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Docosahexaenoic acid up‐regulates both PI 3K/AKT‐dependent FABP 7–PPAR γ interaction and MKP 3 that enhance GFAP in developing rat brain astrocytes

Tripathi, Sachin, Kushwaha, Rajesh, Mishra, Juhi, Gupta, Manoj Kumar, Kumar, Harish, Sanyal, Somali, Singh, Dhirendra, Sanyal, Sabyasachi, Sahasrabuddhe, Amogh Anant, Kamthan, Mohan, Mudiam, Mohana Krishna Reddy, Bandyopadhyay, Sanghamitra·2017·Journal of Neurochemistry
DOI 10.1111/jnc.13879
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Abstract

The astrocyte marker, glial fibrillary acidic protein (GFAP), has essential functions in the brain, but may trigger astroglial scarring when expressed in excess. Docosahexaenoic acid (DHA) is an n‐3 fatty acid that is protective during brain development. However, the effect of DHA on GFAP levels of developing brain remains unexplored. Here, we detected that treating developing rats with DHA‐enriched fish‐oil caused dose‐dependent GFAP augmentation. We investigated the mechanism promoting GFAP, hypothesizing the participation of fatty acid‐binding protein‐7 (FABP 7), known to bind DHA. We identified that DHA stimulated FABP 7 expression in astrocytes, and FABP 7‐silencing suppressed DHA‐induced GFAP, indicating FABP 7‐mediated GFAP increase. Further investigation proved FABP 7 expression to be phosphatidylinositide 3‐kinases (PI 3K)/AKT and nuclear receptor peroxisome proliferator‐activated receptor‐gamma (PPAR γ)‐dependent. We found that PI 3K/AKT activated PPAR γ that triggered FABP 7 expression via PPAR γ‐responsive elements within its gene. Towards identifying FABP 7‐downstream pathways, we considered our previous report that demonstrated cyclin‐dependent kinase‐5 (CDK 5)‐PPAR γ‐protein–protein complex to suppress GFAP. We found that the DHA‐induced FABP 7 underwent protein‐protein interaction with PPAR γ, which impeded CDK 5‐PPAR γ formation. Hence, it appeared that enhanced FABP7‐PPAR γ in lieu of CDK 5‐PPAR γ resulted in increased GFAP. PI3K/AKT not only stimulated formation of FABP 7‐PPAR γ protein‐protein complex, but also up‐regulated a FABP 7‐independent MAP‐kinase‐phosphatase‐3 pathway that inactivated CDK 5 and hence attenuated CDK 5‐PPAR γ. Overall, our data reveal that via the proximal PI 3K/AKT, DHA induces FABP 7‐PPAR γ, through genomic and non‐genomic mechanisms, and MAP‐kinase‐phosphatase‐3 that converged at attenuated CDK 5‐PPAR γ and therefore, enhanced GFAP. Accordingly, our study demonstrates a DHA‐mediated astroglial hyperactivation, pointing toward a probable injurious role of DHA in brain development. image

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Metadata

Authors
Tripathi, S., Kushwaha, R., Mishra, J., Gupta, M. K., Kumar, H., Sanyal, S., Singh, D., Sanyal, S., Sahasrabuddhe, A. A., Kamthan, M., Mudiam, M. K. R., & Bandyopadhyay, S.
Affiliations
  • Developmental Toxicology Laboratory Systems Toxicology & Health Risk Assessment Group CSIR‐Indian Institute of Toxicology Research (IITR) Lucknow India
  • Academy of Scientific and Innovative Research (AcSIR) CSIR‐IITR campus Lucknow India
  • Division of Biochemistry CSIR‐Central Drug Research Institute (CDRI) Lucknow India
  • Amity Institute of Biotechnology Amity University (Lucknow campus) Lucknow India
  • Central Pathology Laboratory CSIR‐IITR Lucknow India
  • Division of Molecular and Structural Biology CSIR‐CDRI Lucknow India
  • Environmental Biotechnology Laboratory Environmental Toxicology Group CSIR‐IITR Lucknow India
  • Mass& Analytical (NCMS) Division CSIR‐Indian Institute of Chemical Technology Hyderabad Telangana India
ORCID
Bandyopadhyay, Sanghamitra
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2016-12-07
Volume
140
Issue
1
Pages
96-113
ISSN
  • 0022-3042
  • 1471-4159
DOI
10.1111/jnc.13879
Cited by
49
References
1
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Funders
Department of Biotechnology , Ministry of Science and Technology (GAP285)

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