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Mitochondrial Fission Mediates Endothelial Inflammation.

Steven J Forrester1, Kyle J Preston1, Hannah A Cooper1

  • 1From the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (S.J.F., K.J.P., H.A.C., M.J.B., K.M.E., A.J.P., K.J.E., R.K., M.M., V.R., R.S., S.E.).

Hypertension (Dallas, Tex. : 1979)
|May 12, 2020
PubMed
Summary

This study reveals a link between mitochondrial fission and inflammation in blood vessels. Inhibiting dynamin-related protein 1 (Drp1) reduces inflammation by controlling mitochondrial fragmentation and nuclear factor-kappa B (NF-κB) activation.

Keywords:
dynaminsendotheliuminflammationleukocytesmitochondria

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Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Inflammation Research

Background:

  • Endothelial inflammation and mitochondrial dysfunction are key in cardiovascular diseases.
  • Mitochondrial dysfunction is linked to mitochondrial fission, regulated by dynamin-related protein 1 (Drp1).
  • Nuclear factor-kappa B (NF-κB) is a critical regulator of endothelial inflammation.

Purpose of the Study:

  • To investigate the causal link between mitochondrial fission and NF-κB activation in endothelial inflammatory responses.
  • To elucidate the role of Drp1 in mediating inflammation-induced mitochondrial fragmentation.
  • To explore the reciprocal relationship between NF-κB signaling and mitochondrial dynamics.

Main Methods:

  • Utilized cultured endothelial cells and Drp1 heterodeficient/silenced mice models.
  • Assessed mitochondrial fragmentation, NF-κB activation, and inflammatory markers like VCAM-1.
  • Investigated the effects of inhibiting Drp1 and canonical NF-κB signaling pathways.

Main Results:

  • Pro-inflammatory stimuli (TNF-α, LPS) induced mitochondrial fragmentation in endothelial cells.
  • Inhibition of Drp1 suppressed mitochondrial fission, NF-κB activation, and leukocyte adhesion.
  • Inhibition of NF-κB signaling reduced endothelial mitochondrial fission, implicating NF-κB p65/RelA in fission.
  • Salicylate maintained mitochondrial balance by inhibiting NF-κB.

Conclusions:

  • A novel mechanism links the canonical NF-κB pathway and mitochondrial fission in regulating endothelial inflammation.
  • Drp1 plays a crucial role in mediating inflammatory responses through mitochondrial dynamics.
  • Targeting the interplay between NF-κB and mitochondrial fission presents a potential therapeutic strategy for cardiovascular diseases.