantation · 2019Article
- Genomic and Genetic Approaches to Deciphering Acute Respiratory Distress Syndrome Risk and Mortality.Antioxidants & redox signaling · 2019Review
- Article
- RPA1 binding to NRF2 switches ARE-dependent transcriptional activation to ARE-NRE-dependent repression.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- RNA‑sequencing analysis of aberrantly expressed long non‑coding RNAs and mRNAs in a mouse model of ventilator‑induced lung injury.Molecular medicine reports · 2018Article
- Genome-Wide Association Study in African Americans with Acute Respiratory Distress Syndrome Identifies the Selectin P Ligand Gene as a Risk Factor.American journal of respiratory and critical care medicine · 2018Article
- The Splicing Factor hnRNPA1 Regulates Alternate Splicing of the MYLK Gene.American journal of respiratory cell and molecular biology · 2018Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Acute lung injury (ALI) and mechanical ventilator-induced lung injury (VILI), major causes of acute respiratory failure with elevated morbidity and mortality, are characterized by significant pulmonary inflammation and alveolar/vascular barrier dysfunction. Previous studies highlighted the role of the non-muscle myosin light chain kinase isoform (nmMLCK) as an essential element of the inflammatory response, with variants in the MYLK gene that contribute to ALI susceptibility. To define nmMLCK involvement further in acute inflammatory syndromes, we used two murine models of inflammatory lung injury, induced by either an intratracheal administration of lipopolysaccharide (LPS model) or mechanical ventilation with increased tidal volumes (the VILI model). Intravenous delivery of the membrane-permeant MLC kinase peptide inhibitor, PIK, produced a dose-dependent attenuation of both LPS-induced lung inflammation and VILI (~50% reductions in alveolar/vascular permeability and leukocyte influx). Intravenous injections of nmMLCK silencing RNA, either directly or as cargo within angiotensin-converting enzyme (ACE) antibody-conjugated liposomes (to target the pulmonary vasculature selectively), decreased nmMLCK lung expression (∼70% reduction) and significantly attenuated LPS-induced and VILI-induced lung inflammation (∼40% reduction in bronchoalveolar lavage protein). Compared with wild-type mice, nmMLCK knockout mice were significantly protected from VILI, with significant reductions in VILI-induced gene expression in biological pathways such as nrf2-mediated oxidative stress, coagulation, p53-signaling, leukocyte extravasation, and IL-6-signaling. These studies validate nmMLCK as an attractive target for ameliorating the adverse effects of dysregulated lung inflammation.
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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.