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
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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