{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ye F"],"funding":["Young Talent Cultivation Program of Military Medical Science and Technology, Army Medical University","National Natural Science Foundation of China"],"pagination":["1034-1044"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8557681"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(5)"],"pubmed_abstract":["Sulfur mustard (a type of vesicant) can directly damage lung bronchial epithelium via aerosol inhalation, and prevalent cell death is an early event that obstructs the respiratory tract. JNK/c-Jun is a stress response pathway, but its role in cell death of the injured cells is not clear. Here, we report that JNK/c-Jun was activated in immortalized human bronchial epithelial (HBE) cells exposed to a lethal dose (20 μM) of nitrogen mustard (NM, a sulfur mustard analog). c-Jun silencing using small-interfering RNA (siRNA) rendered the cells resistant to NM-mediated cell death by blocking poly(ADP-ribose) polymerase 1 (PARP1) cleavage and DNA fragmentation. In addition, the transduction of upstream extrinsic (Fasl-Fas-caspase-8) and intrinsic (loss of Bcl-2 and mitochondrial membrane potential"],"journal":["Toxicology research"],"pubmed_title":["Small-interfering RNA for c-Jun attenuates cell death by preventing JNK-dependent PARP1 cleavage and DNA fragmentation in nitrogen mustard-injured immortalized human bronchial epithelial cells."],"pmcid":["PMC8557681"],"funding_grant_id":["20QNPY001","81502711","81803279"],"pubmed_authors":["Zou Z","Dan G","Chen M","Yu W","Ye F","Sai Y","Zhao Y","Cheng J"],"additional_accession":[]},"is_claimable":false,"name":"Small-interfering RNA for c-Jun attenuates cell death by preventing JNK-dependent PARP1 cleavage and DNA fragmentation in nitrogen mustard-injured immortalized human bronchial epithelial cells.","description":"Sulfur mustard (a type of vesicant) can directly damage lung bronchial epithelium via aerosol inhalation, and prevalent cell death is an early event that obstructs the respiratory tract. JNK/c-Jun is a stress response pathway, but its role in cell death of the injured cells is not clear. Here, we report that JNK/c-Jun was activated in immortalized human bronchial epithelial (HBE) cells exposed to a lethal dose (20 μM) of nitrogen mustard (NM, a sulfur mustard analog). c-Jun silencing using small-interfering RNA (siRNA) rendered the cells resistant to NM-mediated cell death by blocking poly(ADP-ribose) polymerase 1 (PARP1) cleavage and DNA fragmentation. In addition, the transduction of upstream extrinsic (Fasl-Fas-caspase-8) and intrinsic (loss of Bcl-2 and mitochondrial membrane potential","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2025-04-04T21:48:16.635Z","creation":"2024-11-21T10:31:16.028Z"},"accession":"S-EPMC8557681","cross_references":{"pubmed":["34733488"],"doi":["10.1093/toxres/tfab081"]}}