Why the study?
Disruptions to astrocyte endfoot vascular coverage coincide with breaches in blood-brain barrier integrity, raising the question of whether focal ablation of an astrocyte is sufficient to disrupt the barrier.
Astrocytes maintain cerebrovascular coverage and blood-brain barrier integrity via substitution from nearby cells following focal ablation or stroke, a plasticity response that declines with normal aging.
Suggests age-related delay in astrocyte BBB coverage; hypothesis-generating for neurovascular repair in aging and disease.
Astrocytes extend endfeet that enwrap the vasculature. Disruptions to this association in disease coincide with breaches in blood-brain barrier (BBB) integrity, so we asked if the focal ablation of an astrocyte is sufficient to disrupt the BBB. 2Phatal ablation of astrocytes induced a plasticity response whereby surrounding astrocytes extended processes to cover vascular vacancies. This occurred prior to endfoot retraction in young mice yet occurred with significant delay in aged animals. Laser-stimulating replacement astrocytes showed them to induce constrictions in pre-capillary arterioles indicating that replacement astrocytes are functional. Inhibition of EGFR and pSTAT3 significantly reduced astrocyte replacement post-ablation yet without perturbations to BBB integrity. Identical endfoot replacement following astrocyte cell death due to reperfusion post-stroke supports the conclusion that astrocyte plasticity ensures continual vascular coverage so as to retain the BBB. Together, these studies uncover the ability of astrocytes to maintain cerebrovascular coverage via substitution from nearby cells and may represent a novel therapeutic target for vessel recovery post-stroke.
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Mills et al. (2021) studied this question.
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