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Expression of the Nrf2-system at the blood-CSF barrier is modulated by neonatal inflammation and hypoxia-ischemia
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- D'angelo, Barbara (author)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
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- Ek, C. Joakim (author)
- Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology
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- Sandberg, Mats, 1953 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för biomedicin,Institute of Biomedicine
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- (creator_code:org_t)
- 2012-10-30
- 2013
- English.
- In: Journal of Inherited Metabolic Disease. - : Wiley. - 0141-8955 .- 1573-2665. ; 36:3, s. 479-490
- Journal article (peer-reviewed)
Abstract
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- ORIGINAL ARTICLE Expression of the Nrf2-system at the blood-CSF barrier is modulated by neonatal inflammation and hypoxia-ischemia Barbara D ’ Angelo & C. Joakim Ek & Mats Sandberg & Carina Mallard Received: 29 May 2012 /Revised: 14 September 2012 /Accepted: 10 October 2012 /Published online: 30 October 2012 # SSIEM and Springer Science+Business Media Dordrecht 2012 Abstract Transcription factor NF-E2-related factor-2 (Nrf2) is a key regulator of endogenous anti-oxidant sys- tems shown to play a neuroprotective role in the adult by preserving blood – brain barrier function. The choroid plex- us, site for the blood-CSF barrier, has been suggested to be particularly important in maintaining brain barrier function in development. We investigated the expression of Nrf2- and detoxification-system genes in choroid plexus following systemic LPS injections, unilateral cerebral hypoxia- ischemia (HI) as well as the combination of LPS and HI (LPS/HI). Plexuses were collected at different time points after LPS, HI and LPS/HI in 9-day old mice. mRNA levels of Nrf2 and many of its target genes were analyzed by quantitative PCR. Cell death was analyzed by caspase-3 immunostaining and TUNEL. LPS caused down-regulation of the Nrf2-system genes while HI increased expression at earlier time points. LPS exposure prior to HI prevented many of the HI-induced gene increases. None of the insults resulted in any apparent cell death to choroidal epithelium. These data imply that the function of the inducible anti- oxidant system in the choroid plexus is down-regulated by inflammation, even if choroid cells are not structurally damaged. Further, LPS prevented the endogenous antioxi- dant response following HI, suggesting the possibility that the choroid plexus may be at risk if LPS is united with an insult that increases oxidative stress such as hypoxia- ischemia.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Physiology (hsv//eng)
Keyword
- cerebrospinal-fluid
- choroid-plexus
- brain-injury
- multidrug-resistance
- heme oxygenase-1
- gene-expression
- nervous-system
- immature brain
- mouse
- model
- protects
Publication and Content Type
- ref (subject category)
- art (subject category)
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