Till sidans topp

Sidansvarig: Webbredaktion
Sidan uppdaterades: 2012-09-11 15:12

Tipsa en vän
Utskriftsversion

Expression of the Nrf2-sy… - Göteborgs universitet Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

Expression of the Nrf2-system at the blood-CSF barrier is modulated by neonatal inflammation and hypoxia-ischemia

Artikel i vetenskaplig tidskrift
Författare Barbara D'angelo
C. Joakim Ek
Mats Sandberg
Carina Mallard
Publicerad i Journal of Inherited Metabolic Disease
Volym 36
Nummer/häfte 3
Sidor 479-490
ISSN 0141-8955
Publiceringsår 2013
Publicerad vid Institutionen för neurovetenskap och fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för biomedicin
Sidor 479-490
Språk en
Länkar dx.doi.org/10.1007/s10545-012-9551-...
Ämnesord cerebrospinal-fluid, choroid-plexus, brain-injury, multidrug-resistance, heme oxygenase-1, gene-expression, nervous-system, immature brain, mouse, model, protects
Ämneskategorier Fysiologi

Sammanfattning

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.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?

Denna text är utskriven från följande webbsida:
http://www.gu.se/forskning/publikation/?publicationId=180072
Utskriftsdatum: 2020-01-23