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dc.contributor.authorZiraldo, Cordelia
dc.contributor.authorVodovotz, Yoram
dc.contributor.authorNamas, Rami A.
dc.contributor.authorAlmahmoud, Khalid
dc.contributor.authorTapias, Victor
dc.contributor.authorMi, Qi
dc.contributor.authorBarclay, Derek
dc.contributor.authorJefferson, Bahiyyah S.
dc.contributor.authorChen, Guoqiang
dc.contributor.authorBilliar, Timothy R.
dc.contributor.authorZamora, Ruben
dc.date.accessioned2024-01-01T21:35:42Z
dc.date.available2024-01-01T21:35:42Z
dc.date.issued2013
dc.identifier.citationPLoS ONE, Diciembre 2013, vol. 8, n. 12, p. e79804es
dc.identifier.issn1932-6203
dc.identifier.urihttps://uvadoc.uva.es/handle/10324/63880
dc.descriptionProducción Científicaes
dc.description.abstractThe translation of in vitro findings to clinical outcomes is often elusive. Trauma/hemorrhagic shock (T/HS) results in hepatic hypoxia that drives inflammation. We hypothesize that in silico methods would help bridge in vitro hepatocyte data and clinical T/HS, in which the liver is a primary site of inflammation. Primary mouse hepatocytes were cultured under hypoxia (1% O2) or normoxia (21% O2) for 1-72 h, and both the cell supernatants and protein lysates were assayed for 18 inflammatory mediators by Luminex™ technology. Statistical analysis and data-driven modeling were employed to characterize the main components of the cellular response. Statistical analyses, hierarchical and k-means clustering, Principal Component Analysis, and Dynamic Network Analysis suggested MCP-1/CCL2 and IL-1α as central coordinators of hepatocyte-mediated inflammation in C57BL/6 mouse hepatocytes. Hepatocytes from MCP-1-null mice had altered dynamic inflammatory networks. Circulating MCP-1 levels segregated human T/HS survivors from non-survivors. Furthermore, T/HS survivors with elevated early levels of plasma MCP-1 post-injury had longer total lengths of stay, longer intensive care unit lengths of stay, and prolonged requirement for mechanical ventilation vs. those with low plasma MCP-1. This study identifies MCP-1 as a main driver of the response of hepatocytes in vitro and as a biomarker for clinical outcomes in T/HS, and suggests an experimental and computational framework for discovery of novel clinical biomarkers in inflammatory diseases.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.titleCentral Role for MCP-1/CCL2 in Injury-Induced Inflammation Revealed by In Vitro, In Silico, and Clinical Studieses
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.1371/journal.pone.0079804es
dc.identifier.publicationfirstpagee79804es
dc.identifier.publicationissue12es
dc.identifier.publicationtitlePLoS ONEes
dc.identifier.publicationvolume8es
dc.peerreviewedSIes
dcterms.rightsAtribución 4.0 Internacional
dc.identifier.essn1932-6203es
dc.type.hasVersioninfo:eu-repo/semantics/draftes


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