{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(1)"],"submitter":["Li XH"],"pubmed_abstract":["N-methyl-d-aspartate (NMDA) receptor (NMDAR) activation mediates glutamate (Glu) toxicity and involves bleomycin (BLM)-induced acute lung injury (ALI). We have reported that bone marrow-derived mesenchymal stem cells (BM-MSCs) are NMDAR-regulated target cells, and NMDAR activation inhibits the protective effect of BM-MSCs on BLM-induced pulmonary fibrosis, but its effect on ALI remains unknown. Here, we found that Glu release was significantly elevated in plasma of mice at d 7 after intratracheally injected with BLM. BM-MSCs were pretreated with NMDA (the selective agonist of NMDAR) and transplanted into the recipient mice after the BLM challenge. BM-MSCs administration significantly alleviated the pathological changes, inflammatory response, myeloperoxidase activity, and malondialdehyde c"],"journal":["Heliyon"],"pagination":["e23723"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10776937"],"repository":["biostudies-literature"],"pubmed_title":["NMDAR activation attenuates the protective effect of BM-MSCs on bleomycin-induced ALI via the COX-2/PGE<sub>2</sub> pathway."],"pmcid":["PMC10776937"],"pubmed_authors":["Yue SJ","Cheng HP","Feng DD","Luo ZQ","Han Y","Li XH","Zhou Y","Huang P"],"additional_accession":[]},"is_claimable":false,"name":"NMDAR activation attenuates the protective effect of BM-MSCs on bleomycin-induced ALI via the COX-2/PGE<sub>2</sub> pathway.","description":"N-methyl-d-aspartate (NMDA) receptor (NMDAR) activation mediates glutamate (Glu) toxicity and involves bleomycin (BLM)-induced acute lung injury (ALI). We have reported that bone marrow-derived mesenchymal stem cells (BM-MSCs) are NMDAR-regulated target cells, and NMDAR activation inhibits the protective effect of BM-MSCs on BLM-induced pulmonary fibrosis, but its effect on ALI remains unknown. Here, we found that Glu release was significantly elevated in plasma of mice at d 7 after intratracheally injected with BLM. BM-MSCs were pretreated with NMDA (the selective agonist of NMDAR) and transplanted into the recipient mice after the BLM challenge. BM-MSCs administration significantly alleviated the pathological changes, inflammatory response, myeloperoxidase activity, and malondialdehyde c","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jan","modification":"2025-04-05T23:39:49.985Z","creation":"2025-04-05T23:39:49.985Z"},"accession":"S-EPMC10776937","cross_references":{"pubmed":["38205313"],"doi":["10.1016/j.heliyon.2023.e23723"]}}