Journal Article Review Epublish 22 citations
PubMed: 37962453 DOI: 10.14336/AD.2023.1010
Role of Crosstalk between Glial Cells and Immune Cells in Blood-Brain Barrier Damage and Protection after Acute Ischemic Stroke.
Aging Dis 15(6):2507-2525
Authors: Yihui Wang, Wencao Liu, Panpan Geng, Weihong Du, Chun Guo, Qian Wang, Guo-Qing Zheng, Xinchun Jin
Affiliations
- Beijing Key Laboratory of Cancer Invasion and Metastasis Research, Department of Histology and Embryology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing, 100069, China.
- Shanxi Provincial People's Hospital, Taiyuan 030001, China.
- School of Biosciences, University of Sheffield, Firth Court, Western Bank, Sheffield, UK.
- Department of Neurology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Abstract
Blood-brain barrier (BBB) damage is the main pathological basis for acute ischemic stroke (AIS)-induced cerebral vasogenic edema and hemorrhagic transformation (HT). Glial cells, including microglia, astrocytes, and oligodendrocyte precursor cells (OPCs)/oligodendrocytes (OLs) play critical roles in BBB damage and protection. Recent evidence indicates that immune cells also have an important role in BBB damage, vasogenic edema and HT. Therefore, regulating the crosstalk between glial cells and immune cells would hold the promise to alleviate AIS-induced BBB damage. In this review, we first introduce the roles of glia cells, pericytes, and crosstalk between glial cells in the damage and protection of BBB after AIS, emphasizing the polarization, inflammatory response and crosstalk between microglia, astrocytes, and other glia cells. We then describe the role of glial cell-derived exosomes in the damage and protection of BBB after AIS. Next, we specifically discuss the crosstalk between glial cells and immune cells after AIS. Finally, we propose that glial cells could be a potential target for alleviating BBB damage after AIS and we discuss some molecular targets and potential strategies to alleviate BBB damage by regulating glial cells after AIS.
MeSH
Neuroglia, Blood-Brain Barrier, Edema, Astrocytes, Oligodendroglia, Microglia, Oligodendrocyte Precursor Cells, Ischemic Stroke
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- Ischemic Postconditioning Regulates New Cell Death Mechanisms in Stroke: Disulfidptosis. Biomolecules, 2024
- hUMSC-Exosomes suppress TREM1-p38 MAPK signaling via HMGB1-dependent mechanisms to reprogram microglial function and promote neuroprotection in ischemic stroke. J Nanobiotechnology, 2025
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