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  1. Article ; Online: Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

    Ojiaku, Christie A / Yoo, Edwin J / Panettieri, Reynold A

    American journal of respiratory cell and molecular biology

    2017  Volume 56, Issue 4, Page(s) 432–442

    Abstract: The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and ... ...

    Abstract The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and epithelial cells, mediate all three aspects of asthma pathogenesis. Although studies show a connection between airway remodeling and changes in bronchomotor tone, the relationship between the two remains unclear. Transforming growth factor β1 (TGF-β1), a growth factor elevated in the airway of patients with asthma, plays a role in airway remodeling and in the shortening of various airway structural cells. However, the role of TGF-β1 in mediating airway hyperresponsiveness remains unclear. In this review, we summarize the literature addressing the role of TGF-β1 in airway remodeling and shortening. Through our review, we aim to further elucidate the role of TGF-β1 in asthma pathogenesis and the link between airway remodeling and airway hyperresponsiveness in asthma and to define TGF-β1 as a potential therapeutic target for reducing asthma morbidity and mortality.
    MeSH term(s) Airway Remodeling ; Animals ; Humans ; Lung/pathology ; Models, Biological ; Molecular Targeted Therapy ; Respiratory Hypersensitivity/metabolism ; Respiratory Hypersensitivity/physiopathology ; Transforming Growth Factor beta1/metabolism
    Chemical Substances Transforming Growth Factor beta1
    Language English
    Publishing date 2017-04
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2016-0307TR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    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)

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  2. Article ; Online: Phosphoinositide 3-Kinase in Asthma: Novel Roles and Therapeutic Approaches.

    Yoo, Edwin J / Ojiaku, Christie A / Sunder, Krishna / Panettieri, Reynold A

    American journal of respiratory cell and molecular biology

    2017  Volume 56, Issue 6, Page(s) 700–707

    Abstract: Asthma manifests as airway hyperresponsiveness and inflammation, including coughing, wheezing, and shortness of breath. Immune cells and airway structural cells orchestrate asthma pathophysiology, leading to mucus secretion, airway narrowing, and ... ...

    Abstract Asthma manifests as airway hyperresponsiveness and inflammation, including coughing, wheezing, and shortness of breath. Immune cells and airway structural cells orchestrate asthma pathophysiology, leading to mucus secretion, airway narrowing, and obstruction. Phosphoinositide 3-kinase, a lipid kinase, plays a crucial role in many of the cellular and molecular mechanisms driving asthma pathophysiology and represents an attractive therapeutic target. Here, we summarize the diverse roles of phosphoinositide 3-kinase in the pathogenesis of asthma and discuss novel therapeutic approaches to treatment.
    MeSH term(s) Animals ; Asthma/drug therapy ; Asthma/enzymology ; Asthma/immunology ; Asthma/therapy ; Humans ; Lymphocytes/immunology ; Models, Biological ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
    Chemical Substances Protein Kinase Inhibitors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
    Language English
    Publishing date 2017-06
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2016-0308TR
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

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    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)

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  3. Article ; Online: Dexamethasone rescues TGF-β1-mediated β

    Chung, Elena / Ojiaku, Christie A / Cao, Gaoyuan / Parikh, Vishal / Deeney, Brian / Xu, Shengjie / Wang, Serena / Panettieri, Reynold A / Koziol-White, Cynthia

    Respiratory research

    2020  Volume 21, Issue 1, Page(s) 256

    Abstract: Glucocorticoids (GCs) and ... ...

    Abstract Glucocorticoids (GCs) and β
    MeSH term(s) Anti-Inflammatory Agents/pharmacology ; Cyclic Nucleotide Phosphodiesterases, Type 4/biosynthesis ; Cyclic Nucleotide Phosphodiesterases, Type 4/genetics ; Dexamethasone/pharmacology ; Dose-Response Relationship, Drug ; Gene Expression Regulation, Enzymologic ; Humans ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Phosphodiesterase 4 Inhibitors/pharmacology ; Receptors, Adrenergic, beta-2/metabolism ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/metabolism ; Trachea/chemistry ; Trachea/drug effects ; Trachea/metabolism ; Transforming Growth Factor beta1/toxicity
    Chemical Substances Anti-Inflammatory Agents ; Phosphodiesterase 4 Inhibitors ; Receptors, Adrenergic, beta-2 ; TGFB1 protein, human ; Transforming Growth Factor beta1 ; Dexamethasone (7S5I7G3JQL) ; Cyclic Nucleotide Phosphodiesterases, Type 4 (EC 3.1.4.17)
    Language English
    Publishing date 2020-10-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041675-1
    ISSN 1465-993X ; 1465-993X
    ISSN (online) 1465-993X
    ISSN 1465-993X
    DOI 10.1186/s12931-020-01522-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: TGF-β1 Evokes Human Airway Smooth Muscle Cell Shortening and Hyperresponsiveness via Smad3.

    Ojiaku, Christie A / Cao, Gaoyuan / Zhu, Wanqu / Yoo, Edwin J / Shumyatcher, Maya / Himes, Blanca E / An, Steven S / Panettieri, Reynold A

    American journal of respiratory cell and molecular biology

    2017  Volume 58, Issue 5, Page(s) 575–584

    Abstract: Transforming growth factor β1 (TGF-β1), a cytokine whose levels are elevated in the airways of patients with asthma, perpetuates airway inflammation and modulates airway structural cell remodeling. However, the role of TGF-β1 in excessive airway ... ...

    Abstract Transforming growth factor β1 (TGF-β1), a cytokine whose levels are elevated in the airways of patients with asthma, perpetuates airway inflammation and modulates airway structural cell remodeling. However, the role of TGF-β1 in excessive airway narrowing in asthma, or airway hyperresponsiveness (AHR), remains unclear. In this study, we set out to investigate the direct effects of TGF-β1 on human airway smooth muscle (HASM) cell shortening and hyperresponsiveness. The dynamics of AHR and single-cell excitation-contraction coupling were measured in human precision-cut lung slices and in isolated HASM cells using supravital microscopy and magnetic twisting cytometry, respectively. In human precision-cut lung slices, overnight treatment with TGF-β1 significantly augmented basal and carbachol-induced bronchoconstriction. In isolated HASM cells, TGF-β1 increased basal and methacholine-induced cytoskeletal stiffness in a dose- and time-dependent manner. TGF-β1-induced single-cell contraction was corroborated by concomitant increases in myosin light chain and myosin phosphatase target subunit 1 phosphorylation levels, which were attenuated by small interfering RNA-mediated knockdown of Smad3 and pharmacological inhibition of Rho kinase. Strikingly, these physiological effects of TGF-β1 occurred through a RhoA-independent mechanism, with little effect on HASM cell [Ca
    MeSH term(s) Asthma/metabolism ; Asthma/physiopathology ; Bronchial Hyperreactivity/metabolism ; Bronchial Hyperreactivity/physiopathology ; Bronchoconstriction/drug effects ; Calcium Signaling/drug effects ; Cells, Cultured ; Excitation Contraction Coupling/drug effects ; Humans ; Muscle, Smooth/drug effects ; Muscle, Smooth/metabolism ; Muscle, Smooth/physiopathology ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Myosin Light Chains/metabolism ; Myosin-Light-Chain Phosphatase/metabolism ; Phosphorylation ; Smad3 Protein/genetics ; Smad3 Protein/metabolism ; Transforming Growth Factor beta1/pharmacology ; rho-Associated Kinases/metabolism ; rhoA GTP-Binding Protein/metabolism
    Chemical Substances Myosin Light Chains ; SMAD3 protein, human ; Smad3 Protein ; Transforming Growth Factor beta1 ; RHOA protein, human (124671-05-2) ; rho-Associated Kinases (EC 2.7.11.1) ; Myosin-Light-Chain Phosphatase (EC 3.1.3.53) ; PPP1R12A protein, human (EC 3.1.3.53) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2017-10-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2017-0247OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    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)

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  5. Article ; Online: Transforming Growth Factor-β1 Decreases β

    Ojiaku, Christie A / Chung, Elena / Parikh, Vishal / Williams, Jazmean K / Schwab, Anthony / Fuentes, Ana Lucia / Corpuz, Maia L / Lui, Victoria / Paek, Sam / Bexiga, Natalia M / Narayan, Shreya / Nunez, Francisco J / Ahn, Kwangmi / Ostrom, Rennolds S / An, Steven S / Panettieri, Reynold A

    American journal of respiratory cell and molecular biology

    2019  Volume 61, Issue 2, Page(s) 209–218

    Abstract: Helper T effector cytokines implicated in asthma modulate the contractility of human airway smooth muscle (HASM) cells. We have reported recently that a profibrotic cytokine, transforming growth factor (TGF)-β1, induces HASM cell shortening and airway ... ...

    Abstract Helper T effector cytokines implicated in asthma modulate the contractility of human airway smooth muscle (HASM) cells. We have reported recently that a profibrotic cytokine, transforming growth factor (TGF)-β1, induces HASM cell shortening and airway hyperresponsiveness. Here, we assessed whether TGF-β1 affects the ability of HASM cells to relax in response to β
    MeSH term(s) Asthma/drug therapy ; Asthma/metabolism ; Asthma/physiopathology ; Bronchodilator Agents/pharmacology ; Carbachol/pharmacology ; Cyclic AMP/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 4/metabolism ; Cytokines/metabolism ; Gene Expression Regulation ; Humans ; Isoproterenol/pharmacology ; Lung/metabolism ; Muscle, Smooth/drug effects ; Muscle, Smooth/metabolism ; Myosin Light Chains/metabolism ; Phosphorylation ; RNA, Small Interfering/metabolism ; Smad2 Protein/metabolism ; Smad3 Protein/metabolism ; Trachea/drug effects ; Trachea/metabolism ; Transforming Growth Factor beta1/metabolism ; Transforming Growth Factor beta2/agonists ; Transforming Growth Factor beta2/metabolism
    Chemical Substances Bronchodilator Agents ; Cytokines ; Myosin Light Chains ; RNA, Small Interfering ; SMAD2 protein, human ; SMAD3 protein, human ; Smad2 Protein ; Smad3 Protein ; TGFB1 protein, human ; TGFB2 protein, human ; Transforming Growth Factor beta1 ; Transforming Growth Factor beta2 ; Carbachol (8Y164V895Y) ; Cyclic AMP (E0399OZS9N) ; Cyclic Nucleotide Phosphodiesterases, Type 4 (EC 3.1.4.17) ; Isoproterenol (L628TT009W)
    Language English
    Publishing date 2019-03-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2018-0301OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    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)

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  6. Article ; Online: Gα

    Yoo, Edwin J / Cao, Gaoyuan / Koziol-White, Cynthia J / Ojiaku, Christie A / Sunder, Krishna / Jude, Joseph A / Michael, James V / Lam, Hong / Pushkarsky, Ivan / Damoiseaux, Robert / Di Carlo, Dino / Ahn, Kwangmi / An, Steven S / Penn, Raymond B / Panettieri, Reynold A

    British journal of pharmacology

    2017  Volume 174, Issue 23, Page(s) 4383–4395

    Abstract: Background and purpose: PI3K-dependent activation of Rho kinase (ROCK) is necessary for agonist-induced human airway smooth muscle cell (HASMC) contraction, and inhibition of PI3K promotes bronchodilation of human small airways. The mechanisms driving ... ...

    Abstract Background and purpose: PI3K-dependent activation of Rho kinase (ROCK) is necessary for agonist-induced human airway smooth muscle cell (HASMC) contraction, and inhibition of PI3K promotes bronchodilation of human small airways. The mechanisms driving agonist-mediated PI3K/ROCK axis activation, however, remain unclear. Given that G
    Experimental approach: Gα
    Key results: Knockdown of M
    Conclusions and implications: Gα
    MeSH term(s) Airway Obstruction/physiopathology ; Asthma/physiopathology ; Carbachol/pharmacology ; Cells, Cultured ; GTP-Binding Protein alpha Subunits, G12-G13/genetics ; GTP-Binding Protein alpha Subunits, G12-G13/metabolism ; Gene Knockdown Techniques ; Humans ; Muscle Contraction/physiology ; Muscle, Smooth/metabolism ; Myosin Light Chains/metabolism ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphorylation ; Receptor, Muscarinic M3/genetics ; Receptor, Muscarinic M3/metabolism ; Signal Transduction/physiology ; rhoA GTP-Binding Protein/metabolism
    Chemical Substances Myosin Light Chains ; Receptor, Muscarinic M3 ; Carbachol (8Y164V895Y) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; GTP-Binding Protein alpha Subunits, G12-G13 (EC 3.6.5.1) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2017-11-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.14040
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uf I Zs.146: Show issues Location:
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