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Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing

Fei-Fei Xu1, Zi-Bin Zhang1, Yang-Yang Wang1

  • 1Institute of Neurological Disease, Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, 610041, China.

Neuroscience Bulletin
|September 8, 2018
PubMed

Insights

Acute cerebral ischemia (ACI) up-regulates glia maturation factor beta (GMFB) in astrocytes. Brain-derived GMFB then damages lung endothelial cells, initiating lung injury after ACI.

Area of Science:

  • Neuroscience
  • Pulmonology
  • Cell Biology

Background:

  • Brain damage, specifically acute cerebral ischemia (ACI), is known to precipitate lung injury.
  • The precise molecular mechanisms linking ACI to lung damage remain incompletely understood.
  • Glia maturation factor beta (GMFB) emerged as a potential key mediator from proteomic analysis.

Purpose of the Study:

  • To investigate the role of glia maturation factor beta (GMFB) in the pathogenesis of lung injury following acute cerebral ischemia (ACI).
  • To elucidate the cellular source and mechanism by which ACI-induced GMFB affects pulmonary microvascular endothelial cells (PMVECs).

Main Methods:

  • Established a middle cerebral artery occlusion (MCAO) rat model to simulate ACI.
  • Utilized polymerase chain reaction, western blotting, and immunofluorescence to detect GMFB expression in astrocytes.
  • Employed oxygen-glucose deprivation (OGD) on primary astrocytes and RNA interference to modulate GMFB levels.
  • Assessed PMVEC viability and reactive oxygen species (ROS) production using conditioned medium from treated astrocytes and recombinant GMFB.

Main Results:

  • GMFB was significantly over-expressed in astrocytes within the brain following MCAO.
  • Primary astrocytes cultured under OGD conditions also showed increased GMFB levels.
  • Blocking GMFB in astrocytes improved the viability of co-cultured pulmonary microvascular endothelial cells (PMVECs).
  • Recombinant GMFB exposure to PMVECs increased ROS levels and impaired cell status.

Conclusions:

  • Glia maturation factor beta (GMFB) is demonstrably up-regulated in astrocytes subsequent to acute cerebral ischemia.
  • Brain-derived GMFB directly contributes to pulmonary microvascular endothelial cell (PMVEC) damage by elevating reactive oxygen species (ROS).
  • GMFB is identified as a potential initiating factor in ACI-induced lung injury.
Keywords:
Acute cerebral ischemiaGlial maturation factor βLung injuryPulmonary microvascular endothelial cellsRNA interferenceReactive oxygen species

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