Proteomic Signature of Dysfunctional Circulating Endothelial Colony‐Forming Cells of Young Adults

• DOI: 10.1161/jaha.121.021119
• Publication Date: 2021-07-19T09:01:55Z
• Authors: Cheryl M. J. Tan; Adam J. Lewandowski; Wilby Williamson; Odaro J. Huckstep; Grace Z. Yu; Roman Fischer; Jillian N. Simon; Maryam Alsharqi; Afifah Mohamed; Paul Leeson; Mariane Bertagnolli
• Keywords: 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

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