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Updated: Oct 2, 2025

Development of an Insert Co-culture System of Two Cellular Types in the Absence of Cell-Cell Contact

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Published on: July 17, 2016

LPS Administration Impacts Glial Immune Programs by Alternative Splicing.

Vladimir N Babenko¹, Galina T Shishkina¹, Dmitriy A Lanshakov¹

¹Laboratory of Functional Neurogenomics, Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Science, 630090 Novosibirsk, Russia.

|February 25, 2022

Summary

This summary is machine-generated.

Lipopolysaccharide (LPS) exposure alters gene expression in the brain, particularly in glial cells. Alternative splicing, especially of Ptbp1, plays a key role in modulating immune responses in the brain.

Keywords:

RNA-Seq alternative splicing hippocampus immune response lipopolysaccharide

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Area of Science:

Neuroscience
Immunology
Molecular Biology

Background:

Lipopolysaccharide (LPS) administration is a common method to induce neuroinflammation.
Transcriptome analysis reveals changes in gene expression following LPS exposure.

Purpose of the Study:

To investigate the role of differential gene expression and alternative splicing in the hippocampus after LPS administration.
To elucidate the function of Ptbp1 and Ptbp3 splicing factors in glial cells during neuroinflammation.

Main Methods:

Transcriptome analysis of hippocampus 24 hours after LPS administration.
Differential gene expression (DGE) and differential alternative splicing (DAS) analyses.
Isoform switching analysis of Ptbp1 and Ptbp3 genes.

Main Results:

Glial-specific genes constituted two-thirds of differentially expressed genes (DEGs), with microglia showing the most DEGs.
Astrocytes exhibited the highest number of DAS events.
Ptbp1 showed major isoform switching, with exon 8 skipping in the LPS group, potentially de-repressing immune responses.
Ptbp3 (NOD1) splicing factor was de-repressed by the short Ptbp1 isoform in glial cells.
Immune-related genes altered their major isoforms upon LPS exposure.

Conclusions:

Alternative splicing significantly modulates immune responses in the brain.
The Ptbp1 short isoform plays a crucial role in regulating immune-specific splicing in glial cells.
Ptbp1 and Ptbp3 are key regulators of immune responses in microglial and endothelial brain cells.