Title : α1-nAchR-Mediated Signaling Through Lipid Raft Is Required for Nicotine-Induced NLRP3 Inflammasome Activation and Nicotine-Accelerated Atherosclerosis.

Pub. Date : 2021

PMID : 34490270






8 Functional Relationships(s)
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1 alpha1-nAchR-Mediated Signaling Through Lipid Raft Is Required for Nicotine-Induced NLRP3 Inflammasome Activation and Nicotine-Accelerated Atherosclerosis. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
2 alpha1-nAchR-Mediated Signaling Through Lipid Raft Is Required for Nicotine-Induced NLRP3 Inflammasome Activation and Nicotine-Accelerated Atherosclerosis. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
3 Mechanically, nicotine increased the expression of alpha1-nAChR and stimulated the accumulation of alpha1-nAChR in lipid raft, leading to NLRP3 inflammasome activation in macrophage. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
4 Conversely, silencing of alpha1-nAChR in macrophage sufficiently blocked the pro-inflammasome activation effect of nicotine, indicating that alpha1-nAChR was the specific receptor for nicotine in triggering NLRP3 inflammasome in macrophage. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
5 Conversely, silencing of alpha1-nAChR in macrophage sufficiently blocked the pro-inflammasome activation effect of nicotine, indicating that alpha1-nAChR was the specific receptor for nicotine in triggering NLRP3 inflammasome in macrophage. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
6 Furthermore, both the destruction of lipid raft by methyl-beta-cyclodextrin and the interference of lipid raft clustering by silencing acid sphingomyelinase reversed nicotine-induced NLRP3 inflammasome activation by reducing the accumulation of alpha1-nAChR in lipid raft in macrophage, suggesting lipid raft-mediated accumulation of alpha1-nAChR was the key event in regulating the pro-inflammatory effects of nicotine in macrophage. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
7 Furthermore, both the destruction of lipid raft by methyl-beta-cyclodextrin and the interference of lipid raft clustering by silencing acid sphingomyelinase reversed nicotine-induced NLRP3 inflammasome activation by reducing the accumulation of alpha1-nAChR in lipid raft in macrophage, suggesting lipid raft-mediated accumulation of alpha1-nAChR was the key event in regulating the pro-inflammatory effects of nicotine in macrophage. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
8 Conclusion: alpha1-nAChR-mediated signaling through lipid raft is required for NLRP3 inflammasome activation and pro-atherosclerotic property of nicotine. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus