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Optineurin Shapes Basal and LPS-Induced Transcriptomes in BV2 Microglia.

Sara Cappelli1, Josip Peradinovic2, Nikolina Mohovic2

  • 1International Centre for Genetic Engineering and Biotechnology (ICGEB), Padriciano 99, 34149 Trieste, Italy.

International Journal of Molecular Sciences
|November 13, 2025
PubMed
Summary
This summary is machine-generated.

Optineurin (OPTN) is crucial for microglial immune responses. Its absence impairs the inflammatory gene expression and cell cycle regulation in microglia, impacting neuroinflammation in diseases like ALS and FTD.

Keywords:
BV2 microgliaCRISPR-Cas9LPSRNA-Seqinflammationinterferon signalingneuroinflammationoptineurin

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • The OPTN gene, encoding optineurin, is linked to neurodegenerative diseases involving microglial activation.
  • Optineurin's precise function in microglia, particularly in inflammatory signaling and immune response, is not fully understood.

Purpose of the Study:

  • To investigate the role of optineurin in microglial gene expression and inflammatory response.
  • To characterize the impact of optineurin deficiency on the microglial transcriptome under basal and stimulated conditions.

Main Methods:

  • Utilized CRISPR-Cas9 to create optineurin knockout (KO) BV2 microglia.
  • Performed bulk RNA sequencing on wild-type and KO microglia under basal and LPS-stimulated conditions.
  • Analyzed differential gene expression to identify optineurin-dependent pathways.

Main Results:

  • Optineurin KO altered basal microglial transcriptome, downregulating interferon and antiviral pathways.
  • LPS stimulation significantly reprogrammed wild-type microglia, while the response was blunted in optineurin KO cells.
  • Optineurin deficiency led to impaired inflammatory gene induction and persistent cell cycle transcripts upon LPS stimulation, with unique DEG profiles.

Conclusions:

  • Optineurin is a key regulator of the microglial transcriptome, essential for innate immune responses.
  • Loss of optineurin reshapes microglial immune and cell cycle programs, offering insights into neuroinflammation in diseases like ALS and FTD.
  • Provides a systems-level understanding of optineurin's role in microglia and its implications for neurodegeneration.