DHA upregulates FADS2 expression in primary cortical astrocytes exposed to vitamin A

Title:

DHA upregulates FADS2 expression in primary cortical astrocytes exposed to vitamin A

Creator:

Dziedzic, B., Bewicz-Binkowska, D., Zgorzynska, E., Stulczewski, D., Wieteska, L., Kaza, B., and Walczewska, A.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:65f67383-8f63-498c-a3b7-416b96546695
uuid:65f67383-8f63-498c-a3b7-416b96546695
issn:0862-8408

Subject:

vitamin A, palmitic acid, FADS2, α-linolenic acid, docosahexaenoic acid, astrocytes, 14, and 612

Type:

model:article and TEXT

Format:

print, bez média, and svazek

Description:

The fads2 gene encoding Δ6-desaturase, the rate-limiting enzyme of the LCPUFA biosynthesis is expressed in astrocytes. Dietary fatty acids, which cross the blood-brain barrier, may regulate the transcription of lipogenic enzymes through activation of transcription factors such as peroxisome proliferator-activated receptors (PPARs). The PPARs form the transcription complex with retinoid X receptors (RXRs) that are activated by 9-cis retinoic acid, a metabolite of vitamin A (VA). The study examines whether challenge of astrocytes with VA, prior 24-h treatment with palmitic acid (PA), α-linolenic acid (ALA) or docosahexaenoic acid (DHA) has the effect on the FADS2 expression. RT-qPCR showed that in astrocytes not challenged with VA, PA increased fads2 gene expression and DHA decreased it. However, in VA-primed astrocytes, PA doubled the FADS2 mRNA levels, while DHA increased fads2 gene expression, oppositely to non-primed cells. Furthermore, similar changes were seen in VA-primed astrocytes with regard to Δ6-desaturase protein levels following PA and DHA treatment. ALA did not have any effect on the FADS2 mRNA and protein levels in either VA-primed or non-primed astrocytes. These findings indicate that in the presence of vitamin A, DHA upregulates fads2 gene expression in astrocytes., B. Dziedzic, D. Bewicz-Binkowska, E. Zgorzynska, D. Stulczewski, L. Wieteska, B. Kaza, A.Walczewska., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:4

Harvested from:

CDK

Metadata only:

false