scholarly journals The role of bone marrow-derived endothelial progenitor cells and angiogenic responses in chronic obstructive pulmonary disease

2017 ◽  
Vol 9 (7) ◽  
pp. 2168-2177 ◽  
Author(s):  
Brittany Salter ◽  
Roma Sehmi
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Bone Marrow ◽  
Progenitor Cells ◽  
Pulmonary Disease ◽  
Endothelial Progenitor Cells ◽  
Chronic Obstructive ◽  
Endothelial Progenitor ◽  
Obstructive Pulmonary Disease

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.

Role of exhaled nitric oxide in predicting steroid response in chronic obstructive pulmonary disease

2010 ◽  
Vol 151 (51) ◽  
pp. 2083-2088 ◽  
Author(s):  
Balázs Antus
Keyword(s):  
Nitric Oxide ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Exhaled Nitric Oxide ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Steroid Response

A kilégzett levegőben mérhető nitrogén-monoxid a legszélesebb körben vizsgált légúti biomarker. A stabil állapotú krónikus obstruktív tüdőbetegségben a kilégzett nitrogén-monoxid-szint hasonló vagy csak kismértékben emelkedett az egészségesekhez képest. Mivel a nitrogén-monoxid-szint szoros összefüggést mutat a légúti eosinophilia mértékével, és mivel az eosinophil típusú légúti gyulladás szteroidokra érzékenyebb, az emelkedett nitrogén-monoxid-szinttel rendelkező betegek jobb válaszkészséget mutatnak az inhalációs vagy szisztémás kortikoszteroidkezelésre. A krónikus obstruktív tüdőbetegség akut exacerbatiója során a kilégzett nitrogén-monoxid szintje megemelkedik, majd ennek kezelése után csökken. Mivel a nitrogén-monoxid-szint és a kezelés során elért légzésfunkciós javulás szoros korrelációt mutat egymással, a nitrogén-monoxid-méréssel a terápiás válasz megjósolható. Összefoglalva: a nitrogén-monoxid-méréssel a krónikus obstruktív tüdőbetegségben szenvedő betegek olyan alcsoportját lehet elkülöníteni, amelynek szteroidérzékenysége nagyobb. Orv. Hetil., 2010, 151, 2083–2088.

Participation of ABCA1 transporter in development of chronic obstructive pulmonary disease

2020 ◽  
Vol 28 (3) ◽  
pp. 360-370
Author(s):  
Stanislav N. Kotlyarov ◽  
Anna A. Kotlyarova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Significant Contribution ◽  
Modern Medicine ◽  
Lipid Homeostasis ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Reverse Transport ◽  
Current Paradigm

Despite all achievements of the modern medicine, the problem of chronic obstructive pulmonary disease (COPD) does not lose its relevance. The current paradigm suggests a key role of macrophages in inflammation in COPD. Macrophages are known to be heterogeneous in their functions. This heterogeneity is determined by their immunometabolic profile and also by peculiarities of lipid homeostasis of cells. Aim. To analyze the role of the ABCA1 transporter, a member of the ABC A subfamily, in the pathogenesis of COPD. The expression of ABCA1 in lung tissues is on the second place after the liver, which shows the important role of the carrier and of lipid homeostasis in the function of lungs. Analysis of the literature shows that participation of the transporter in inflammation consists in regulation of the content of cholesterol in the lipid rafts of the membranes, in phagocytosis and apoptosis. Conclusion. Through regulation of the process of reverse transport of cholesterol in macrophages of lungs, ABCA1 can change their inflammatory response, which makes a significant contribution to the pathogenesis of COPD.

scholarly journals Chronic Obstructive Pulmonary Disease: Epidemiology, Biomarkers, and Paving the Way to Lung Cancer

2021 ◽  
Vol 10 (13) ◽  
pp. 2889
Author(s):  
Klára Szalontai ◽  
Nikolett Gémes ◽  
József Furák ◽  
Tünde Varga ◽  
Patrícia Á. Neuperger ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Alveolar Wall ◽  
Obstructive Pulmonary Disease ◽  
Major Health Problem ◽  
Chronic Inflammatory Response ◽  
Disease Epidemiology

Chronic obstructive pulmonary disease (COPD), the frequently fatal pathology of the respiratory tract, accounts for half a billion cases globally. COPD manifests via chronic inflammatory response to irritants, frequently to tobacco smoke. The progression of COPD from early onset to advanced disease leads to the loss of the alveolar wall, pulmonary hypertension, and fibrosis of the respiratory epithelium. Here, we focus on the epidemiology, progression, and biomarkers of COPD with a particular connection to lung cancer. Dissecting the cellular and molecular players in the progression of the disease, we aim to shed light on the role of smoking, which is responsible for the disease, or at least for the more severe symptoms and worse patient outcomes. We summarize the inflammatory conditions, as well as the role of EMT and fibroblasts in establishing a cancer-prone microenvironment, i.e., the soil for ‘COPD-derived’ lung cancer. We highlight that the major health problem of COPD can be alleviated via smoking cessation, early diagnosis, and abandonment of the usage of biomass fuels on a global basis.

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