| http://purl.uniprot.org/citations/38069081 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/38069081 | http://www.w3.org/2000/01/rdf-schema#comment | "Acute lung injury (ALI) is characterized by endothelial barrier disruption and associated inflammatory responses, and transient receptor potential cation channel 6 (TRPC6)-mediated Ca2+ influx is critical for endothelial hyperpermeability. In this study, we investigated the role of TRPC6 in LPS-induced ALI, analyzed gene expression in WT and TRPC6-/- lungs using RNA sequencing, and explored the effects of TRPC6 in the LPS-induced hyperpermeability in human umbilical vein endothelial cells (HUVECs) to elucidate the underlying mechanisms. Intratracheal instillation of LPS caused edema in the mouse lungs. Deletion of TRPC6 reduced LPS-induced lung edema and decreased cell infiltration. RNA sequencing analysis suggested that downregulated cell adhesion molecules in TRPC6-/- lungs may be responsible for their resistance to LPS-induced injury. In addition, downregulation of TRPC6 significantly alleviated the LPS-induced decrease in eNOS expression in lung tissue as well as in HUVECs. Moreover, inhibition of TRPC6 with the channel antagonist larixyl led to a decrease in LPS-induced hyperpermeability and ROS production in HUVECs, which could be reversed by blocking eNOS. Our findings suggest that inhibition of TRPC6 ameliorates LPS-induced ALI, which may be achieved by acting on the cell adhesion molecule signaling pathway and participating in the regulation of eNOS levels in endothelial cells."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.org/dc/terms/identifier | "doi:10.3390/ijms242316756"xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/author | "Chen X."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/author | "Guo J."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/author | "Zhang X."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/author | "Wang M."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/author | "Yang F."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/author | "Yang S."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/name | "Int J Mol Sci"xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/pages | "16756"xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/title | "TRPC6 Deletion Enhances eNOS Expression and Reduces LPS-Induced Acute Lung Injury."xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://purl.uniprot.org/core/volume | "24"xsd:string |
| http://purl.uniprot.org/citations/38069081 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/38069081 |
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