ArticleBrain pathology (Zurich, Switzerland)2012
NF-κB activity in perinatal brain during infectious and hypoxic-ischemic insults revealed by a reporter mouse.
Article in Brain pathology (Zurich, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Endothelial TDP-43 depletion disrupts core blood-brain barrier pathways in neurodegeneration.Nature neuroscience · 2025Article
- NKG2D knockdown improves hypoxic-ischemic brain damage by inhibiting neuroinflammation in neonatal mice.Scientific reports · 2024Article
- A20 regulates lymphocyte adhesion in murine neuroinflammation by restricting endothelial ICOSL expression in the CNS.The Journal of clinical investigation · 2023Article
- Targeted inCITE-Seq Analysis Identifies the Loss of Nuclear TDP-43 in Endothelium as a Mediator of Blood Brain Barrier Signaling Pathway Dysfunction in Neurodegeneration.bioRxiv : the preprint server for biology · 2023Article
- NF-kappa-B activation unveils the presence of inflammatory hotspots in human gut xenografts.PloS one · 2021Article
- Survival and Inflammatory Response in Adipose-derived Mesenchymal Stem Cell-enriched Mouse Fat Grafts.Plastic and reconstructive surgery. Global open · 2016Article
- Brain endothelial TAK1 and NEMO safeguard the neurovascular unit.The Journal of experimental medicine · 2015Article
- 17β-Estradiol Ameliorates Tight Junction Disruption via Repression of MMP Transcription.Molecular endocrinology (Baltimore, Md.) · 2015Article
- In vivo bioimaging with tissue-specific transcription factor activated luciferase reporters.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infants suffering from infection or hypoxia-ischemia around the time of birth can develop brain damage resulting in life-long impairment such as cerebral palsy, epilepsy and cognitive disability. Inflammation appears to be an important contributor irrespective of whether the primary event is infection or hypoxia-ischemia. Activation of the transcription factor NF-κB is a hallmark of inflammation. To study perinatal brain inflammation, we developed a transgenic reporter mouse for imaging NF-κB activity in live animals and tissue samples. The reporter genes firefly luciferase and a destabilized version of enhanced GFP (dEGFP) were regulated by common NF-κB sites using a bidirectional promoter. Luciferase activity was imaged in vivo, while dEGFP was detected at cellular level in tissue sections. In newborn mice subjected to experimental models of infections or hypoxia-ischemia; luciferase signal increased in brains of live animals. In brain sections dEGFP expression, revealing NF-κB activation was observed in the endothelial cells of the blood-brain barrier in all disease models. In meningitis and hypoxia-ischemia expression of dEGFP was also induced in perivascular astrocytes. In conclusion, by using this transgenic reporter mouse in experimental models of perinatal complications, we could assess NF-κB activity in vivo and subsequently determine the cellular origin in the tissues.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.