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Article ; Online: Bidirectional interaction of airway epithelial remodeling and inflammation in asthma.

Banno, Asoka / Reddy, Aravind T / Lakshmi, Sowmya P / Reddy, Raju C

Clinical science (London, England : 1979)

2020 Volume 134, Issue 9, Page(s) 1063–1079

Abstract: Asthma is a chronic disease of the airways that has long been viewed predominately as an inflammatory condition. Accordingly, current therapeutic interventions focus primarily on resolving inflammation. However, the mainstay of asthma therapy neither ... ...

Abstract	Asthma is a chronic disease of the airways that has long been viewed predominately as an inflammatory condition. Accordingly, current therapeutic interventions focus primarily on resolving inflammation. However, the mainstay of asthma therapy neither fully improves lung function nor prevents disease exacerbations, suggesting involvement of other factors. An emerging concept now holds that airway remodeling, another major pathological feature of asthma, is as important as inflammation in asthma pathogenesis. Structural changes associated with asthma include disrupted epithelial integrity, subepithelial fibrosis, goblet cell hyperplasia/metaplasia, smooth muscle hypertrophy/hyperplasia, and enhanced vascularity. These alterations are hypothesized to contribute to airway hyperresponsiveness, airway obstruction, airflow limitation, and progressive decline of lung function in asthmatic individuals. Consequently, targeting inflammation alone does not suffice to provide optimal clinical benefits. Here we review asthmatic airway remodeling, focusing on airway epithelium, which is critical to maintaining a healthy respiratory system, and is the primary defense against inhaled irritants. In asthma, airway epithelium is both a mediator and target of inflammation, manifesting remodeling and resulting obstruction among its downstream effects. We also highlight the potential benefits of therapeutically targeting airway structural alterations. Since pathological tissue remodeling is likewise observed in other injury- and inflammation-prone tissues and organs, our discussion may have implications beyond asthma and lung disease.
MeSH term(s)	Airway Remodeling/drug effects ; Animals ; Anti-Asthmatic Agents/pharmacology ; Asthma/drug therapy ; Asthma/physiopathology ; Epithelium/drug effects ; Humans ; Inflammation/drug therapy ; Inflammation/physiopathology ; Lung/drug effects ; Lung/physiopathology
Chemical Substances	Anti-Asthmatic Agents
Language	English
Publishing date	2020-05-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	206835-7
ISSN	1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
ISSN (online)	1470-8736
ISSN	0301-0538 ; 0009-0360 ; 0143-5221
DOI	10.1042/CS20191309
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Article ; Online: Glucocorticoid Receptor α Mediates Roflumilast's Ability to Restore Dexamethasone Sensitivity in COPD.

Reddy, Aravind T / Lakshmi, Sowmya P / Banno, Asoka / Reddy, Raju C

International journal of chronic obstructive pulmonary disease

2020 Volume 15, Page(s) 125–134

Abstract: Background: Glucocorticoids are commonly prescribed to treat inflammation of the respiratory system; however, they are mostly ineffective for controlling chronic obstructive pulmonary disease (COPD)-associated inflammation. This study aimed to elucidate ...

Abstract	Background: Glucocorticoids are commonly prescribed to treat inflammation of the respiratory system; however, they are mostly ineffective for controlling chronic obstructive pulmonary disease (COPD)-associated inflammation. This study aimed to elucidate the molecular mechanisms responsible for such glucocorticoid inefficacy in COPD, which may be instrumental to providing better patient outcomes. Roflumilast is a selective phosphodiesterase-4 (PDE4) inhibitor with anti-inflammatory properties in severe COPD patients who have a history of exacerbations. Roflumilast has a suggested ability to mitigate glucocorticoid resistance, but the mechanism is unknown. Methods: To understand the mechanism that mediates roflumilast-induced restoration of glucocorticoid sensitivity in COPD, we tested the role of glucocorticoid receptor α (GRα). Roflumilast's effects on GRα expression and transcriptional activity were assessed in bronchial epithelial cells from COPD patients. Results: We found that both GRα expression and activity are downregulated in bronchial epithelial cells from COPD patients and that roflumilast stimulates both GRα mRNA synthesis and GRα's transcriptional activity in COPD bronchial epithelial cells. We also demonstrate that roflumilast enhances dexamethasone's ability to suppress pro-inflammatory mediator production, in a GRα-dependent manner. Discussion: Our findings highlight the significance of roflumilast-induced GRα upregulation for COPD therapeutic strategies by revealing that roflumilast restores glucocorticoid sensitivity by sustaining GRα expression.
MeSH term(s)	Aminopyridines/pharmacology ; Benzamides/pharmacology ; Cells, Cultured ; Cyclopropanes/pharmacology ; Dexamethasone/pharmacology ; Drug Resistance ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Glucocorticoids/pharmacology ; Humans ; Inflammation Mediators/metabolism ; Interleukin-8/metabolism ; Lung/drug effects ; Lung/metabolism ; Lung/physiopathology ; Phosphodiesterase 4 Inhibitors/pharmacology ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Receptors, Glucocorticoid/agonists ; Receptors, Glucocorticoid/genetics ; Receptors, Glucocorticoid/metabolism ; Transcription Factor RelA/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation
Chemical Substances	Aminopyridines ; Benzamides ; CXCL8 protein, human ; Cyclopropanes ; Glucocorticoids ; Inflammation Mediators ; Interleukin-8 ; Phosphodiesterase 4 Inhibitors ; RELA protein, human ; Receptors, Glucocorticoid ; TNF protein, human ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha ; glucocorticoid receptor alpha ; Roflumilast (0P6C6ZOP5U) ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2020-01-14
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2212419-6
ISSN	1178-2005 ; 1176-9106
ISSN (online)	1178-2005
ISSN	1176-9106
DOI	10.2147/COPD.S230188
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Article ; Online: Molecular, chemical, and structural characterization of prostaglandin A2 as a novel agonist for Nur77.

Lakshmi, Sowmya P / Reddy, Aravind T / Banno, Asoka / Reddy, Raju C

The Biochemical journal

2019 Volume 476, Issue 19, Page(s) 2757–2767

Abstract: Nur77 is a transcription factor belonging to the NR4A subfamily of nuclear hormone receptors. Upon induction, Nur77 modulates the expression of its target genes and controls a variety of biological and pathophysiological processes. Prior research that ... ...

Abstract	Nur77 is a transcription factor belonging to the NR4A subfamily of nuclear hormone receptors. Upon induction, Nur77 modulates the expression of its target genes and controls a variety of biological and pathophysiological processes. Prior research that revealed a structurally atypical ligand-binding domain (LBD) and failed to locate an endogenous ligand had led to a classification of Nur77 as an orphan receptor. However, several more recent studies indicate that small synthetic molecules and unsaturated fatty acids can bind to Nur77. Discovery of additional endogenous ligands will facilitate our understanding of the receptor's functions and regulatory mechanisms. Our data have identified prostaglandin A2 (PGA2), a cyclopentenone prostaglandin (PG), as such a ligand. Cyclopentenone PGs exert their biological effects primarily by forming protein adducts via the characteristic electrophilic β-carbon(s) located in their cyclopentenone rings. Our data show that PGA2 induces Nur77 transcriptional activity by forming a covalent adduct between its endocyclic β-carbon, C9, and Cys566 in the receptor's LBD. The importance of this endocyclic β-carbon was substantiated by the failure of PGs without such electrophilic properties to react with Nur77. Calculated chemical properties and data from reactive molecular dynamic simulations, intrinsic reaction co-ordinate modeling, and covalent molecular docking also corroborate the selectivity of PGA2's C9 β-carbon towards Nur77's Cys. In summary, our molecular, chemical, and structural characterization of the PGA2-Nur77 interaction provides the first evidence that PGA2 is an endogenous Nur77 agonist.
MeSH term(s)	Cell Line ; Humans ; Nuclear Receptor Subfamily 4, Group A, Member 1/agonists ; Nuclear Receptor Subfamily 4, Group A, Member 1/metabolism ; Prostaglandins A/chemistry ; Prostaglandins A/metabolism ; Prostaglandins A/physiology ; Protein Binding ; Protein Domains
Chemical Substances	NR4A1 protein, human ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Prostaglandins A ; prostaglandin A2 (K6VT5BDY9E)
Language	English
Publishing date	2019-09-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20190253
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Article ; Online: Identification and Molecular Characterization of Peroxisome Proliferator-Activated Receptor δ as a Novel Target for Covalent Modification by 15-Deoxy-Δ

Reddy, Aravind T / Lakshmi, Sowmya P / Banno, Asoka / Reddy, Raju C

ACS chemical biology

2018 Volume 13, Issue 12, Page(s) 3269–3278

Abstract: PPARδ belongs to the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors. Upon activation by an agonist, PPARδ controls a variety of physiological processes via regulation of its target genes. 15-Deoxy- ... ...

Abstract	PPARδ belongs to the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors. Upon activation by an agonist, PPARδ controls a variety of physiological processes via regulation of its target genes. 15-Deoxy-Δ
MeSH term(s)	Alkylation ; Cell Line ; Cysteine/chemistry ; Density Functional Theory ; Humans ; Ligands ; Models, Chemical ; Molecular Dynamics Simulation ; Mutation ; PPAR delta/agonists ; PPAR delta/chemistry ; PPAR delta/genetics ; PPAR delta/metabolism ; Prostaglandin D2/analogs & derivatives ; Prostaglandin D2/chemistry ; Prostaglandin D2/metabolism ; Prostaglandin D2/pharmacology ; Protein Binding ; Protein Domains
Chemical Substances	15-deoxy-delta(12,14)-prostaglandin J2 ; Ligands ; PPAR delta ; Cysteine (K848JZ4886) ; Prostaglandin D2 (RXY07S6CZ2)
Language	English
Publishing date	2018-11-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Video-Audio Media
ISSN	1554-8937
ISSN (online)	1554-8937
DOI	10.1021/acschembio.8b00584
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Article: PPAR Agonists for the Prevention and Treatment of Lung Cancer.

Lakshmi, Sowmya P / Reddy, Aravind T / Banno, Asoka / Reddy, Raju C

PPAR research

2017 Volume 2017, Page(s) 8252796

Abstract: Lung cancer is the most common and most fatal of all malignancies worldwide. Furthermore, with more than half of all lung cancer patients presenting with distant metastases at the time of initial diagnosis, the overall prognosis for the disease is poor. ... ...

Abstract	Lung cancer is the most common and most fatal of all malignancies worldwide. Furthermore, with more than half of all lung cancer patients presenting with distant metastases at the time of initial diagnosis, the overall prognosis for the disease is poor. There is thus a desperate need for new prevention and treatment strategies. Recently, a family of nuclear hormone receptors, the peroxisome proliferator-activated receptors (PPARs), has attracted significant attention for its role in various malignancies including lung cancer. Three PPARs, PPAR
Language	English
Publishing date	2017-02-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2237981-2
ISSN	1687-4765 ; 1687-4757
ISSN (online)	1687-4765
ISSN	1687-4757
DOI	10.1155/2017/8252796
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Article ; Online: Airway Epithelial Cell Peroxisome Proliferator-Activated Receptor γ Regulates Inflammation and Mucin Expression in Allergic Airway Disease.

Lakshmi, Sowmya P / Reddy, Aravind T / Banno, Asoka / Reddy, Raju C

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 201, Issue 6, Page(s) 1775–1783

Abstract: Airway epithelial cells (AECs) orchestrate inflammatory responses to airborne irritants that enter the respiratory system. A viscous mucus layer produced by goblet cells in the airway epithelium also contributes to a physiological defense mechanism ... ...

Abstract	Airway epithelial cells (AECs) orchestrate inflammatory responses to airborne irritants that enter the respiratory system. A viscous mucus layer produced by goblet cells in the airway epithelium also contributes to a physiological defense mechanism through the physical and chemical barriers it provides. Dysregulation or impairment in these functions has been implicated as a cause of the chronic inflammation and tissue remodeling that constitute major pathological features of asthma. In particular, mucus hypersecretion leading to airway obstruction and impaired pulmonary function is associated with morbidity and mortality in asthma patients. Peroxisome proliferator-activated receptor γ (PPARγ) is a ligand-activated transcription factor involved in a variety of cellular processes. Accumulating evidence indicates that PPARγ agonists antagonize exaggerated inflammatory responses, yet PPARγ's precise role in airway remodeling/mucus hypersecretion has yet to be defined. In this study, we created an AEC-specific PPARγ (AEC-PPARγ) deletion to investigate PPARγ's functions in a murine model of allergic airway disease. AEC-PPARγ deficiency exaggerated airway hyperresponsiveness, inflammation, cytokine expression, and tissue remodeling. We also found that PPARγ directly bound to a PPAR response element found in
MeSH term(s)	Animals ; Asthma/genetics ; Asthma/immunology ; Asthma/pathology ; Cells, Cultured ; Epithelial Cells/immunology ; Epithelial Cells/pathology ; Female ; Gene Expression Regulation/immunology ; Humans ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Male ; Mice ; Mice, Knockout ; Mucin 5AC/genetics ; Mucin 5AC/immunology ; PPAR gamma/genetics ; PPAR gamma/immunology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/pathology ; Response Elements/immunology
Chemical Substances	MUC5AC protein, human ; Muc5ac protein, mouse ; Mucin 5AC ; PPAR gamma ; PPARG protein, human
Language	English
Publishing date	2018-07-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1800649
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Article ; Online: Role of GPx3 in PPARγ-induced protection against COPD-associated oxidative stress.

Reddy, Aravind T / Lakshmi, Sowmya P / Banno, Asoka / Reddy, Raju C

Free radical biology & medicine

2018 Volume 126, Page(s) 350–357

Abstract: Cigarette smoke, a source of numerous oxidants, produces oxidative stress and exaggerated inflammatory responses that lead to irreversible lung tissue damage. It is the single, most significant risk factor for chronic obstructive pulmonary disease (COPD). ...

Abstract	Cigarette smoke, a source of numerous oxidants, produces oxidative stress and exaggerated inflammatory responses that lead to irreversible lung tissue damage. It is the single, most significant risk factor for chronic obstructive pulmonary disease (COPD). Although an intrinsic defense system that includes both enzymatic and non-enzymatic modulators exists to protect lung tissues against oxidative stress, impairment of these protective mechanisms has been demonstrated in smokers and COPD patients. The antioxidant enzyme GSH peroxidase (GPx) is an important part of this intrinsic defense system. Although cigarette smoke has been shown to downregulate its expression and activity, the underlying mechanism is not known. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear hormone receptor with antioxidant effects. PPARγ activation has demonstrated protective effects against cigarette smoke-induced oxidative stress and inflammation. Molecular mechanisms for PPARγ's antioxidant function likewise remain to be elucidated. This study explored the link between PPARγ and GPx3 and found a positive association in cigarette smoke extract (CSE)-exposed human bronchial epithelial cells. Moreover, we provide evidence that identifies GPx3 as a PPARγ transcriptional target. Attenuation of antioxidant effects in the absence of GPx3 highlights the antioxidant's prominent role in mediating PPARγ's function. We also demonstrate that ligand-mediated PPARγ activation blocks CSE-induced reactive oxygen species and hydrogen peroxide production via upregulation of GPx3. In summary, our findings describing the molecular mechanisms involving GPx3 and PPARγ in CSE-induced oxidative stress and inflammation may provide valuable information for the development of more effective therapeutics for COPD.
MeSH term(s)	Antioxidants/metabolism ; Bronchi/drug effects ; Bronchi/metabolism ; Cell Line ; Cigarette Smoking/adverse effects ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Glutathione Peroxidase/genetics ; Glutathione Peroxidase/metabolism ; Humans ; Oxidative Stress/genetics ; PPAR gamma/genetics ; PPAR gamma/metabolism ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/pathology ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Smoking/adverse effects
Chemical Substances	Antioxidants ; PPAR gamma ; Reactive Oxygen Species ; GPX3 protein, human (EC 1.11.1.-) ; Glutathione Peroxidase (EC 1.11.1.9)
Language	English
Publishing date	2018-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2018.08.014
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Article: PPARs: Key Regulators of Airway Inflammation and Potential Therapeutic Targets in Asthma.

Banno, Asoka / Reddy, Aravind T / Lakshmi, Sowmya P / Reddy, Raju C

Nuclear receptor research

2017 Volume 5

Abstract: Asthma affects approximately 300 million people worldwide, significantly impacting quality of life and healthcare costs. While current therapies are effective in controlling many patients' symptoms, a large number continue to experience exacerbations or ... ...

Abstract	Asthma affects approximately 300 million people worldwide, significantly impacting quality of life and healthcare costs. While current therapies are effective in controlling many patients' symptoms, a large number continue to experience exacerbations or treatment-related adverse effects. Alternative therapies are thus urgently needed. Accumulating evidence has shown that the peroxisome proliferator-activated receptor (PPAR) family of nuclear hormone receptors, comprising PPARα, PPARβ/δ, and PPARγ, is involved in asthma pathogenesis and that ligand-induced activation of these receptors suppresses asthma pathology. PPAR agonists exert their anti-inflammatory effects primarily by suppressing pro-inflammatory mediators and antagonizing the pro-inflammatory functions of various cell types relevant to asthma pathophysiology. Experimental findings strongly support the potential clinical benefits of PPAR agonists in the treatment of asthma. We review current literature, highlighting PPARs' key role in asthma pathogenesis and their agonists' therapeutic potential. With additional research and rigorous clinical studies, PPARs may become attractive therapeutic targets in this disease.
Language	English
Publishing date	2017-12-11
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2834982-9
ISSN	2314-5714 ; 2314-5706
ISSN (online)	2314-5714
ISSN	2314-5706
DOI	10.11131/2018/101306
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Article ; Online: Cigarette smoke downregulates Nur77 to exacerbate inflammation in chronic obstructive pulmonary disease (COPD).

Reddy, Aravind T / Lakshmi, Sowmya P / Banno, Asoka / Jadhav, Shantanu Krishna / Pulikkal Kadamberi, Ishaque / Kim, Seong C / Reddy, Raju C

PloS one

2020 Volume 15, Issue 2, Page(s) e0229256

Abstract: Cigarette smoke (CS) contains multiple gaseous and particulate materials that can cause lung inflammation, and smoking is the major cause of chronic obstructive pulmonary disease (COPD). We sought to determine the mechanisms of how CS triggers lung ... ...

Abstract	Cigarette smoke (CS) contains multiple gaseous and particulate materials that can cause lung inflammation, and smoking is the major cause of chronic obstructive pulmonary disease (COPD). We sought to determine the mechanisms of how CS triggers lung inflammation. Nur77, a nuclear hormone receptor belonging to the immediate-early response gene family, controls inflammatory responses, mainly by suppressing the NF-κB signaling pathway. Because it is unknown if Nur77's anti-inflammatory role modulates COPD, we assessed if and how Nur77 expression and activity are altered in CS-induced airway inflammation. In lung tissues and bronchial epithelial cells from COPD patients, we found Nur77 was downregulated. In a murine model of CS-induced airway inflammation, CS promoted lung inflammation and also reduced Nur77 activity in wild type (WT) mice, whereas lungs of Nur77-deficient mice showed exaggerated CS-induced inflammatory responses. Our findings in in vitro studies of human airway epithelial cells complemented those in vivo data in mice, together showing that CS induced threonine-phosphorylation of Nur77, which is known to interfere with its anti-inflammatory functions. In summary, our findings point to Nur77 as an important regulator of CS-induced inflammatory responses and support the potential benefits of Nur77 activation for COPD treatment.
MeSH term(s)	Animals ; Down-Regulation/drug effects ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Humans ; Inflammation/genetics ; Lung/pathology ; Mice ; Nuclear Receptor Subfamily 4, Group A, Member 1/genetics ; Phosphorylation/drug effects ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/pathology ; Smoke/adverse effects ; Threonine/metabolism ; Nicotiana/chemistry
Chemical Substances	Nuclear Receptor Subfamily 4, Group A, Member 1 ; Smoke ; Threonine (2ZD004190S)
Language	English
Publishing date	2020-02-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0229256
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Article ; Online: Cigarette smoke downregulates Nur77 to exacerbate inflammation in chronic obstructive pulmonary disease (COPD).

Aravind T Reddy / Sowmya P Lakshmi / Asoka Banno / Shantanu Krishna Jadhav / Ishaque Pulikkal Kadamberi / Seong C Kim / Raju C Reddy

PLoS ONE, Vol 15, Iss 2, p e

2020 Volume 0229256

Abstract	Cigarette smoke (CS) contains multiple gaseous and particulate materials that can cause lung inflammation, and smoking is the major cause of chronic obstructive pulmonary disease (COPD). We sought to determine the mechanisms of how CS triggers lung inflammation. Nur77, a nuclear hormone receptor belonging to the immediate-early response gene family, controls inflammatory responses, mainly by suppressing the NF-κB signaling pathway. Because it is unknown if Nur77's anti-inflammatory role modulates COPD, we assessed if and how Nur77 expression and activity are altered in CS-induced airway inflammation. In lung tissues and bronchial epithelial cells from COPD patients, we found Nur77 was downregulated. In a murine model of CS-induced airway inflammation, CS promoted lung inflammation and also reduced Nur77 activity in wild type (WT) mice, whereas lungs of Nur77-deficient mice showed exaggerated CS-induced inflammatory responses. Our findings in in vitro studies of human airway epithelial cells complemented those in vivo data in mice, together showing that CS induced threonine-phosphorylation of Nur77, which is known to interfere with its anti-inflammatory functions. In summary, our findings point to Nur77 as an important regulator of CS-induced inflammatory responses and support the potential benefits of Nur77 activation for COPD treatment.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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