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Published on: September 22, 2023
Brain endothelial cells as phagocytes: mechanisms and implications.
Rudy T Chang1, Mark J Fisher2,3, Rachita K Sumbria4,5
1Department of Biomedical and Pharmaceutical Sciences, School of Pharmacy, Chapman University, Irvine, CA, USA.
Brain endothelial cells (BECs) lining the blood-brain barrier (BBB) can engulf various materials, acting as non-professional phagocytes. This phagocytosis is crucial for brain homeostasis, debris clearance, and understanding conditions like cerebral microhemorrhages.
Area of Science:
- Neuroscience
- Cell Biology
- Immunology
Background:
- Brain microvascular endothelial cells (BECs) form the blood-brain barrier (BBB), traditionally viewed as a passive barrier.
- Emerging evidence suggests BECs possess phagocytic capabilities, challenging conventional understanding.
- This phagocytosis is critical for maintaining brain homeostasis and responding to pathological conditions.
Purpose of the Study:
- To review the phagocytic capacity of BECs.
- To summarize the mechanisms underlying BEC phagocytosis.
- To discuss the clinical implications of BEC phagocytosis in brain health and disease.
Main Methods:
- Literature review of studies on BEC phagocytosis.
- Analysis of mechanisms including phosphatidylserine exposure, adhesion molecules (ICAM-1, VCAM-1), opsonization, and cytoskeleton remodeling.
- Examination of clinical relevance in conditions like capillary stalling, debris clearance, and hemorrhagic lesions.
Main Results:
- BECs actively phagocytose diverse cargos like aged red blood cells (RBCs), myelin debris, and embolic particles.
- Phagocytosis is triggered by specific molecular cues and involves cytoskeletal changes.
- BEC phagocytosis plays roles in regulating microvascular patency, clearing debris, and contributing to hemorrhagic lesions.
Conclusions:
- BECs function as non-professional phagocytes, significantly impacting brain homeostasis.
- Understanding BEC phagocytosis mechanisms is key to addressing neurological disorders.
- Further research is needed to fully elucidate the complexities and therapeutic potential of BEC phagocytosis.
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