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Article ; Online: Abi1 mediates airway smooth muscle cell proliferation and airway remodeling via Jak2/STAT3 signaling

Ruping Wang / Yinna Wang / Guoning Liao / Bohao Chen / Reynold A. Panettieri, Jr. / Raymond B. Penn / Dale D. Tang

iScience, Vol 25, Iss 2, Pp 103833- (2022)

2022

Abstract: Summary: Asthma is a complex pulmonary disorder with multiple pathological mechanisms. A key pathological feature of chronic asthma is airway remodeling, which is largely attributed to airway smooth muscle (ASM) hyperplasia that contributes to thickening ...

Abstract	Summary: Asthma is a complex pulmonary disorder with multiple pathological mechanisms. A key pathological feature of chronic asthma is airway remodeling, which is largely attributed to airway smooth muscle (ASM) hyperplasia that contributes to thickening of the airway wall and further drives asthma pathology. The cellular processes that mediate ASM cell proliferation are not completely elucidated. Using multiple approaches, we demonstrate that the adapter protein Abi1 (Abelson interactor 1) is upregulated in ∼50% of ASM cell cultures derived from patients with asthma. Loss-of-function studies demonstrate that Abi1 regulates the activation of Jak2 (Janus kinase 2) and STAT3 (signal transducers and activators of transcription 3) as well as the proliferation of both nonasthmatic and asthmatic human ASM cell cultures. These findings identify Abi1 as a molecular switch that activates Jak2 kinase and STAT3 in ASM cells and demonstrate that a dysfunctional Abi1-associated pathway contributes to the progression of asthma.
Keywords	Respiratory medicine ; Molecular biology ; Cell biology ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: An inherent dysfunction in soluble guanylyl cyclase is present in the airway of severe asthmatics and is associated with aberrant redox enzyme expression and compromised NO-cGMP signaling

Arnab Ghosh / Cynthia J. Koziol-White / William F. Jester, Jr. / Serpil C. Erzurum / Kewal Asosingh / Reynold A. Panettieri, Jr. / Dennis J. Stuehr

Redox Biology, Vol 39, Iss , Pp 101832- (2021)

2021

Abstract: A subset of asthmatics develop a severe form of the disease whose etiology involves airway inflammation along with inherent drivers that remain ill-defined. To address this, we studied human airway smooth muscle cells (HASMC), whose relaxation drives ... ...

Abstract	A subset of asthmatics develop a severe form of the disease whose etiology involves airway inflammation along with inherent drivers that remain ill-defined. To address this, we studied human airway smooth muscle cells (HASMC), whose relaxation drives airway bronchodilation and whose dysfunction contributes to airway obstruction and hypersensitivity in severe asthma. Because HASMC relaxation can be driven by the NO-soluble guanylyl cyclase (sGC)-cGMP signaling pathway, we questioned if HASMC from severe asthma donors might possess inherent defects in their sGC or in redox enzymes that support sGC function. We analyzed HASMC primary lines derived from 17 severe asthma and 16 normal donors and corresponding lung tissue samples regarding sGC activation by NO or by pharmacologic agonists, and also determined expression levels of sGC α1 and β1 subunits, supporting redox enzymes, and related proteins. We found a majority of the severe asthma donor HASMC (12/17) and lung samples primarily expressed a dysfunctional sGC that was NO-unresponsive and had low heterodimer content and high Hsp90 association. This sGC phenotype correlated with lower expression levels of the supporting redox enzymes cytochrome b5 reductase, catalase, and thioredoxin-1, and higher expression of heme oxygenases 1 and 2. Together, our work reveals that severe asthmatics are predisposed toward defective NO-sGC-cGMP signaling in their airway smooth muscle due to an inherent sGC dysfunction, which in turn is associated with inherent changes in the cell redox enzymes that impact sGC maturation and function.
Keywords	Inflammation ; Cell Signaling ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Vitamin D modulates airway smooth muscle function in COPD

Banerjee, Audreesh / Panettieri, Reynold, Jr

Current opinion in pharmacology. 2012 June, v. 12, no. 3

2012

Abstract: COPD is a disease manifested as persistent airflow obstruction with an enhanced inflammatory response in the airways and lungs to noxious particles and gases which evokes symptoms of dyspnea on exertion, cough and mucus production. Airway smooth muscle ... ...

Abstract	COPD is a disease manifested as persistent airflow obstruction with an enhanced inflammatory response in the airways and lungs to noxious particles and gases which evokes symptoms of dyspnea on exertion, cough and mucus production. Airway smooth muscle plays a central role in the COPD diathesis and is implicated in many aspects of COPD pathogenesis. Vitamin D deficiency has been associated with COPD severity and studies suggest a role for Vitamin D as a treatment for COPD. In this review, we describe the effects of 1,25-dihydroxyvitamin D on airway smooth muscle function, including agonist-induced shortening, secretion of inflammatory mediators, and myocyte hypertrophy and hyperplasia.
Keywords	air flow ; cough ; dyspnea ; gases ; hyperplasia ; hypertrophy ; inflammation ; lungs ; mucus ; pathogenesis ; secretion ; smooth muscle ; vitamin D ; vitamin D deficiency
Language	English
Dates of publication	2012-06
Size	p. 266-274.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2012.01.014
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Article: p38 MAPK inhibitors, IKK2 inhibitors, and TNFα inhibitors in COPD

Banerjee, Audreesh / Koziol-White, Cynthia / Panettieri, Reynold, Jr

Current opinion in pharmacology. 2012 June, v. 12, no. 3

2012

Abstract: COPD represents a major respiratory disorder, causing significant morbidity and mortality throughout the world. While therapies exist for COPD, they are not always effective, and many patients experience exacerbations and morbidity despite current ... ...

Abstract	COPD represents a major respiratory disorder, causing significant morbidity and mortality throughout the world. While therapies exist for COPD, they are not always effective, and many patients experience exacerbations and morbidity despite current therapies. Study of the molecular mechanisms involved in the underlying physiological manifestations of COPD has yielded multiple new targets for therapeutic intervention. In this review, we discuss signaling pathways involved in COPD pathogenesis and review clinical studies of p38 MAPK inhibitors, TNFα inhibitors, and IKK2 inhibitors as potential COPD therapies.
Keywords	clinical trials ; mitogen-activated protein kinase ; morbidity ; mortality ; pathogenesis ; patients ; respiratory tract diseases ; signal transduction ; tumor necrosis factor-alpha
Language	English
Dates of publication	2012-06
Size	p. 287-292.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2012.01.016
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Article: Drug development for severe asthma: What are the metrics?

Robinson, Cynthia B / Leonard, Joanne / Panettieri, Reynold A., Jr

Pharmacology and therapeutics. 2012 Aug., v. 135, no. 2

2012

Abstract: Although reversible airway obstruction in part defines asthma, lung function as measured by spirometry alone inadequately predicts the value of new therapeutic agents in the treatment of severe asthma. Our objectives are 1) to review whether pulmonary ... ...

Abstract	Although reversible airway obstruction in part defines asthma, lung function as measured by spirometry alone inadequately predicts the value of new therapeutic agents in the treatment of severe asthma. Our objectives are 1) to review whether pulmonary function and bronchodilator reversibility are endpoints for drug discovery and 2) to identify parameters that predict efficacy in drug development in severe asthma. An English language literature search using MedLine and PubMed was conducted from 1997 to present concerning pathophysiology, diagnosis and therapy of severe asthma using the terms “severe asthma,” “irreversible asthma,” “difficult asthma,” “airway remodeling,” “fixed airway obstruction,” “reversibility” and “bronchodilator reversibility” as index terms. Eight studies were characterized that encompass 1424 subjects with asthma. Our review identified the limitations of using bronchodilator reversibility as a predictor in drug development for severe asthma. Neither improvement in lung function nor bronchodilator reversibility characterized the benefit of new drugs in the treatment of severe asthma. Newly approved drugs in the treatment of severe asthma show decreased asthma exacerbations and improved quality of life associated with steroid-sparing benefits without altering bronchodilator responsiveness or improving lung function. Although changes in lung function predict asthma control in mild/moderate asthma, lung function alone is inadequate to assess improvement in asthma control in severe asthma manifested by fixed airway obstruction. Endpoints that focus on asthma control, as defined by the Expert Panel Report 3 and GINA guidelines, may predict the value of new therapeutics in the management of severe asthma.
Keywords	asthma ; bronchodilators ; guidelines ; lung function ; new drugs ; pathophysiology ; quality of life ; therapeutics
Language	English
Dates of publication	2012-08
Size	p. 176-181.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2012.05.005
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Article ; Online: Guidance for the use and reporting of anaesthetic agents in BJP manuscripts involving work with animals.

British journal of pharmacology

2022 Volume 180, Issue 3, Page(s) 255–263

Abstract: Scientists who plan to publish in the British Journal of Pharmacology (BJP) should read this article before undertaking studies utilising anaesthetics in mammalian animals. This editorial identifies certain gaps in the reporting of details on the use of ... ...

Abstract	Scientists who plan to publish in the British Journal of Pharmacology (BJP) should read this article before undertaking studies utilising anaesthetics in mammalian animals. This editorial identifies certain gaps in the reporting of details on the use of anaesthetics in animal research studies published in the BJP. The editorial also provides guidance, based upon current best practices, for performing in vivo experiments that require anaesthesia. In addition, mechanisms of action and physiological impact of specific anaesthetic agents are discussed. Our goal is to identify best practices and to provide guidance on the information required for manuscripts submitted to the BJP that involve the use of anaesthetic agents in studies with experimental animals.
MeSH term(s)	Animals ; Anesthetics/pharmacology ; Anesthesia ; Animal Experimentation ; Mammals
Chemical Substances	Anesthetics
Language	English
Publishing date	2022-12-18
Publishing country	England
Document type	Editorial
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15992
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Article ; Online: Mucins MUC5AC and MUC5B Are Variably Packaged in the Same and in Separate Secretory Granules.

American journal of respiratory and critical care medicine

2022 Volume 206, Issue 9, Page(s) 1081–1095

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Humans ; Mice ; Animals ; Swine ; Mucin-5B ; Mucin 5AC ; Lung/metabolism ; Pulmonary Disease, Chronic Obstructive ; Secretory Vesicles/metabolism ; Mammals/metabolism
Chemical Substances	Mucin-5B ; Mucin 5AC ; MUC5B protein, human ; MUC5AC protein, human ; Muc5ac protein, mouse ; Muc5b protein, mouse
Language	English
Publishing date	2022-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202202-0309OC
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Article ; Online: Asthma Yardstick: Practical recommendations for a sustained step-up in asthma therapy for poorly controlled asthma.

Chipps, Bradley E / Corren, Jonathan / Israel, Elliot / Katial, Rohit / Lang, David M / Panettieri, Reynold A / Peters, Stephen P / Farrar, Judith R

Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology

2017 Volume 118, Issue 2, Page(s) 133–142.e3

Abstract: Current asthma guidelines recommend a control-based approach to management that involves assessment of impairment and risk followed by implementation of treatment strategies individualized according to the patient's needs and preferences. The fact that ... ...

Abstract	Current asthma guidelines recommend a control-based approach to management that involves assessment of impairment and risk followed by implementation of treatment strategies individualized according to the patient's needs and preferences. The fact that many patients still experience severe symptoms that negatively affect quality of life suggests that asthma control remains an objective to be achieved. Tools are available to help patients (and families) manage the day-to-day and short-term variability in asthma symptoms; however, when and how to implement a sustained step-up in therapy is less clear. The Asthma Yardstick is a comprehensive update on how to conduct a sustained step-up in asthma therapy for the patient with not well-controlled or poorly controlled asthma. Patient profiles and step-up strategies are based on current guidelines, newer data, and the authors' combined clinical experience and are intended to provide a practical and clinically meaningful guide toward the goal of well-controlled asthma for every patient. The development of this tool comes in response to the continued need to proactively address the sustained loss of asthma control at all levels of severity.
MeSH term(s)	Algorithms ; Anti-Asthmatic Agents/administration & dosage ; Anti-Asthmatic Agents/therapeutic use ; Asthma/diagnosis ; Asthma/immunology ; Asthma/therapy ; Disease Management ; Eosinophils/drug effects ; Eosinophils/immunology ; Eosinophils/metabolism ; Humans ; Immunoglobulin E/immunology ; Molecular Targeted Therapy ; Neutrophils/drug effects ; Neutrophils/immunology ; Neutrophils/metabolism ; Practice Guidelines as Topic ; Severity of Illness Index ; Workflow
Chemical Substances	Anti-Asthmatic Agents ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2017-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1228189-x
ISSN	1534-4436 ; 0003-4738 ; 1081-1206
ISSN (online)	1534-4436
ISSN	0003-4738 ; 1081-1206
DOI	10.1016/j.anai.2016.12.010
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Article: Regulator of G protein signaling 2 is a key modulator of airway hyperresponsiveness

Xie, Yan / Jiang, Haihong / Nguyen, Hoai / Jia, Shuping / Berro, Abdo / Panettieri, Reynold A., Jr / Wolff, Dennis W / Abel, Peter W / Casale, Thomas B / Tu, Yaping

The Journal of Allergy and Clinical Immunology. 2012 Oct., v. 130, no. 4

2012

Abstract: BACKGROUND: Drugs targeting individual G protein–coupled receptors are used as asthma therapies, but this strategy is limited because of G protein–coupled receptor signal redundancy. Regulator of G protein signaling 2 (RGS2), an intracellular selective ... ...

Abstract	BACKGROUND: Drugs targeting individual G protein–coupled receptors are used as asthma therapies, but this strategy is limited because of G protein–coupled receptor signal redundancy. Regulator of G protein signaling 2 (RGS2), an intracellular selective inhibitor of multiple bronchoconstrictor receptors, may play a central role in the pathophysiology and treatment of asthma. OBJECTIVE: We defined functions and mechanisms of RGS2 in regulating airway hyperresponsiveness (AHR), the pathophysiologic hallmark of asthma. METHODS: Real-time PCR and Western blot were used to determine changes in RGS2 expression in ovalbumin-sensitized/-challenged mice. We also used immunohistochemistry and real-time PCR to compare RGS2 expression between human asthmatic and control subjects. The AHR of RGS2 knockout mice was assessed by using invasive tracheostomy and unrestrained plethysmography. Effects of loss of RGS2 on mouse airway smooth muscle (ASM) remodeling, contraction, intracellular Ca²⁺, and mitogenic signaling were determined in vivo and in vitro. RESULTS: RGS2 was highly expressed in human and murine bronchial epithelium and ASM and was markedly downregulated in lungs of ovalbumin-sensitized/-challenged mice. Lung tissues and blood monocytes from asthma patients expressed significantly lower RGS2 protein (lung) and mRNA (monocytes) than from nonasthma subjects. The extent of reduction of RGS2 on human monocytes correlated with increased AHR. RGS2 knockout caused spontaneous AHR in mice. Loss of RGS2 augmented Ca²⁺ mobilization and contraction of ASM cells. Loss of RGS2 also increased ASM mass and stimulated ASM cell growth via extracellular signal-regulated kinase and phosphatidylinositol 3-kinase pathways. CONCLUSION: We identified RGS2 as a potent modulator of AHR and a potential novel therapeutic target for asthma.
Keywords	1-phosphatidylinositol 4-kinase ; G-protein coupled receptors ; Western blotting ; asthma ; calcium ; cell growth ; drugs ; epithelium ; immunohistochemistry ; knockout mutants ; lungs ; messenger RNA ; mice ; mitogen-activated protein kinase ; monocytes ; pathophysiology ; patients ; phosphatidylinositol 3-kinase ; quantitative polymerase chain reaction ; smooth muscle
Language	English
Dates of publication	2012-10
Size	p. 968-976.e3.
Publishing place	Mosby, Inc.
Document type	Article
ZDB-ID	121011-7
ISSN	1085-8725 ; 1097-6825 ; 0091-6749
ISSN (online)	1085-8725 ; 1097-6825
ISSN	0091-6749
DOI	10.1016/j.jaci.2012.05.004
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Article ; Online: The BJP expects authors to share data.

George, Christopher H / Alexander, Stephen P H / Cirino, Giuseppe / Docherty, James R / Hoyer, Daniel / Insel, Paul A / Izzo, Angelo A / Ji, Yong / Panettieri, Reynold A / Sobey, Christopher G / Stanford, S Clare / Stefanska, Barbara / Stephens, Gary / Teixeira, Mauro / Ahluwalia, Amrita

British journal of pharmacology

2020 Volume 176, Issue 24, Page(s) 4595–4598

MeSH term(s)	Editorial Policies ; Information Dissemination
Language	English
Publishing date	2020-01-16
Publishing country	England
Document type	Editorial
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.14907
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