ApoA-I deficiency has a subtle effect on acute inflammatory responses after experimental Traumatic Brain Injury

Authors

  • Honor Cheung University of British Columbia
  • Wai Hang Cheng 1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  • Emily Beth Button Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  • Asma Bashir 1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  • Carlos Juan Barron Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  • Anna Wilkinson Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  • Cheryl Lea Wellington Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Abstract

Cerebral vascular injury is a common phenomenon after traumatic brain injury (TBI), with complications including vascular inflammation, decreased cerebral blood flow, and increased vessel tortuosity following TBI. Promoting cerebrovascular health may therefore be a useful therapeutic intervention after TBI. High density lipoproteins (HDL) are an attractive target due to their vasoprotective and anti-inflammatory roles in periphery vessels, but little is known on whether these benefits extend to the brain. Recently, deficiency of ApoA-I, the major protein constituent of circulating HDL, was shown to increase vascular associated plaque load in Alzheimer’s Disease (AD) mice, which may imply a vessel protective function of ApoA-I in the brain. This study was designed to test the novel hypothesis that ApoA-I deficiency would worsen acute vascular and inflammatory outcomes in mice after Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA) TBI. ApoA-I KO and WT mice underwent single moderate-severe TBI. Histopathological outcomes at 6hr and 2 days (2D) post injury were assessed. ApoA-I deficient mice exhibited greater ICAM-1 immunoreactivity at the cortex at 2D post TBI compared to WT controls, and a subtle increase in brain cytokine levels, potentially suggesting role of ApoA-I in protecting from TBI induced inflammation.

Author Biographies

Honor Cheung, University of British Columbia

Affiliation

  1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  2. Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Wai Hang Cheng, 1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Affiliation

  1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  2. Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Emily Beth Button, Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

AFFILIATIONS:

  1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  2. Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Asma Bashir, 1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

AFFILIATIONS:

  1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  2. Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Carlos Juan Barron, Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

AFFILIATIONS:

  1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  2. Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Anna Wilkinson, Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

AFFILIATIONS:

  1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  2. Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Cheryl Lea Wellington, Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

AFFILIATIONS:

  1. Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3
  2. Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z3

Published

2021-05-04

Issue

Vol. 6 No. 1 (2021)

Section

Articles

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