Proteomic Signature of Dysfunctional Circulating Endothelial Colony‐Forming Cells of Young Adults
Adult
CD36 Antigens
Male
Proteomics
0301 basic medicine
Lumican
cardiovascular disease risk factors
Neovascularization, Physiologic
Exocytosis
angiogenesis
03 medical and health sciences
proteomics
0302 clinical medicine
Diseases of the circulatory (Cardiovascular) system
Humans
Osteonectin
hypertension/high blood pressure
Cells, Cultured
endothelial progenitor cells
Original Research
Cell Proliferation
Endothelial Progenitor Cells
blood pressure
3. Good health
Serum Amyloid P-Component
C-Reactive Protein
Heart Disease Risk Factors
RC666-701
Hypertension
Female
Endothelium, Vascular
Transcriptome
DOI:
10.1161/jaha.121.021119
Publication Date:
2021-07-19T09:01:55Z
AUTHORS (11)
ABSTRACT
Background A subpopulation of endothelial progenitor cells called colony-forming (ECFCs) may offer a platform for cellular assessment in clinical studies because their remarkable angiogenic and expansion potentials vitro. Despite cell function being influenced by cardiovascular risk factors, no have yet provided comprehensive proteomic profile to distinguish functional (ie, more expansive cells) versus dysfunctional circulating ECFCs young adults. The aim this study was provide detailed comparison between ECFCs. Methods Results Peripheral blood were isolated from 11 subjects (45% men, aged 27±5 years) using Ficoll density gradient centrifugation. expressed surface markers displayed cobblestone-patterned morphology with clonal capacities deemed if <1 closed tube formed during the vitro formation assay proliferation rate <20%. Hierarchical clustering revealed distinct ECFC signatures changes mechanisms involved exocytosis, vesicle transport, extracellular matrix organization, metabolism, apoptosis. Targeted antiangiogenic proteins included SPARC (secreted protein acidic rich cysteine), CD36 (cluster differentiation 36), LUM (lumican), PTX3 (pentraxin-related PYX3). Conclusions Circulating impaired angiogenesis significant phenotype compared highly cells. Impaired underlie link dysfunction disease risks
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