ArticleThe Journal of biological chemistry2006
Spatial compartmentalization of tumor necrosis factor (TNF) receptor 1-dependent signaling pathways in human airway smooth muscle cells. Lipid rafts are essential for TNF-alpha-mediated activation of RhoA but dispensable for the activation of the NF-kappaB and MAPK pathways.
Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 89 citations in OpenAlex.
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- Selective Blockade of TNFR1 Improves Clinical Disease and Bronchoconstriction in Experimental RSV Infection.Viruses · 2020Article
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- Palmitoylation is required for TNF-R1 signaling.Cell communication and signaling : CCS · 2019Article
- New insight into the interaction of TRAF2 C-terminal domain with lipid raft microdomains.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Article
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- Sphingosylphosphorylcholine inhibits macrophage adhesion to vascular smooth muscle cells.Biochemical pharmacology · 2016Article
- Clinical perspectives of TRAIL: insights into central nervous system disorders.Cellular and molecular life sciences : CMLS · 2016Review
- Roles and Clinical Applications of OPG and TRAIL as Biomarkers in Cardiovascular Disease.BioMed research international · 2016Review
- Simvastatin reduces burn injury-induced splenic apoptosis via downregulation of the TNF-α/NF-κB pathway.Annals of surgery · 2015Article
- Dual regulation of tumor necrosis factor-α on myosin light chain phosphorylation in vascular smooth muscle.American journal of physiology. Heart and circulatory physiology · 2015Article
- The Tm7sf2 Gene Deficiency Protects Mice against Endotoxin-Induced Acute Kidney Injury.PloS one · 2015Article
- Antigen-induced airway hyperresponsiveness and obstruction is related to caveolin-1 expression in airway smooth muscle in a guinea pig asthma model.Clinical and translational allergy · 2015Article
- TRAIL modulates the immune system and protects against the development of diabetes.Journal of immunology research · 2015Review
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2 authors at 1 institution in 1 country.
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Abstract
Tumor necrosis factor (TNF)-alpha-induced activation of RhoA, mediated by TNF receptor 1 (TNFR1), is a prerequisite step in a pathway that leads to increased 20-kDa light chain of myosin (MLC20) phosphorylation and airway smooth muscle contraction. In this study, we have investigated the proximal events in TNF-alpha-induced RhoA activation. TNFR1 is localized to both lipid raft and nonraft regions of the plasma membrane in primary human airway smooth muscle cells. TNF-alpha engagement of TNFR1 recruited the adaptor proteins TRADD, TRAF-2, and RIP into lipid rafts and activated RhoA, NF-kappaB, and MAPK pathways. Depletion of cholesterol from rafts with methyl-beta-cyclodextrin caused a redistribution of TNFR1 to nonraft plasma membrane and prevented ligand-induced RhoA activation. By contrast, TNF-alpha-induced activation of NF-kappaB and MAPKs was unaffected by methyl-beta-cyclodextrin indicating that, in airway smooth muscle cells, activation of these pathways occurred independently of lipid rafts. Targeted knockdown of caveolin-1 completely abrogated TNF-alpha-induced RhoA activation, identifying this raft-resident protein as a positive regulator of the activation process. The signaling adaptors TRADD and RIP were also found to be necessary for ligand-induced RhoA activation. Taken together, our results suggest that in airway smooth muscle cells, spatial compartmentalization of TNFR1 provides a mechanism for generating distinct signaling outcomes in response to ligand engagement and define a mechanistic role for lipid rafts and caveolin-1 in TNF-alpha-induced activation of RhoA.
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