Abstract
The gliovascular unit (GVU) is composed of the brain microvascular endothelial cells forming blood–brain barrier and the neighboring surrounding “mural” cells (e.g., pericytes) and astrocytes. Modulation of the GVU/BBB features could be observed in a variety of vascular, immunologic, neuro-psychiatric diseases, and cancers, which can disrupt the brain homeostasis. Ca2+ dynamics have been regarded as a major factor in determining BBB/GVU properties, and previous studies have demonstrated the role of transient receptor potential vanilloid (TRPV) channels in modulating Ca2+ and BBB/GVU properties. The physiological role of thermosensitive TRPV channels in the BBB/GVU, as well as their possible therapeutic potential as targets in treating brain diseases via preserving the BBB are reviewed. TRPV2 and TRPV4 are the most abundant isoforms in the human BBB, and TRPV2 was evidenced to play a main role in regulating human BBB integrity. Interspecies differences in TRPV2 and TRPV4 BBB expression complicate further preclinical validation. More studies are still needed to better establish the physiopathological TRPV roles such as in astrocytes, vascular smooth muscle cells, and pericytes. The effect of the chronic TRPV modulation should also deserve further studies to evaluate their benefit and innocuity in vivo.
Highlights
The brain gliovascular unit (GVU) consists firstly of brain microvascular endothelial cells (BMECs) forming the blood–brain barrier (BBB) and secondly of the neighboring surrounded “mural” cells and astrocytes [1]
We focus our attention on thermosensitive TRPV1–4 in the GVU and in particular in BMECs (Table 3)
The expression of TRPV2 in astrocytes was recently identified by biochemical and functional methods showing that TRPV2 was mainly detected in the plasma membrane of primary cultured astrocytes from mice, which can be activated by a high temperature
Summary
The brain gliovascular unit (GVU) consists firstly of brain microvascular endothelial cells (BMECs) forming the blood–brain barrier (BBB) and secondly of the neighboring surrounded “mural” cells (e.g., pericytes) and astrocytes [1]. Several chemical/physical stimuli from the blood and/or brain parenchyma compartments can modulate the BBB features and lead to changes in the vascular flow, immune cell trafficking, and/or the tight junction integrity. The functions of TRPV1 [44], and more recently for TRPV2 [45] and TRPV4 [46], in brain endothelial cells forming the BBB showed their participation in modulating BBB properties Their localization at the vascular interface enhances their role in mechanotransduction mechanisms and possibly responses to vascular/shear stress (e.g., migration, adhesion), as TRPV2 and TRPV4 are known to be associated with actin/cytoskeleton proteins [47]. We will summarize the role of TRPV channels in the GVU with a particular focus on the BBB and discuss their physiological and/or potential as drug targets in CNS diseases
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