| http://purl.uniprot.org/citations/27693468 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27693468 | http://www.w3.org/2000/01/rdf-schema#comment | "The acute respiratory distress syndrome (ARDS) is a serious condition resulting from direct or indirect lung injury that is associated with high mortality and morbidity. A key biological event in the pathogenesis of the acute lung injury (ALI) that causes acute respiratory distress syndrome is activation of the lung endothelium cells (ECs), which is triggered by a variety of inflammatory insults leading to barrier disruption and excessive accumulation of neutrophils. Recently, we demonstrated that imatinib protects against lipopolysaccharide (LPS)-induced EC activation by inhibiting c-Abl kinase. In the present study, we explored the role of parkin, a novel c-Abl substrate, in ALI. Parkin is an E3 ubiquitin ligase originally characterized in the pathogenesis of Parkinson disease; however, its potential role in acute inflammatory processes and lung EC function remains largely unknown. Using parkin deficient (PARK2-/-) mice, we now demonstrate that parkin mediates LPS-induced ALI. After LPS, PARK2-/-mice have reduced total protein and cell levels in bronchoalveolar lavage (BAL) compared to wild type. Moreover, in LPS-treated PARK2-/-lungs, the sequestration and activation of neutrophils and release of inflammatory cytokines (interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α]) are significantly reduced. The BAL levels of soluble VCAM-1 and ICAM-1 are also decreased in LPS-treated PARK2-/-mice compared to wild type. In cultured human lung endothelial cells, downregulation of parkin by small interfering RNA decreases LPS-induced VCAM-1 expression, IL-8 and IL-6 secretion, and NF-kB phosphorylation. These results suggest a previously unidentified role of parkin in mediating endotoxin-induced endothelial proinflammatory signaling and indicate that it may play a critical role in acute inflammation."xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.trsl.2016.09.002"xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/author | "Wang H."xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/author | "Dudek S.M."xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/author | "Sammani S."xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/author | "Letsiou E."xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/author | "Belvitch P."xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/name | "Transl Res"xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/pages | "71-82"xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/title | "Parkin regulates lipopolysaccharide-induced proinflammatory responses in acute lung injury."xsd:string |
| http://purl.uniprot.org/citations/27693468 | http://purl.uniprot.org/core/volume | "181"xsd:string |
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