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@ARTICLE{Morton:275866,
author = {Morton, Lorena and Garza, Alejandra P and Debska-Vielhaber,
Grazyna and Villafuerte, Luis E and Henneicke, Solveig and
Ulbrich, Philipp and Meuth, Sven G and Schreiber, Stefanie
and Dunay, Ildiko R},
title = {{P}ericytes and {E}xtracellular {V}esicle {I}nteractions in
{N}eurovascular {A}daptation to {C}hronic {A}rterial
{H}ypertension.},
journal = {Journal of the American Heart Association},
volume = {14},
number = {1},
issn = {2047-9980},
address = {New York, NY},
publisher = {Association},
reportid = {DZNE-2025-00101},
pages = {e038457},
year = {2025},
abstract = {Chronic arterial hypertension restructures the vascular
architecture of the brain, leading to a series of
pathological responses that culminate in cerebral
small-vessel disease. Pericytes respond dynamically to
vascular challenges; however, how they manifest under the
continuous strain of hypertension has not been elucidated.In
this study, we characterized pericyte behavior alongside
hypertensive states in the spontaneously hypertensive
stroke-prone rat model, focusing on their phenotypic and
metabolic transformation. Flow cytometry was used to
characterize pericytes by their expression of
platelet-derived growth factor receptor β, neuroglial
antigen 2, cluster of differentiation 13-alanyl
aminopeptidase, and antigen Kiel 67. Microvessels were
isolated for gene expression profiling and in vitro pericyte
expansion. Immunofluorescence validated the cell culture
model. Plasma-derived extracellular vesicles from
hypertensive rodents were applied as a treatment to assess
their effects on pericyte function and detailed metabolic
assessments on enriched pericytes measured oxidative
phosphorylation and glycolysis. Our results reveal a shift
in platelet-derived growth factor receptor β+ pericytes
toward increased neuroglial antigen 2 and cluster of
differentiation 13-alanyl aminopeptidase coexpression,
indicative of their critical role in vascular stabilization
and inflammatory responses within the hypertensive milieu.
Significant alterations were found within key pathways
including angiogenesis, blood-brain barrier integrity,
hypoxia, and inflammation. Circulating extracellular
vesicles from hypertensive rodents distinctly influenced
pericyte mitochondrial function, evidencing their dual role
as carriers of disease pathology and potential therapeutic
agents. Furthermore, a shift toward glycolytic metabolism in
hypertensive pericytes was confirmed, coupled with ATP
production dysregulation.Our findings demonstrate that
cerebral pericytes undergo phenotypic and metabolic
reprogramming in response to hypertension, with
hypertensive-derived plasma-derived extracellular vesicles
impairing their mitochondrial function. Importantly,
plasma-derived extracellular vesicles from normotensive
controls restore this function, suggesting their potential
as both therapeutic agents and precision biomarkers for
hypertensive vascular complications. Further investigation
into plasma-derived extracellular vesicle cargo is essential
to further explore their therapeutic potential in vascular
health.},
keywords = {Pericytes: metabolism / Pericytes: pathology / Animals /
Extracellular Vesicles: metabolism / Hypertension:
physiopathology / Hypertension: metabolism / Rats, Inbred
SHR / Male / Rats / Disease Models, Animal / Chronic Disease
/ Cells, Cultured / Adaptation, Physiological / Blood-Brain
Barrier: metabolism / Blood-Brain Barrier: pathology /
blood–brain barrier (Other) / extracellular vesicles
(Other) / hypertension (Other) / mitochondrial membrane
potential (Other) / pericytes (Other) / spontaneously
hypertensive stroke‐prone rat (SHRSP) (Other) / vascular
remodeling (Other)},
cin = {AG Schreiber},
ddc = {610},
cid = {I:(DE-2719)1310010},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39719419},
doi = {10.1161/JAHA.124.038457},
url = {https://pub.dzne.de/record/275866},
}