{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Husain MA"],"funding":["U.S. Department of Veterans Affairs (VA)","U.S. Department of Veterans Affairs"],"pagination":["e70588"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12046946"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(9)"],"pubmed_abstract":["Neuroinflammation is a major driver of secondary tissue damage after spinal cord injury (SCI). Within minutes after SCI, activated microglia and astrocytes produce proinflammatory mediators such as TNF-α, IL-6, iNOS, and COX-2 which induce tissue injury through cytotoxicity, vascular hyperpermeability, and secondary ischemia. The inflammatory cascade is amplified by chemokines like CCL2 and CXCL1 which recruit immune cells to the injured site. HuR is an RNA regulator that promotes glial expression of many proinflammatory factors by binding to adenylate- and uridylate-rich elements in the 3' untranslated regions of their mRNAs. SRI-42127 is a small molecule which blocks HuR function by preventing its nucleocytoplasmic translocation. This study aimed to evaluate the potential of SRI-42127 to"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Inhibition of the RNA Regulator HuR Mitigates Spinal Cord Injury by Potently Suppressing Post-Injury Neuroinflammation."],"pmcid":["PMC12046946"],"funding_grant_id":["BX006244","BX005899"],"pubmed_authors":["DeBerry JJ","Husain MA","Guha A","Andrabi SA","Kaimari A","Nabors LB","Filippova N","Sorge RE","Si Y","Webb CK","Smith R","Cardozo CP","Hassan AZ","Smith KA","King PH"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of the RNA Regulator HuR Mitigates Spinal Cord Injury by Potently Suppressing Post-Injury Neuroinflammation.","description":"Neuroinflammation is a major driver of secondary tissue damage after spinal cord injury (SCI). Within minutes after SCI, activated microglia and astrocytes produce proinflammatory mediators such as TNF-α, IL-6, iNOS, and COX-2 which induce tissue injury through cytotoxicity, vascular hyperpermeability, and secondary ischemia. The inflammatory cascade is amplified by chemokines like CCL2 and CXCL1 which recruit immune cells to the injured site. HuR is an RNA regulator that promotes glial expression of many proinflammatory factors by binding to adenylate- and uridylate-rich elements in the 3' untranslated regions of their mRNAs. SRI-42127 is a small molecule which blocks HuR function by preventing its nucleocytoplasmic translocation. This study aimed to evaluate the potential of SRI-42127 to","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-04-23T03:18:55.86Z","creation":"2025-07-02T03:04:57.131Z"},"accession":"S-EPMC12046946","cross_references":{"pubmed":["40317946"],"doi":["10.1096/fj.202500236R"]}}