A calpain inhibitor protects against fractalkine production in lipopolysaccharide-treated endothelial cells
DC Field | Value | Language |
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dc.contributor.author | Jang, Jaewoong | - |
dc.contributor.author | Yoon, Yoo Sik | - |
dc.contributor.author | Oh, Dong-Jin | - |
dc.date.available | 2019-03-08T07:58:29Z | - |
dc.date.issued | 2017-09 | - |
dc.identifier.issn | 2211-9132 | - |
dc.identifier.issn | 2211-9140 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/4058 | - |
dc.description.abstract | Background: Fractalkine (CX3CL1) is a chemokine with a unique CX3C motif and is produced by endothelial cells stimulated with lipopolysaccharide (LPS), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, and interferon-gamma. There have been several reports that the caspase/calpain system is activated in endotoxemia, which leads to cellular apoptosis and acute inflammatory processes. We aimed to determine the role of the caspase/calpain system in cell viability and regulation of fractalkine production in LPS-treated endothelial cells. Methods: Human umbilical vein endothelial cells (HUVECs) were stimulated with 0.01-100 mu g/mL of LPS to determine cell viability. The changes of CX3CL1 expression were compared in control, LPS (1 mu g/mL)-, IL-1 alpha (1 mu g/ mL)-, and IL-1 beta (1 mu g/mL)-treated HUVECs. Cell viability and CX3CL1 production were compared with 50 mu M of inhibitors of caspase-1, caspase-3, caspase-9, and calpain in LPS-treated HUVECs. Results: Cell viability was significantly decreased from 1 to 100 mu g/mL of LPS. Cell viability was significantly restored with inhibitors of caspase-1, caspase-3, caspase-9, and calpain in LPS-treated HUVECs. The expression of CX3CL1 was highest in IL-1 beta-treated HUVECs. CX3CL1 production was highly inhibited with a calpain inhibitor and significantly decreased with the individual inhibitors of caspase-1, caspase-3, and caspase-9. Conclusion: The caspase/calpain system is an important modulator of cell viability and CX3CL1 production in LPS-treated endothelial cells. | - |
dc.format.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | ELSEVIER INC | - |
dc.title | A calpain inhibitor protects against fractalkine production in lipopolysaccharide-treated endothelial cells | - |
dc.type | Article | - |
dc.identifier.doi | 10.23876/j.krcp.2017.36.3.224 | - |
dc.identifier.bibliographicCitation | KIDNEY RESEARCH AND CLINICAL PRACTICE, v.36, no.3, pp 224 - 231 | - |
dc.identifier.kciid | ART002258097 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.wosid | 000425053700003 | - |
dc.identifier.scopusid | 2-s2.0-85034837373 | - |
dc.citation.endPage | 231 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 224 | - |
dc.citation.title | KIDNEY RESEARCH AND CLINICAL PRACTICE | - |
dc.citation.volume | 36 | - |
dc.type.docType | Article | - |
dc.publisher.location | 대한민국 | - |
dc.subject.keywordAuthor | Calpain | - |
dc.subject.keywordAuthor | Caspase | - |
dc.subject.keywordAuthor | CX3CL1 | - |
dc.subject.keywordAuthor | Endothelial cells | - |
dc.subject.keywordAuthor | Lipopolysaccharides | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | ACUTE-RENAL-FAILURE | - |
dc.subject.keywordPlus | VASCULAR DYSFUNCTION | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | INDUCED SEPSIS | - |
dc.subject.keywordPlus | TNF-ALPHA | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | CHEMOKINE | - |
dc.subject.keywordPlus | CHEMOATTRACTANT | - |
dc.relation.journalResearchArea | Urology & Nephrology | - |
dc.relation.journalWebOfScienceCategory | Urology & Nephrology | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | esci | - |
dc.description.journalRegisteredClass | kci | - |
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