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Updated: Jun 2, 2026
Isolation of Primary Murine Brain Microvascular Endothelial Cells
Published on: November 14, 2014
Involvement of the cellular prion protein in the migration of brain microvascular endothelial cells
Takuya Watanabe1, Yuki Yasutaka, Tsuyoshi Nishioku
1Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. twatanabe@fukuoka-u.ac.jp
Abstract:
The conversion of cellular prion protein (PrP(C)) to its protease-resistant isoform is involved in the pathogenesis of prion disease. Although PrP(C) is a ubiquitous glycoprotein that is present in various cell types, the physiological role of PrP(C) remains obscure. The present study aimed to determine whether PrP(C) mediates migration of brain microvascular endothelial cells. Small interfering RNAs (siRNAs) targeting PrP(C) were transfected into a mouse brain microvascular endothelial cell line (bEND.3 cells). siPrP1, selected among three siRNAs, reduced mRNA and protein levels of PrP(C) in bEND.3 cells. Cellular migration was evaluated with a scratch-wound assay. siPrP1 suppressed migration without significantly affecting cellular proliferation. This study provides the first evidence that PrP(C) may be necessary for brain microvascular endothelial cells to migrate into damaged regions in the brain. This function of PrP(C) in the brain endothelium may be a mechanism by which the neurovascular unit recovers from an injury such as an ischemic insult.
Insights
Cellular prion protein (PrP(C)) is essential for brain microvascular endothelial cells to migrate to damaged brain areas. This finding suggests a role for PrP(C) in neurovascular repair after injury.
Area of Science:
- Neuroscience
- Cell Biology
- Prion Biology
Background:
- The cellular prion protein (PrP(C)) is a glycoprotein with an unknown physiological function.
- Prion diseases involve the conversion of PrP(C) to a pathogenic isoform.
- Understanding PrP(C)'s normal function is crucial for comprehending prion disease pathogenesis.
Purpose of the Study:
- To investigate the role of PrP(C) in the migration of brain microvascular endothelial cells.
- To determine if PrP(C) is necessary for endothelial cell movement in the brain.
Main Methods:
- Used small interfering RNAs (siRNAs) to reduce PrP(C) expression in mouse brain microvascular endothelial cells (bEND.3).
- Evaluated cellular migration using a scratch-wound assay.
- Assessed the impact of PrP(C) reduction on cell proliferation.
Main Results:
- One siRNA (siPrP1) effectively reduced PrP(C) mRNA and protein levels.
- Reduced PrP(C) levels significantly suppressed endothelial cell migration.
- Cell proliferation remained unaffected by PrP(C) reduction.
Conclusions:
- PrP(C) plays a critical role in mediating brain microvascular endothelial cell migration.
- This function of PrP(C) may be vital for the neurovascular unit's recovery from injuries like ischemic stroke.
- PrP(C) is potentially a key factor in brain repair mechanisms.
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