{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ramos RB"],"funding":["National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["jcs261323"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10560554"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["136(18)"],"pubmed_abstract":["Endothelial dysfunction is a crucial factor in promoting organ failure during septic shock. However, the underlying mechanisms are unknown. Here, we show that kidney injury after lipopolysaccharide (LPS) insult leads to strong endothelial transcriptional and epigenetic responses. Furthermore, SOCS3 loss leads to an aggravation of the responses, demonstrating a causal role for the STAT3-SOCS3 signaling axis in the acute endothelial response to LPS. Experiments in cultured endothelial cells demonstrate that IL-6 mediates this response. Furthermore, bioinformatics analysis of in vivo and in vitro transcriptomics and epigenetics suggests a role for STAT, AP1 and interferon regulatory family (IRF) transcription factors. Knockdown of STAT3 or the AP1 member JunB partially prevents the changes in"],"journal":["Journal of cell science"],"pubmed_title":["Shock drives a STAT3 and JunB-mediated coordinated transcriptional and DNA methylation response in the endothelium."],"pmcid":["PMC10560554"],"funding_grant_id":["R01GM124133","R01 GM124133"],"pubmed_authors":["Ramos RB","Balasubramanian U","Di John Portela I","Adam AP","Zuo MXG","Chuy D","Lu S","Martino N","Vincent PA"],"additional_accession":[]},"is_claimable":false,"name":"Shock drives a STAT3 and JunB-mediated coordinated transcriptional and DNA methylation response in the endothelium.","description":"Endothelial dysfunction is a crucial factor in promoting organ failure during septic shock. However, the underlying mechanisms are unknown. Here, we show that kidney injury after lipopolysaccharide (LPS) insult leads to strong endothelial transcriptional and epigenetic responses. Furthermore, SOCS3 loss leads to an aggravation of the responses, demonstrating a causal role for the STAT3-SOCS3 signaling axis in the acute endothelial response to LPS. Experiments in cultured endothelial cells demonstrate that IL-6 mediates this response. Furthermore, bioinformatics analysis of in vivo and in vitro transcriptomics and epigenetics suggests a role for STAT, AP1 and interferon regulatory family (IRF) transcription factors. Knockdown of STAT3 or the AP1 member JunB partially prevents the changes in","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Sep","modification":"2026-04-29T11:57:55.586Z","creation":"2025-04-06T16:07:24.252Z"},"accession":"S-EPMC10560554","cross_references":{"pubmed":["37667913"],"doi":["10.1242/jcs.261323"]}}