Abstract
In the neurovascular units of the central nervous system, astrocytes form extensive networks that physically and functionally connect the neuronal synapses and the cerebral vascular vessels. This astrocytic network is thought to be critically important for coupling neuronal signaling activity and energy demand with cerebral vascular tone and blood flow. To establish and maintain this elaborate network, astrocytes must precisely calibrate their perisynaptic and perivascular processes in order to sense and regulate neuronal and vascular activities, respectively. Integrins, a prominent family of cell-adhesion molecules that support astrocytic migration in the brain during developmental and normal adult stages, have been implicated in regulating the integrity of the blood brain barrier and the tripartite synapse to facilitate the formation of a functionally integrated neurovascular unit. This paper describes the significant roles that integrins and connexins play not only in regulating astrocyte migration during the developmental and adult stages of the neurovascular unit, but also in general health and in such diseases as hepatic encephalopathy.
Highlights
The microenvironment of the central nervous system (CNS) must function correctly if the signaling activities of neurons are to be fully supported [1, 2, 6]
Our emphasis will be on integrins, the foremost family of cell-adhesion molecules, whose mediation of cell migration and astrocyte adhesion [13, 14] ideally positions them for further interaction with blood-brain barrier (BBB) endothelial cells, as well as with neurons in the neurovascular units
During the developmental stages of the neurovascular unit, Sonic hedgehog (Shh) released from astrocytes binds to Hedgehog receptors expressed on BBB-endothelial cells
Summary
The microenvironment of the central nervous system (CNS) must function correctly if the signaling activities of neurons are to be fully supported [1, 2, 6]. The ability of the BBB to physically separate the brain microenvironment from its systemic counterpart principally derives from the tight intercellular junctional complexes that form among BBB endothelial cells This mechanism blocks the paracellular passage of ionic molecules, thereby restricting molecular passage solely through transcellular routes. Studies have addressed, far, a potential role by which the molecular and cellular interactions at the neurovascular unit might play in the pathogenesis and progression of chronic pain. Addressing this problem could lead to innovative therapies that ameliorate chronic inflammatory pain [12]. Our emphasis will be on integrins, the foremost family of cell-adhesion molecules, whose mediation of cell migration and astrocyte adhesion [13, 14] ideally positions them for further interaction with BBB endothelial cells, as well as with neurons in the neurovascular units
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