ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Thrombin selectively engages LIM kinase 1 and slingshot-1L phosphatase to regulate NF-κB activation and endothelial cell inflammation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
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- Integrative multi-omics analysisiScience · 2025Article
- LIM kinases in cardiovascular health and disease.Frontiers in physiology · 2024Review
- Review
- Synthesis and Development of a Novel First-in-Class Cofilin Inhibitor for Neuroinflammation in Hemorrhagic Brain Injury.ACS chemical neuroscience · 2022Article
- Autophagy protein ATG7 is a critical regulator of endothelial cell inflammation and permeability.Scientific reports · 2020Article
- Critical role of autophagy regulator Beclin1 in endothelial cell inflammation and barrier disruption.Cellular signalling · 2019Article
- The cofilin phosphatase slingshot homolog 1 restrains angiotensin II-induced vascular hypertrophy and fibrosis in vivo.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Noncanonical Matrix Metalloprotease 1-Protease-Activated Receptor 1 Signaling Drives Progression of Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Importins α and β signaling mediates endothelial cell inflammation and barrier disruption.Cellular signalling · 2018Article
- Cofilin Mediates LPS-Induced Microglial Cell Activation and Associated Neurotoxicity Through Activation of NF-κB and JAK-STAT Pathway.Molecular neurobiology · 2018Article
- Shigella depends on SepA to destabilize the intestinal epithelial integrity via cofilin activation.Gut microbes · 2017Article
- Phospholipase C-ε signaling mediates endothelial cell inflammation and barrier disruption in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Cofilin as a Promising Therapeutic Target for Ischemic and Hemorrhagic Stroke.Translational stroke research · 2016Review
- Inducible Bronchus-Associated Lymphoid Tissue: Taming Inflammation in the Lung.Frontiers in immunology · 2016Review
- G Protein-Coupled Receptor and RhoA-Stimulated Transcriptional Responses: Links to Inflammation, Differentiation, and Cell Proliferation.Molecular pharmacology · 2015Review
- Nuclear factor-κB mediates the phenotype switching of airway smooth muscle cells in a murine asthma model.International journal of clinical and experimental pathology · 2015Article
- Novel regulators of endothelial barrier function.American journal of physiology. Lung cellular and molecular physiology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial cell (EC) inflammation is a central event in the pathogenesis of many pulmonary diseases such as acute lung injury and its more severe form acute respiratory distress syndrome. Alterations in actin cytoskeleton are shown to be crucial for NF-κB regulation and EC inflammation. Previously, we have described a role of actin binding protein cofilin in mediating cytoskeletal alterations essential for NF-κB activation and EC inflammation. The present study describes a dynamic mechanism in which LIM kinase 1 (LIMK1), a cofilin kinase, and slingshot-1Long (SSH-1L), a cofilin phosphatase, are engaged by procoagulant and proinflammatory mediator thrombin to regulate these responses. Our data show that knockdown of LIMK1 destabilizes whereas knockdown of SSH-1L stabilizes the actin filaments through modulation of cofilin phosphorylation; however, in either case thrombin-induced NF-κB activity and expression of its target genes (ICAM-1 and VCAM-1) is inhibited. Further mechanistic analyses reveal that knockdown of LIMK1 or SSH-1L each attenuates nuclear translocation and thereby DNA binding of RelA/p65. In addition, LIMK1 or SSH-1L depletion inhibited RelA/p65 phosphorylation at Ser(536), a critical event conferring transcriptional competency to the bound NF-κB. However, unlike SSH-1L, LIMK1 knockdown also impairs the release of RelA/p65 by blocking IKKβ-dependent phosphorylation/degradation of IκBα. Interestingly, LIMK1 or SSH-1L depletion failed to inhibit TNF-α-induced RelA/p65 nuclear translocation and proinflammatory gene expression. Thus this study provides evidence for a novel role of LIMK1 and SSH-1L in selectively regulating EC inflammation associated with intravascular coagulation.
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