| http://purl.uniprot.org/citations/28181168 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28181168 | http://www.w3.org/2000/01/rdf-schema#comment | "Endothelial dysfunction plays a vital role during the initial stage of atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) induces vascular endothelial injury and vessel wall inflammation. Sphingosine-1-phosphate (S1P) exerts numerous vasoprotective effects by binding to diverse S1P receptors (S1PRs; S1PR1-5). A number of studies have shown that in endothelial cells (ECs), S1PR2 acts as a pro-atherosclerotic mediator by stimulating vessel wall inflammation through the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Scavenger receptor class B member I (SR-BI), a high-affinity receptor for apolipoprotein A-I (apoA-I)/high-density lipoprotein (HDL), inhibits nuclear factor-κB (NF-κB) translocation and decreases the plasma levels of inflammatory mediators via the PI3K/Akt pathway. We hypothesized that the inflammatory effects of S1P/S1PR2 on ECs may be regulated by apoA-I/SR-BI. The results showed that ox-LDL, a pro-inflammatory factor, augmented the S1PR2 level in human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner. In addition, S1P/S1PR2 signaling influenced the levels of inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-10, aggravating inflammation in HUVECs. Moreover, the pro-inflammatory effects induced by S1P/S1PR2 were attenuated by SR-BI overexpression and enhanced by an SR-BI inhibitor, BLT-1. Further experiments showed that the PI3K/Akt signaling pathway was involved in this process. Taken together, these results demonstrate that apoA-I/SR-BI negatively regulates S1P/S1PR2-mediated inflammation in HUVECs by activating the PI3K/Akt signaling pathway."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.org/dc/terms/identifier | "doi:10.1007/s13105-017-0553-5"xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Jiang Y."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Li L."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Lu Y.J."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Ren K."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Zhang Q.H."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Tang Z.L."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Yi G.H."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Mo Z.C."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "Peng X.S."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/author | "-Liu X."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/name | "J Physiol Biochem"xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/pages | "287-296"xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/title | "ApoA-I/SR-BI modulates S1P/S1PR2-mediated inflammation through the PI3K/Akt signaling pathway in HUVECs."xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://purl.uniprot.org/core/volume | "73"xsd:string |
| http://purl.uniprot.org/citations/28181168 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28181168 |
| http://purl.uniprot.org/citations/28181168 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/28181168 |
| http://purl.uniprot.org/uniprot/#_A0A024R3E3-mappedCitation-28181168 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28181168 |
| http://purl.uniprot.org/uniprot/#_A0A0S2Z3N2-mappedCitation-28181168 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28181168 |
| http://purl.uniprot.org/uniprot/#_A0A0S2Z3I2-mappedCitation-28181168 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28181168 |
| http://purl.uniprot.org/uniprot/#_B4E3I1-mappedCitation-28181168 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28181168 |
| http://purl.uniprot.org/uniprot/#_B4DZ71-mappedCitation-28181168 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/28181168 |