LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 31

Search options

  1. Article: Airway and Extracellular Matrix Mechanics in COPD.

    Bidan, Cécile M / Veldsink, Annemiek C / Meurs, Herman / Gosens, Reinoud

    Frontiers in physiology

    2015  Volume 6, Page(s) 346

    Abstract: ... Cells and extracellular matrix in the airway and parenchymal compartments respond both passively and ... constituents of the extracellular matrix and their biomechanical impact on airway obstruction. We then review ... the changes in extracellular matrix composition in the airway and parenchymal compartments at different stages ...

    Abstract Chronic obstructive pulmonary disease (COPD) is one of the most common lung diseases worldwide, and is characterized by airflow obstruction that is not fully reversible with treatment. Even though airflow obstruction is caused by airway smooth muscle contraction, the extent of airway narrowing depends on a range of other structural and functional determinants that impact on active and passive tissue mechanics. Cells and extracellular matrix in the airway and parenchymal compartments respond both passively and actively to the mechanical stimulation induced by smooth muscle contraction. In this review, we summarize the factors that regulate airway narrowing and provide insight into the relative contributions of different constituents of the extracellular matrix and their biomechanical impact on airway obstruction. We then review the changes in extracellular matrix composition in the airway and parenchymal compartments at different stages of COPD, and finally discuss how these changes impact airway narrowing and the development of airway hyperresponsiveness. Finally, we position these data in the context of therapeutic research focused on defective tissue repair. As a conclusion, we propose that future works should primarily target mild or early COPD, prior to the widespread structural changes in the alveolar compartment that are more characteristic of severe COPD.
    Language English
    Publishing date 2015-12-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2015.00346
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article: Research trends on airway remodeling: A bibliometrics analysis.

    Liu, Pengcheng / Wang, Yu / Chen, Chen / Liu, Hui / Ye, Jing / Zhang, Xiaoming / Ma, Changxiu / Zhao, Dahai

    Heliyon

    2024  Volume 10, Issue 3, Page(s) e24824

    Abstract: ... remodeling, extracellular matrix, and non-coding RNA are the research hotspots in the field of airway ... such as asthma and COPD, which is significantly related to pulmonary function and clinical symptoms. And ... of airway remodeling to clarify current research hotspots and future research trends.: Methods: A comprehensive ...

    Abstract Background: Airway remodeling is an essential pathological basis of respiratory diseases such as asthma and COPD, which is significantly related to pulmonary function and clinical symptoms. And pulmonary disease can be improved by regulating airway remodeling. This study aimed to establish a knowledge map of airway remodeling to clarify current research hotspots and future research trends.
    Methods: A comprehensive search was performed to analyze all relevant articles on airway remodeling using the Web of Science Core Collection Database from January 01, 2004 to June 03, 2023.2 reviewers screened the retrieved literature. Besides, the CiteSpace (6.2. R3) and VOSviewer (1.6.19) were utilized to visualize the research focus and trend regarding the effect of airway remodeling.
    Results: A total of 4077 articles about airway remodeling were retrieved. The United States is the country with the most published literature, underscoring the country's role in airway remodeling. In recent years, China has been the country with the fastest growth in the number of published literature, suggesting that China will play a more critical role in airway remodeling in the future. From the perspective of co-operation among countries, European co-operation was closer than Asian co-operation. The co-citation analysis showed that 98,313 citations were recorded in 3594 articles, and 25 clusters could be realized. In recent years, Burst detection shows that oxidative stress and epithelial-mesenchymal transition are hot words.
    Conclusions: Based on the bibliometric analysis of airway remodeling studies in the past 20 years, a multi-level knowledge structure map was drawn, it mainly includes countries, institutions, research fields, authors, journals, keywords and so on. The research directions represented by obstructive airway disease, PDGF-BB treatment of airway smooth muscle, allergen-induced airway remodeling, extracellular matrix, and non-coding RNA are the research hotspots in the field of airway remodeling. While the risk factors for airway remodeling, the application of new noninvasively assessing tools, biomarkers as well as The molecular mechanism represented by EMT and autophagy had been frontiers in recent years.
    Language English
    Publishing date 2024-01-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 2835763-2
    ISSN 2405-8440
    ISSN 2405-8440
    DOI 10.1016/j.heliyon.2024.e24824
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Stiffness Mediated-Mechanosensation of Airway Smooth Muscle Cells on Linear Stiffness Gradient Hydrogels.

    Tan, Yong Hwee / Wang, Kimberley C W / Chin, Ian L / Sanderson, Rowan W / Li, Jiayue / Kennedy, Brendan F / Noble, Peter B / Choi, Yu Suk

    Advanced healthcare materials

    2024  , Page(s) e2304254

    Abstract: ... the extracellular matrix (ECM) protein amount and composition of the airway smooth muscle (ASM) is often remodelled, likely ... In obstructive airway diseases such as asthma and chronic obstructive pulmonary disease (COPD ... by uniaxial compression tester using porcine ASM layers under 0, 5 and 10% longitudinal stretch above in situ ...

    Abstract In obstructive airway diseases such as asthma and chronic obstructive pulmonary disease (COPD), the extracellular matrix (ECM) protein amount and composition of the airway smooth muscle (ASM) is often remodelled, likely altering tissue stiffness. The underlying mechanism of how human ASM cell (hASMC) mechanosenses the aberrant microenvironment is not well understood. Physiological stiffnesses of the ASM were measured by uniaxial compression tester using porcine ASM layers under 0, 5 and 10% longitudinal stretch above in situ length. Linear stiffness gradient hydrogels (230 kPa range) were fabricated and functionalized with ECM proteins, collagen I (ColI), fibronectin (Fn) and laminin (Ln), to recapitulate the above-measured range of stiffnesses. Overall, hASMC mechanosensation exhibited a clear correlation with the underlying hydrogel stiffness. Cell size, nuclear size and contractile marker alpha-smooth muscle actin (αSMA) expression showed a strong correlation to substrate stiffness. Mechanosensation, assessed by Lamin-A intensity and nuc/cyto YAP, exhibited stiffness-mediated behaviour only on ColI and Fn-coated hydrogels. Inhibition studies using blebbistatin or Y27632 attenuated most mechanotransduction-derived cell morphological responses, αSMA and Lamin-A expression and nuc/cyto YAP (blebbistatin only). This study highlights the interplay and complexities between stiffness and ECM protein type on hASMC mechanosensation, relevant to airway remodelling in obstructive airway diseases.
    Language English
    Publishing date 2024-04-09
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2649576-4
    ISSN 2192-2659 ; 2192-2640
    ISSN (online) 2192-2659
    ISSN 2192-2640
    DOI 10.1002/adhm.202304254
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 6966: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression?

    Bu, Tegeleqi / Wang, Li Fang / Yin, Yi Qing

    International journal of chronic obstructive pulmonary disease

    2020  Volume 15, Page(s) 107–116

    Abstract: ... disorganization, mucus hypersecretion, and extracellular matrix deposition. Dendritic cells (DCs) exhibit ... the activation of inflammatory cells could possibly delay the progression of airway remodeling in COPD, and ... over-simplified in descriptions of the mechanism of COPD progression. As a form of first-line airway ...

    Abstract Recently, the therapeutic potential of immune-modulation during the progression of chronic obstructive pulmonary disease (COPD) has been attracting increasing interest. However, chronic inflammatory response has been over-simplified in descriptions of the mechanism of COPD progression. As a form of first-line airway defense, epithelial cells exhibit phenotypic alteration, and participate in epithelial layer disorganization, mucus hypersecretion, and extracellular matrix deposition. Dendritic cells (DCs) exhibit attenuated antigen-presenting capacity in patients with advanced COPD. Immature DCs migrate into small airways, where they promote a pro-inflammatory microenvironment and bacterial colonization. In response to damage-associated molecular patterns (DAMPs) in lung tissue affected by COPD, neutrophils are excessively recruited and activated, where they promote a proteolytic microenvironment and fibrotic repair in small airways. Macrophages exhibit decreased phagocytosis in the large airways, while they demonstrate high pro-inflammatory potential in the small airways, and mediate alveolar destruction and chronic airway inflammation. Natural killer T (NKT) cells, eosinophils, and mast cells also play supplementary roles in COPD progression; however, their cellular activities are not yet entirely clear. Overall, during COPD progression, "exhausted" innate immune responses can be observed in the large airways. On the other hand, the innate immune response is enhanced in the small airways. Approaches that inhibit the inflammatory cascade, chemotaxis, or the activation of inflammatory cells could possibly delay the progression of airway remodeling in COPD, and may thus have potential clinical significance.
    MeSH term(s) Airway Remodeling ; Animals ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Disease Progression ; Eosinophils/immunology ; Eosinophils/metabolism ; Humans ; Immunity, Cellular ; Immunity, Innate ; Lung/immunology ; Lung/metabolism ; Lung/physiopathology ; Macrophages/immunology ; Macrophages/metabolism ; Mast Cells/immunology ; Mast Cells/metabolism ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Neutrophils/immunology ; Neutrophils/metabolism ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Signal Transduction
    Language English
    Publishing date 2020-01-10
    Publishing country New Zealand
    Document type Journal Article ; Review
    ISSN 1178-2005
    ISSN (online) 1178-2005
    DOI 10.2147/COPD.S235054
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  5. Article ; Online: HDAC6 Activates ERK in Airway and Pulmonary Vascular Remodeling of Chronic Obstructive Pulmonary Disease.

    Su, Yunchao / Han, Weihong / Kovacs-Kasa, Anita / Verin, Alexander D / Kovacs, Laszlo

    American journal of respiratory cell and molecular biology

    2021  Volume 65, Issue 6, Page(s) 603–614

    Abstract: ... the overproduction of extracellular matrix (e.g., collagen). Cigarette smoke (CS) and several mediators, such as PDGF ... platelet-derived growth factor) and IL-6, play critical roles in COPD pathogenesis. HDAC6 has been shown to be implicated ... in the lungs of patients with COPD and a COPD animal model. We also found that CS extract (CSE), PDGF, and IL-6 ...

    Abstract Chronic obstructive pulmonary disease (COPD) is a multisystemic respiratory disease that is associated with progressive airway and pulmonary vascular remodeling due to the increased proliferation of bronchial smooth muscles cells (BSMCs) and pulmonary arterial smooth muscle cells (PASMCs) and the overproduction of extracellular matrix (e.g., collagen). Cigarette smoke (CS) and several mediators, such as PDGF (platelet-derived growth factor) and IL-6, play critical roles in COPD pathogenesis. HDAC6 has been shown to be implicated in vascular remodeling. However, the role of airway HDAC6 signaling in pulmonary vascular remodeling in COPD and the underlying mechanisms remain undetermined. Here, we show that HDAC6 expression is upregulated in the lungs of patients with COPD and a COPD animal model. We also found that CS extract (CSE), PDGF, and IL-6 increase the protein levels and activation of HDAC6 in BSMCs and PASMCs. Furthermore, CSE and these stimulants induced deacetylation and phosphorylation of ERK1/2 and increased collagen synthesis and BSMC and PASMC proliferation, which were outcomes that were prevented by HDAC6 inhibition. Inhibition of ERK1/2 also diminished the CSE-, PDGF-, and IL-6-caused elevation in collagen levels and cell proliferation. Pharmacologic HDAC6 inhibition with tubastatin A prevented the CS-stimulated increases in the thickness of the bronchial and pulmonary arterial wall, airway resistance, emphysema, and right ventricular systolic pressure and right ventricular hypertrophy in a rat model of COPD. These data demonstrate that the upregulated HDAC6 governs the collagen synthesis and BSMC and PASMC proliferation that lead to airway and vascular remodeling in COPD.
    MeSH term(s) Airway Remodeling ; Animals ; Cytokines/metabolism ; Disease Models, Animal ; Histone Deacetylase 6/antagonists & inhibitors ; Histone Deacetylase 6/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Indoles/pharmacology ; MAP Kinase Signaling System ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/pathology ; Myocytes, Smooth Muscle/enzymology ; Myocytes, Smooth Muscle/pathology ; Pulmonary Artery/enzymology ; Pulmonary Artery/pathology ; Pulmonary Disease, Chronic Obstructive/enzymology ; Pulmonary Disease, Chronic Obstructive/pathology ; Rats ; Rats, Sprague-Dawley ; Vascular Remodeling
    Chemical Substances Cytokines ; Hydroxamic Acids ; Indoles ; tubastatin A (2XTSOX1NF8) ; HDAC6 protein, human (EC 3.5.1.98) ; HDAC6 protein, rat (EC 3.5.1.98) ; Histone Deacetylase 6 (EC 3.5.1.98)
    Language English
    Publishing date 2021-07-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2020-0520OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Mechanisms of airway remodeling.

    Hirota, Nobuaki / Martin, James G

    Chest

    2013  Volume 144, Issue 3, Page(s) 1026–1032

    Abstract: ... affecting airway smooth muscle, epithelium, blood vessels, and extracellular matrix. It occurs in patients ... with chronic inflammatory airway diseases such as asthma, COPD, bronchiectasis, and cystic fibrosis ... Airway remodeling comprises the structural changes of airway walls, induced by repeated injury and ...

    Abstract Airway remodeling comprises the structural changes of airway walls, induced by repeated injury and repair processes. It is characterized by the changes of tissue, cellular, and molecular composition, affecting airway smooth muscle, epithelium, blood vessels, and extracellular matrix. It occurs in patients with chronic inflammatory airway diseases such as asthma, COPD, bronchiectasis, and cystic fibrosis. Airway remodeling is arguably one of the most intractable problems in these diseases, leading to irreversible loss of lung function. Current therapeutics can ameliorate inflammation, but there is no available therapy proven to prevent or reverse airway remodeling, although reversibility of airway remodeling is suggested by studies in animal models of disease. Airway remodeling is often considered the result of longstanding airway inflammation, but it may be present to an equivalent degree in the airways of children with asthma, raising the necessity for early and specific therapeutic interventions. In this review, we consider the factors that may contribute to airway remodeling and discuss the current and potential therapeutic interventions.
    MeSH term(s) Airway Remodeling/physiology ; Animals ; Asthma/pathology ; Asthma/physiopathology ; Humans ; Lung/physiopathology ; Pulmonary Disease, Chronic Obstructive/pathology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Respiratory Mucosa/pathology ; Respiratory Mucosa/physiopathology ; Respiratory Physiological Phenomena
    Language English
    Publishing date 2013-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1378/chest.12-3073
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ui III Zs.45: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 349: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  7. Article ; Online: Investigation of the role of the autophagic protein LC3B in the regulation of human airway epithelium cell differentiation in COPD using a biomimetic model

    Shiue-Luen Chen / Hsiao-Chun Chou / Kuan-Chen Lin / Jia-Wei Yang / Ren-Hao Xie / Chong-You Chen / Xin-Yi Liu / Johnson H.Y. Chung / Guan-Yu Chen

    Materials Today Bio, Vol 13, Iss , Pp 100182- (2022)

    2022  

    Abstract: ... characteristics by regulating the biological microenvironment, extracellular matrix, and air-liquid interface ... LC3B in normal and COPD human small airway epithelial cells and found that the nucleus of COPD cells ... differentiation and function of COPD cells. Our innovative model can be used to further analyze the physiological ...

    Abstract Chronic obstructive pulmonary disease (COPD) is one of the most lethal chronic disease worldwide; however, the establishment of reliable in vitro models for exploring the biological mechanisms of COPD remains challenging. Here, we determined the differences in the expression and characteristics of the autophagic protein LC3B in normal and COPD human small airway epithelial cells and found that the nucleus of COPD cells obviously accumulated LC3B. We next established 3D human small airway tissues with distinct disease characteristics by regulating the biological microenvironment, extracellular matrix, and air-liquid interface culture methods. Using this biomimetic model, we found that LC3B affects the differentiation of COPD cells into basal, secretory, mucous, and ciliated cells. Moreover, although chloroquine and ivermectin effectively inhibited the expression of LC3B in the nucleus, chloroquine specifically maintained the performance of LC3B in cytoplasm, thereby contributing to the differentiation of ciliated cells and subsequent improvement in the beating functions of the cilia, whereas ivermectin only facilitated differentiation of goblet cells. We demonstrated that the autophagic mechanism of LC3B in the nucleus is one factor regulating the ciliary differentiation and function of COPD cells. Our innovative model can be used to further analyze the physiological mechanisms in the in vitro airway environment.
    Keywords Chronic obstructive pulmonary disease ; Airway epithelial cells ; Autophagy ; Cell differentiation ; Cilia beating ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  8. Article ; Online: Let-7 mediated airway remodelling in chronic obstructive pulmonary disease via the regulation of IL-6.

    Di, Tingting / Yang, Yue / Fu, Congli / Zhang, Zixiao / Qin, Chu / Sai, Xiaoyan / Liu, Jiaxin / Hu, Caixia / Zheng, Mingfeng / Wu, Yan / Bian, Tao

    European journal of clinical investigation

    2020  Volume 51, Issue 4, Page(s) e13425

    Abstract: Background: Myofibroblast differentiation and extracellular matrix (ECM) deposition are observed ... serum and primary bronchial epithelial cells of COPD patients and cigarette smoke (CS)-exposed mice. IL ... 6 mRNA was explored in lung tissues of COPD patients and CS-exposed mice. IL-6 protein was detected ...

    Abstract Background: Myofibroblast differentiation and extracellular matrix (ECM) deposition are observed in chronic obstructive pulmonary disease (COPD). However, the mechanisms of regulation of myofibroblast differentiation remain unclear.
    Materials and methods: We detected let-7 levels in peripheral lung tissues, serum and primary bronchial epithelial cells of COPD patients and cigarette smoke (CS)-exposed mice. IL-6 mRNA was explored in lung tissues of COPD patients and CS-exposed mice. IL-6 protein was detected in cell supernatant from primary epithelial cells by ELISA. We confirmed the regulatory effect of let-7 on IL-6 by luciferase reporter assay. Western blotting assay was used to determine the expression of α-SMA, E-cadherin and collagen I. In vitro, cell study was performed to demonstrate the role of let-7 in myofibroblast differentiation and ECM deposition.
    Results: Low expression of let-7 was observed in COPD patients, CS-exposed mice and CS extract (CSE)-treated human bronchial epithelial (HBE) cells. Increased IL-6 was found in COPD patients, CS-exposed mice and CSE-treated HBE cells. Let-7 targets and silences IL-6 protein coding genes through binding to 3' untranslated region (UTR) of IL-6. Normal or CSE-treated HBE cells were co-cultured with human embryonic lung fibroblasts (MRC-5 cells). Reduction of let-7 in HBE cells caused myofibroblast differentiation and ECM deposition, while increase of let-7 mimics decreased myofibroblast differentiation phenotype and ECM deposition.
    Conclusion: We demonstrate that CS reduced let-7 expression in COPD and, further, identify let-7 as a regulator of myofibroblast differentiation through the regulation of IL-6, which has potential value for diagnosis and treatment of COPD.
    MeSH term(s) Actins/metabolism ; Adult ; Aged ; Airway Remodeling/genetics ; Animals ; Cadherins/metabolism ; Cell Differentiation/genetics ; Cigarette Smoking ; Collagen Type I/metabolism ; Epithelial Cells/metabolism ; Extracellular Matrix/metabolism ; Female ; Humans ; In Vitro Techniques ; Interleukin-6/metabolism ; Lung/metabolism ; Male ; Mice ; MicroRNAs/genetics ; Middle Aged ; Myofibroblasts/metabolism ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/pathology ; RNA, Messenger/metabolism ; Respiratory Mucosa/cytology ; Respiratory Mucosa/metabolism ; Smoke ; Tobacco Products
    Chemical Substances ACTA2 protein, human ; Actins ; Cadherins ; Collagen Type I ; Interleukin-6 ; MicroRNAs ; RNA, Messenger ; Smoke ; alpha-smooth muscle actin, mouse ; mirnlet7 microRNA, human ; mirnlet7 microRNA, mouse
    Language English
    Publishing date 2020-10-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 186196-7
    ISSN 1365-2362 ; 0014-2972 ; 0960-135X
    ISSN (online) 1365-2362
    ISSN 0014-2972 ; 0960-135X
    DOI 10.1111/eci.13425
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 677: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  9. Article ; Online: Altered DNA methylation is associated with aberrant gene expression in parenchymal but not airway fibroblasts isolated from individuals with COPD.

    Clifford, Rachel L / Fishbane, Nick / Patel, Jamie / MacIsaac, Julia L / McEwen, Lisa M / Fisher, Andrew J / Brandsma, Corry-Anke / Nair, Parameswaran / Kobor, Michael S / Hackett, Tillie-Louise / Knox, Alan J

    Clinical epigenetics

    2018  Volume 10, Page(s) 32

    Abstract: ... within the airway and parenchyma of the lung and contribute to the aberrant deposition of extracellular matrix ... in COPD. No assessment or comparison of genome-wide DNA methylation profiles in the airway and parenchymal ... into the molecular mechanisms contributing to COPD and the differing pathologies of small airways disease and ...

    Abstract Background: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease of the lungs that is currently the fourth leading cause of death worldwide. Genetic factors account for only a small amount of COPD risk, but epigenetic mechanisms, including DNA methylation, have the potential to mediate the interactions between an individual's genetics and environmental exposure. DNA methylation is highly cell type-specific, and individual cell type studies of DNA methylation in COPD are sparse. Fibroblasts are present within the airway and parenchyma of the lung and contribute to the aberrant deposition of extracellular matrix in COPD. No assessment or comparison of genome-wide DNA methylation profiles in the airway and parenchymal fibroblasts from individuals with and without COPD has been undertaken. These data provide valuable insight into the molecular mechanisms contributing to COPD and the differing pathologies of small airways disease and emphysema in COPD.
    Methods: Genome-wide DNA methylation was evaluated at over 485,000 CpG sites using the Illumina Infinium HumanMethylation450 BeadChip array in the airway (non-COPD
    Results: Differentially methylated DNA regions were identified between cells isolated from individuals with and without COPD in both airway and parenchymal fibroblasts. Only in parenchymal fibroblasts was differential DNA methylation associated with differential gene expression. A second analysis of differential DNA methylation variability identified 359 individual differentially variable CpG sites in parenchymal fibroblasts. No differentially variable CpG sites were identified in the airway fibroblasts. Five differentially variable-methylated CpG sites, associated with three genes, were subsequently assessed for gene expression differences. Two genes (OAT and GRIK2) displayed significantly increased gene expression in cells isolated from individuals with COPD.
    Conclusions: Differential and variable DNA methylation was associated with COPD status in the parenchymal fibroblasts but not airway fibroblasts. Aberrant DNA methylation was associated with altered gene expression imparting biological function to DNA methylation changes. Changes in DNA methylation are therefore implicated in the molecular mechanisms underlying COPD pathogenesis and may represent novel therapeutic targets.
    MeSH term(s) Aged ; Cells, Cultured ; CpG Islands ; DNA Methylation ; Epigenesis, Genetic ; Female ; Fibroblasts/chemistry ; Gene Expression Profiling/methods ; Gene Expression Regulation ; Humans ; Lung/chemistry ; Lung/cytology ; Male ; Middle Aged ; Organ Specificity ; Ornithine-Oxo-Acid Transaminase/genetics ; Parenchymal Tissue/chemistry ; Parenchymal Tissue/cytology ; Pulmonary Disease, Chronic Obstructive/genetics ; Receptors, Kainic Acid/genetics ; Sequence Analysis, DNA ; Up-Regulation ; GluK2 Kainate Receptor
    Chemical Substances Receptors, Kainic Acid ; OAT protein, human (EC 2.6.1.1.13) ; Ornithine-Oxo-Acid Transaminase (EC 2.6.1.13)
    Language English
    Publishing date 2018-03-05
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553921-8
    ISSN 1868-7083 ; 1868-7075
    ISSN (online) 1868-7083
    ISSN 1868-7075
    DOI 10.1186/s13148-018-0464-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  10. Article ; Online: Tiotropium inhibits methacholine-induced extracellular matrix production via β-catenin signaling in human airway smooth muscle cells.

    Huo, Yating / Guan, Lili / Xu, Jiawen / Zhou, Luqian / Chen, Rongchang

    International journal of chronic obstructive pulmonary disease

    2018  Volume 13, Page(s) 1469–1481

    Abstract: ... alteration of the extracellular matrix (ECM) surrounding the airway smooth muscle (ASM) bundle is one ... COPD) that is associated with disease severity and irreversible airflow limitation. An extensive ... to investigate the influence of tiotropium on ECM production by ASMCs and the underlying mechanism.: Methods ...

    Abstract Background: Airway remodeling is an important feature of chronic obstructive pulmonary disease (COPD) that is associated with disease severity and irreversible airflow limitation. An extensive alteration of the extracellular matrix (ECM) surrounding the airway smooth muscle (ASM) bundle is one of the pathological manifestations of airway remodeling, which contributes to the decline in lung function. Tiotropium, a long-acting inhaled muscarinic receptor antagonist, has been confirmed to play a role in preventing airway remodeling including ECM deposition beyond bronchodilation in vivo, but the relationship between ASM cell (ASMC) relaxation and ECM production remains unclear.
    Purpose: In this study, we attempted to investigate the influence of tiotropium on ECM production by ASMCs and the underlying mechanism.
    Methods: Tiotropium was added 30 minutes before the addition of methacholine to primary cultured human ASMCs. Protein expression was analylized by Western Blot and mRNA abundance was determined by real-time PCR.
    Results: We found that tiotropium reduced collagen I protein expression, and the mRNA abundance of
    Conclusion: These findings suggest that relaxation of ASMCs by tiotropium can prevent ECM production through β-catenin signaling.
    MeSH term(s) Adult ; Airway Remodeling/drug effects ; Bronchi/drug effects ; Bronchi/metabolism ; Bronchodilator Agents/pharmacology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Extracellular Matrix/genetics ; Extracellular Matrix/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Male ; Methacholine Chloride/pharmacology ; Middle Aged ; Muscarinic Antagonists/pharmacology ; Muscle, Smooth/drug effects ; Muscle, Smooth/metabolism ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Phosphorylation ; Signal Transduction/drug effects ; Tiotropium Bromide/pharmacology ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances Bronchodilator Agents ; CTNNB1 protein, human ; Extracellular Matrix Proteins ; Muscarinic Antagonists ; beta Catenin ; Methacholine Chloride (0W5ETF9M2K) ; GSK3B protein, human (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Tiotropium Bromide (XX112XZP0J)
    Language English
    Publishing date 2018-05-03
    Publishing country New Zealand
    Document type Journal Article
    ISSN 1178-2005
    ISSN (online) 1178-2005
    DOI 10.2147/COPD.S158552
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top