| http://purl.uniprot.org/citations/38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/38184221 | http://www.w3.org/2000/01/rdf-schema#comment | "Endothelial dysfunction plays a pivotal role in the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Dipeptidyl peptidase IV (DPP-4), a cell surface glycoprotein, has been implicated in endothelial inflammation and barrier dysfunction. In this study, the role of DPP-4 on lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial cells (HPMECs) dysfunction and the underlying mechanism were investigated by siRNA-mediated knockdown of DPP-4. Our results indicated that LPS (1 μg/ml) challenge resulted in either the production and releasing of DPP-4, as well as the secretion of IL-6 and IL-8 in HPMECs. DPP-4 knockdown inhibited chemokine releasing and monolayer hyper-permeability in LPS challenged HPMECs. When cocultured with human polymorphonuclear neutrophils (PMNs), DPP4 knockdown suppressed LPS-induced neutrophil-endothelial adhesion, PMN chemotaxis and trans-endothelial migration. Western blotting showed that DPP-4 knockdown attenuated LPS-induced activation of TLR4/NF-κB pathway. Immunoprecipitation and liquid chromatography-tandem mass spectrometry revealed that DPP-4 mediated LPS-induced endothelial inflammation by interacting with integrin-α5β1. Moreover, exogenous soluble DPP-4 treatment sufficiently activated integrin-α5β1 downstream FAK/AKT/NF-κB signaling, thereafter inducing ICAM-1 upregulation in HPMECs. Collectively, our results suggest that endothelia synthesis and release DPP-4 under the stress of endotoxin, which interact with integrin-α5β1 complex in an autocrine or paracrine manner to exacerbate endothelial inflammation and enhance endothelial cell permeability. Therefore, blocking DDP-4 could be a potential therapeutic strategy to prevent endothelial dysfunction in ALI/ARDS."xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.yexcr.2023.113909"xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/author | "Kong H."xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/author | "Fan J."xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/author | "Liu C."xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/author | "Xu J."xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/author | "Xie W."xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/author | "Liu C.'"xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/date | "2024"xsd:gYear |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/name | "Exp Cell Res"xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/pages | "113909"xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/title | "DPP-4 exacerbates LPS-induced endothelial cells inflammation via integrin-alpha5beta1/FAK/AKT signaling."xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://purl.uniprot.org/core/volume | "435"xsd:string |
| http://purl.uniprot.org/citations/38184221 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/38184221 |
| http://purl.uniprot.org/citations/38184221 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A059VC25-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A7S4ZD15-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A7S4ZD17-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A7S4ZD76-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A7S4ZDQ1-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A7S4ZDW8-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A7S5DJN1-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A0A7S5DJP9-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |
| http://purl.uniprot.org/uniprot/#_A8K6A5-mappedCitation-38184221 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/38184221 |