ArticleCell death & disease2016
PML regulates neuroprotective innate immunity and neuroblast commitment in a hypoxic-ischemic encephalopathy model.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- PML is crucial for neural stem cell differentiation, stress tolerance and mitochondrial integrity.Stem cell reports · 2025Article
- Early transcriptional responses reveal cell type-specific vulnerability and neuroprotective mechanisms in the neonatal ischemic hippocampus.Acta neuropathologica communications · 2025Article
- Lactate receptor HCAR1 regulates neurogenesis and microglia activation after neonatal hypoxia-ischemia.eLife · 2022Article
- Adulthood systemic inflammation accelerates the trajectory of age-related cognitive decline.Aging · 2021Article
- Meteorin Is a Novel Therapeutic Target for Wet Age-Related Macular Degeneration.Journal of clinical medicine · 2021Article
- Profiling the Murine SUMO Proteome in Response to Cardiac Ischemia and Reperfusion Injury.Molecules (Basel, Switzerland) · 2020Article
- PML Regulates the Epidermal Differentiation Complex and Skin Morphogenesis during Mouse Embryogenesis.Genes · 2020Article
- PML Bodies in Mitosis.Cells · 2019Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulation of innate immune responses and activation of tissue regenerative processes are key elements in the pathophysiology of brain injuries. The promyelocytic leukemia (PML) gene was originally identified on a breakpoint of chromosomal translocation t(15;17) associated with acute PML. We have studied the role of PML protein during acute and regenerative phases after hypoxia-ischemia (HI) in brains of neonatal mice. We found that PML prevents tissue loss and apoptotic cell death selectively in subcortical regions of the brain at early stages after damage. In accordance with this, we revealed that PML is important for microglia activation and production of key inflammatory cytokines such as IL1α, IL1β, IL1RN, CXCL10, CCL12 and TNFα. During the regenerative phase, PML-depleted mice were found to have impaired transformation of transit-amplifying precursors into migratory progenitors. This was accompanied by increased ratios of symmetric versus asymmetric neural progenitor cell divisions during tissue repair and a specific defect in tissue restoration within the striatum 42 days after HI. The data demonstrate a dual role of PML in protection and recovery after brain injury.
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