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MPO/HOCl upregulates gene expression of mitophagy in murine macrophages

GSE311973 Mus musculus Expression profiling by high throughput sequencing 12 samples 2026/06/19 GPL24247
Summary
HOCl, the main product of myeloperoxidase in vivo, could induce extensive cell damage, however, how HOCl regulates gene transcription remains unclear. In this study, we treated murine macrophage cell line with different concentrations of HOCl to clarify the regulatory role of MPO on inflammatory environment. Results showed that HOCl could induce the upregulation of autophagy-related genes and extensive changes on mitochondria-related gene expression. These results were validated by other experiments, like RT-qPCR and WB. And we also observed that HOCl could induce colocalization of autophagosomes and mitochondria in confocal images, showing mitophagy. These results were consistent with in vivo experiments showing that macrophage mitophagy was MPO-dependent. One interesting result in our study was that the vehicle of HOCl treatment, HBSS, and the sublethal HOCl could also regulate macrophage function, which was mostly ignored by HOCl-related studies.
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NCBI GEO page ↗ Paper (PMID 42025704) ↗ {# Names what the click gives you. "Open in finder" meant nothing to a visitor who arrived from a search engine and has never seen the tool. #} Find more mouse RNA-seq datasets →
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