Abstract
Astrocytes comprise the major non-neuronal cell population in the mammalian neurovascular unit. Traditionally, astrocytes are known to play broad roles in central nervous system (CNS) homeostasis, including the management of extracellular ion balance and pH, regulation of neurotransmission, and control of cerebral blood flow and metabolism. After CNS injury, cell–cell signaling between neuronal, glial, and vascular cells contribute to repair and recovery in the neurovascular unit. In this mini-review, we propose the idea that astrocytes play a central role in organizing these signals. During CNS recovery, reactive astrocytes communicate with almost all CNS cells and peripheral progenitors, resulting in the promotion of neurogenesis and angiogenesis, regulation of inflammatory response, and modulation of stem/progenitor response. Reciprocally, changes in neurons and vascular components of the remodeling brain should also influence astrocyte signaling. Therefore, understanding the complex and interdependent signaling pathways of reactive astrocytes after CNS injury may reveal fundamental mechanisms and targets for re-integrating the neurovascular unit and augmenting brain recovery.
Highlights
The neurovascular unit is a conceptual framework for investigating the mechanisms of central nervous system (CNS) injury and disease [1]
Fibrous astrocytes are originated from radial glial cells that are capable of differentiating neurons, astrocytes and oligodendrocytes during brain development, and these astrocytes highly express glial fibrillary acidic protein (GFAP), nestin, and vimentin [11,12]
We found that endogenous high-mobility group box 1 (HMGB1) produced by astrocytes was crucial for endothelial progenitor cells (EPCs) homing in vivo in both gray matter and white matter [74,75]
Summary
The neurovascular unit is a conceptual framework for investigating the mechanisms of central nervous system (CNS) injury and disease [1]. Protoplasmic astrocytes widely distributing in gray matter have a larger size (~50 μm) and more organelles than fibrous astrocytes, and at least one process contacts blood vessels through perivascular endfeet as well as forming multiple contacts with neurons. The reader is referred to many detailed reviews that rigorously describe these multiphasic astrocyte phenotypes and functions [15,17,18,19,20,21,22,23,24] In this mini-review, we aim to survey primary principles to support the idea that astrocytes comprise a critical source of crosstalk signaling within the neurovascular unit as the damaged brain begins to transition from initial injury into endogenous repair and recovery after CNS injury, including stroke, white matter injury, and spinal cord injury
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