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FABP7 drives an inflammatory response in human astrocytes

ABSTRACT: To investigate the effect of FABP7 over-expression in human iPCS-derived astrocytes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE214628 | GEO | 2024/02/07

REPOSITORIES: GEO

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FABP7 drives an inflammatory response in human astrocytes

Project description:FABP7 drives an inflammatory response in human astrocytes

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Project description:Patients with epilepsy often experience increased frequency of seizures at night. Given the crucial role glial cells play in modulating neuronal excitability, we hypothesize that circadian changes in glia may affect changes in seizure threshold. Fatty acid binding protein 7 (Fabp7) is expressed in brain astrocytes and is involved in the transport of fatty acids, signal transduction, and gene transcription. Its mRNA expression levels rise and fall in a circadian rhythm and is necessary for normal sleep regulation. We examined if Fabp7 influences electrically induced seizure threshold and differential gene expression in wild type (WT) vs. Fabp7 knockout (KO) mice with and without seizure.

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Project description:To reveal the function of FABP7 in the inner ear, we evaluated gene expressions between Wild-type and Fabp7 KO mice one day after noise exposure at 10 weeks, using RNA sequencing analysis. The read number was approximately 27–32 million paired-end reads per sample. A total of 24 and 23 genes were identified as upregulated and downregulated differentially expressed genes (DEGs), respectively in Fabp7 KO mice. The upregulation of genes related to nicotinamide-adenine dinucleotide (NADH) dehydrogenase (mt-Nd1, 2, 3, 4, and 6) and a glial high-affinity glutamate transporter (solute carrier family 1, member 2: Slc1a2) and downregulation of genes related to C/D box small nucleolar RNAs were observed in Fabp7 KO mice.

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Project description:Fatty acid binding proteins (FABPs) are key regulators of lipid metabolism, energy homeostasis, and inflammation. They participate in fatty acid metabolism by regulating their uptake, transport, and availability of ligands to nuclear receptors. In the adult brain, FABP7 is especially abundant in astrocytes that are rich in cytoplasmic granules originated from damaged mitochondria. Mitochondrial dysfunction and oxidative stress have been implicated in the neurodegenerative process observed in amyotrophic lateral sclerosis (ALS), either as a primary cause or as a secondary component of the pathogenic process. Here we investigated the expression of FABP7 in animal models of human superoxide dismutase 1 (hSOD1)-linked ALS. In the spinal cord of symptomatic mutant hSOD1-expressing mice, FABP7 is upregulated in gray matter astrocytes. Using a coculture model, we examined the effect of increased FABP7 expression in astrocyte-motor neuron interaction. Our data show that FABP7 overexpression directly promotes an NF-κB-driven pro-inflammatory response in nontransgenic astrocytes that ultimately is detrimental for motor neuron survival. Addition of trophic factors, capable of supporting motor neuron survival in pure cultures, did not prevent motor neuron loss in cocultures with FABP7 overexpressing astrocytes. In addition, astrocyte cultures obtained from symptomatic hSOD1-expressing mice display upregulated FABP7 expression. Silencing endogenous FABP7 in these cultures decreases the expression of inflammatory markers and their toxicity toward cocultured motor neurons. Our results identify a key role of FABP7 in the regulation of the inflammatory response in astrocytes and identify FABP7 as a potential therapeutic target to prevent astrocyte-mediated motor neuron toxicity in ALS.

| S-EPMC7573932 | biostudies-literature

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