The role of associated genes of Wnt signaling pathway in chronic obstructive pulmonary disease (COPD)

Gene Reports ◽  
2020 ◽  
Vol 18 ◽  
pp. 100582 ◽  
Author(s):  
Elham Amjad ◽  
Solmaz Asnaashari ◽  
Babak Sokouti
2020 ◽  
Author(s):  
Yi Yang ◽  
Xun Zhou ◽  
Jun Zhang ◽  
Bo Li ◽  
Xinxing Wang ◽  
...  

Abstract Background The effects of Ardisia japonica (AJ) on airway remodeling in chronic obstructive pulmonary disease (COPD) rats, and the mechanisms have not been verified. This study aimed to investigate the effects of a Miao medicine, AJ on airway remodeling in COPD rats, and to assess the mechanisms.Methods COPD model was produced by cigarette smoke and intratracheal injection of lipopolysaccharide (LPS). The experiments were divided into a normal group, a COPD group, different doses of AJ treatment groups and a positive control group. After treatments, matrix metalloprotein (MMP)-9, platelet derived growth factor (PDGF) and transforming growth factor-β1 (TGF-β1) levels in inferior lobes of the right lung tissues were detected by ELISA. Expression of Wnt signaling pathway was detected by immunohistochemistry and Western blotting. To verify the function of Wnt signaling pathway in airway remodeling, airway fibroblasts obtained from COPD rats were treated with Wnt signaling pathway agonists. The cell proliferation, apoptosis, and MMP-9, PDGF, TGF-β1 levels were determined.Results The pathological changes of COPD were confirmed by haematoxylin eosin (H&E) staining. MMP-9, PDGF and TGF-β1 levels were promoted in COPD rats, which were significantly reduced by different doses of AJ treatment. Importantly, components of Wnt signaling pathway, including Wnt5a, β-catenin and RhoA were up-regulated in COPD model, which were also significantly reduced by treatment with different doses of AJ. The airway fibroblasts were obtained from COPD rats and verified based on vimentin expression. Wnt signaling pathway agonists, lithium chloride (Licl), 4-Ethyl-5,6-Dihydro-5-methyl-[1, 3] dioxolo[4,5-j] phenanthridine (HLY78), TPA and epidermal growth factor (EGF) promoted cell proliferation, reduced apoptosis, and promoted MMP-9, PDGF and TGF-β1 levels.Conclusions Our data implicated that AJ could prevent airway remodeling in COPD rats, likely via depressing Wnt signaling pathway.


2010 ◽  
Vol 151 (51) ◽  
pp. 2083-2088 ◽  
Author(s):  
Balázs Antus

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.


2020 ◽  
Vol 28 (3) ◽  
pp. 360-370
Author(s):  
Stanislav N. Kotlyarov ◽  
Anna A. Kotlyarova

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.


2021 ◽  
Vol 10 (13) ◽  
pp. 2889
Author(s):  
Klára Szalontai ◽  
Nikolett Gémes ◽  
József Furák ◽  
Tünde Varga ◽  
Patrícia Á. Neuperger ◽  
...  

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.


2015 ◽  
Vol 3 (4) ◽  
pp. 151-154 ◽  
Author(s):  
Gautam Rawal ◽  
Sankalp Yadav

AbstractCachexia and muscle wasting is a frequent but partly reversible complication in patients with chronic obstructive pulmonary disease (COPD), and affects the disease progression and prognosis. Weight loss in COPD is a consequence of increased energy requirements unbalanced by dietary intake. Nutritional supplement therapy has been shown to be effective for maintaining and improving the muscle strength and exercise tolerance in poorly nourished COPD patients, thereby decreasing morbidity and mortality. This mini review discusses the role of nutritional supplement therapy in the treatment of COPD.


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