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Inflammatory response of microglial BV-2 cells includes a glycolytic shift and is modulated by mitochondrial

Ludmila A Voloboueva1, John F Emery, Xiaoyun Sun

  • 1Department of Anesthesia, Stanford University School of Medicine, 300 Pasteur Drive, Grant Building S272, Stanford, CA 94305, United States. ludmilav@stanford.edu

FEBS Letters
|February 12, 2013
PubMed

Insights

Overexpression of glucose-regulated protein75 (Grp75) protects mitochondria and suppresses inflammation. This finding offers a new strategy for treating inflammation-associated diseases by modulating cytokine production.

Area of Science:

  • Mitochondrial biology
  • Immunology
  • Cellular metabolism

Background:

  • Mitochondria are increasingly linked to the generation of proinflammatory cytokines.
  • Glucose-regulated protein75 (Grp75/mortalin) is a mitochondrial chaperone that protects mitochondria.
  • The role of Grp75 in modulating lipopolysaccharide (LPS)-induced inflammatory responses in microglial cells remains to be fully elucidated.

Purpose of the Study:

  • To investigate the effect of Grp75 on the lipopolisaccharide (LPS)-induced inflammatory response in microglial BV-2 cells.
  • To determine how Grp75 influences metabolic changes and mitochondrial function during LPS-induced activation.
  • To explore the potential of Grp75 as a therapeutic target for inflammation-associated pathologies.

Main Methods:

  • Utilized microglial BV-2 cell line.
  • Induced inflammatory response using lipopolisaccharide (LPS).
  • Overexpressed glucose-regulated protein75 (Grp75).
  • Assessed metabolic changes, mitochondrial function, oxidative stress, and proinflammatory cytokine production.
  • Investigated the involvement of NF-κB activation and lactate.

Main Results:

  • LPS-induced activation caused significant metabolic alterations, including suppressed mitochondrial function and increased glycolysis.
  • Overexpression of Grp75 attenuated LPS-induced oxidative and metabolic responses.
  • Grp75 overexpression suppressed proinflammatory activation, which was dependent on both NF-κB activation and lactate production.
  • LPS-induced inflammation in microglial cells involves metabolic shifts that can be modulated by Grp75.

Conclusions:

  • Overexpression of Grp75 mitigates LPS-induced inflammatory responses in microglial cells.
  • Grp75 plays a protective role by preserving mitochondrial function and reducing metabolic disturbances during inflammation.
  • Targeting Grp75 represents a novel therapeutic strategy for managing inflammation-associated diseases through modulation of cytokine production.

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