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.

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

CONDITION OF HEMODYNAMICS IN THE PULMONARY CIRCULATION OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) CONCURRENT WITH METABOLIC SYNDROME WITH HYPERTROPHY AND ATROPHY OF THE MYOCARDIUM

2019 ◽  
Vol 72 (8) ◽  
pp. 1491-1493
Author(s):  
Viktor P. Boriak ◽  
Svitlana V. Shut’ ◽  
Tetiana A. Trybrat ◽  
Olena V. Filatova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Metabolic Syndrome ◽  
Right Ventricular ◽  
Pulmonary Disease ◽  
Pulmonary Circulation ◽  
Contractile Function ◽  
Ventricular Myocardium ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Right

Introduction: In recent years, COPD is observed as not an isolated, but an associated pathology, in particular, concurrent with metabolic syndrome. The aim of the research is to identify the differences in changes of the rheopulmonography parameters (RPG) depending on the presence of hypertrophy or atrophy of the right ventricular myocardium in patients with COPD concurrent with metabolic syndrome.. Materials and methods: We studied changes in rheopulmonography (RPG) in 145 patients with chronic obstructive pulmonary disease (COPD) concurrent with metabolic syndrome. Results: We detected precapillary hypertension of the pulmonary circulation in patients with right ventricular myocardial hypertrophy: anacrotism serration; flattened peak of the systolic wave; decreased Vcp; high placement of incisura; horizontal course of catacrotism; decreased amplitude of the systolic wave (in this case, due to a greater increase in the resistance of the blood flow in the pulmonary vessels than the decreased impact volume of the right ventricle); prolonged Q-a (in this group of patients, it depends more on hypertension of the pulmonary circulation than on the reduction of contractile function of the myocardium). In atrophy of the right ventricular myocardium, the following changes in the RPG were revealed: decreased systolic wave at its dramatic rise; prolonged Q-a (in this case, due to the weakened heart contraction); Vmax reduction (it reflects the reduction of myocardial contractility); in hypertrophy of the myocardium, Vcp., unlike RPG, does not decrease, which is explained by the decrease in the pressure of the pulmonary circulation. Conclusions: We believe that these changes in RPG allow differentiating hypertrophy and right ventricular myocardial atrophy along with established diagnostic criteria, and can be used as markers for the diagnosis and treatment of COPD concurrent with metabolic syndrome.

Sign in / Sign up

Export Citation Format

Share Document