scholarly journals Dysfunction of Endothelial Progenitor Cells from Smokers and Chronic Obstructive Pulmonary Disease Patients Due to Increased DNA Damage and Senescence

Stem Cells ◽  
2013 ◽  
Vol 31 (12) ◽  
pp. 2813-2826 ◽  
Author(s):  
Koralia E. Paschalaki ◽  
Richard D. Starke ◽  
Yanhua Hu ◽  
Nicolas Mercado ◽  
Andriana Margariti ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Dna Damage ◽  
Progenitor Cells ◽  
Pulmonary Disease ◽  
Endothelial Progenitor Cells ◽  
Chronic Obstructive ◽  
Endothelial Progenitor ◽  
Obstructive Pulmonary Disease

scholarly journals Endothelial progenitor cells in patients with chronic obstructive pulmonary disease

2013 ◽  
Vol 305 (12) ◽  
pp. L964-L969 ◽  
Author(s):  
Mairi Brittan ◽  
Mathilde M. Hoogenboom ◽  
Gareth J. Padfield ◽  
Olga Tura ◽  
Takeshi Fujisawa ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Progenitor Cells ◽  
Pulmonary Disease ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Chronic Obstructive ◽  
Endothelial Progenitor ◽  
Obstructive Pulmonary Disease ◽  
Circulating Endothelial Progenitor Cells ◽  
Colony Forming Units

The pathogenesis of chronic obstructive pulmonary disease is not fully understood. The objective of this study was to compare circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease to age, sex, and cigarette smoking matched healthy controls. Patients with chronic obstructive pulmonary disease ( n = 37) and healthy controls ( n = 19) were matched by age, sex, and smoking status. Circulating hematopoietic progenitor cells (CD34+ or CD133+ mononuclear cells) and endothelial progenitor cells (CD34+KDR+ or CD34+CD133+KDR+ mononuclear cells) were quantified by flow cytometry. Endothelial cell-colony forming units from peripheral blood mononuclear cells were quantified in vitro and phenotypic analysis carried out using immunocytochemistry. Patients with chronic obstructive pulmonary disease had more circulating mononuclear cells compared with controls (8.4 ± 0.6 vs. 5.9 ± 0.4 × 109 cells/l; P = 0.02). CD34+ hematopoietic progenitor cells were reduced as a proportion of mononuclear cells in patients compared with controls (0.99 ± 0.12 vs. 1.9 ± 0.12%; P = 0.02); however, there were no differences in the absolute number of CD34+, CD34+KDR+, or CD34+CD133+KDR+ cells ( P > 0.05 for all). Endothelial cell-colony forming units were increased in patients with chronic obstructive pulmonary disease compared with controls (13.7 ± 5.2 vs. 2.7 ± 0.9 colonies; P = 0.048). In contrast to previous studies, the number of circulating progenitor cells was not reduced in patients with chronic obstructive pulmonary disease compared with carefully matched controls. It seems unlikely that circulating endothelial progenitor cells or failure of angiogenesis plays a central role in the development of emphysema.

scholarly journals Endothelial progenitor cells in chronic obstructive pulmonary disease and emphysema

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0173446 ◽  
Author(s):  
Margaret F. Doyle ◽  
Russell P. Tracy ◽  
Megha A. Parikh ◽  
Eric A. Hoffman ◽  
Daichi Shimbo ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Progenitor Cells ◽  
Pulmonary Disease ◽  
Endothelial Progenitor Cells ◽  
Chronic Obstructive ◽  
Endothelial Progenitor ◽  
Obstructive Pulmonary Disease

scholarly journals Endothelial Progenitor Cells as Pathogenetic and Diagnostic Factors, and Potential Targets for GLP-1 in Combination with Metabolic Syndrome and Chronic Obstructive Pulmonary Disease

2019 ◽  
Vol 20 (5) ◽  
pp. 1105 ◽  
Author(s):  
Evgenii Skurikhin ◽  
Olga Pershina ◽  
Angelina Pakhomova ◽  
Edgar Pan ◽  
Vyacheslav Krupin ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Metabolic Syndrome ◽  
Endothelial Cells ◽  
Progenitor Cells ◽  
Pulmonary Disease ◽  
Endothelial Progenitor Cells ◽  
Cigarette Smoke ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

In clinical practice, there are patients with a combination of metabolic syndrome (MS) and chronic obstructive pulmonary disease (COPD). The pathological mechanisms linking MS and COPD are largely unknown. It remains unclear whether the effect of MS (possible obesity) has a major impact on the progression of COPD. This complicates the development of effective approaches for the treatment of patients with a diagnosis of MS and COPD. Experiments were performed on female C57BL/6 mice. Introduction of monosodium glutamate and extract of cigarette smoke was modeled to simulate the combined pathology of lipid disorders and emphysema. Biological effects of glucagon-like peptide 1 (GLP-1) and GLP-1 on endothelial progenitor cells (EPC) in vitro and in vivo were evaluated. Histological, immunohistochemical methods, biochemical methods, cytometric analysis of markers identifying EPC were used in the study. The CD31+ endothelial cells in vitro evaluation was produced by Flow Cytometry and Image Processing of each well with a Cytation™ 3. GLP-1 reduces the area of emphysema and increases the number of CD31+ endothelial cells in the lungs of mice in conditions of dyslipidemia and damage to alveolar tissue of cigarette smoke extract. The regenerative effects of GLP-1 are caused by a decrease in inflammation, a positive effect on lipid metabolism and glucose metabolism. EPC are proposed as pathogenetic and diagnostic markers of endothelial disorders in combination of MS with COPD. Based on GLP-1, it is proposed to create a drug to stimulate the regeneration of endothelium damaged in MS and COPD.

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