Journal
JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
Volume 15, Issue 5, Pages 1049-1063Publisher
SPRINGER
DOI: 10.1007/s12265-022-10235-y
Keywords
prehypertension; endothelial progenitor cells; CXCR4; shear stress; reendothelialization
Funding
- National Natural Science Foundation of China [81700263, 81370309, 82100348]
- Basic and Applied Basic Research Foundation of Guangdong Province of China [2020A1515110865]
- Science and Technology Projects in Guangzhou City of China [202102021124]
- Medical Science Technology Research Foundation of Guangdong Province of China [B2021162]
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This study investigated the effects of prehypertension and shear stress on the reendothelialization potential of early EPCs in humans and explored the potential mechanisms. The study found that early EPCs from prehypertensive patients exhibited reduced migration and adhesion, as well as significantly impaired in vivo reendothelialization capacity. Shear stress pretreatment could significantly promote the in vivo reendothelialization capacity of EPCs. Additionally, CXCR4 receptor plays a crucial role in modulating the reendothelialization potential of early EPCs through regulating JAK-2 signaling.
This study investigated the effects of prehypertension and shear stress on the reendothelialization potential of human early EPCs and explored its potential mechanisms. Early EPCs from the prehypertensive patients showed reduced migration and adhesion in vitro and demonstrated a significantly impaired in vivo reendothelialization capacity. Shear stress pretreatment markedly promoted the in vivo reendothelialization capacity of EPCs. Although basal CXCR4 expression in early EPCs from prehypertensive donors was similar to that from healthy control, SDF-1-induced phosphorylation of CXCR4 was lower in prehypertensive EPCs. Shear stress up-regulated CXCR4 expression and increased CXCR4 phosphorylation, and restored the SDF-1/CXCR4-dependent JAK-2 phosphorylation in prehypertensive EPCs. CXCR4 knockdown or JAK-2 inhibitor treatment prevents against shear stress-induced increase in the migration, adhesion and reendothelialization capacity of the prehypertensive EPCs. Collectively, CXCR4 receptor profoundly modulates the reendothelialization potential of early EPCs. The abnormal CXCR4-mediated JAK-2 signaling may contribute to impaired functions of EPCs from patients with prehypertension.
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