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  1. Article ; Online: OGR1-dependent regulation of the allergen-induced asthma phenotype.

    Nayak, Ajay P / Deshpande, Deepak A / Shah, Sushrut D / Villalba, Dominic R / Yi, Roslyn / Wang, Nadan / Penn, Raymond B

    American journal of physiology. Lung cellular and molecular physiology

    2021  Volume 321, Issue 6, Page(s) L1044–L1054

    Abstract: The proton-sensing receptor, ovarian cancer G protein-coupled receptor (OGR1), has been shown to be expressed in airway smooth muscle (ASM) cells and is capable of promoting ASM contraction in response to decreased extracellular pH. OGR1 knockout (OGR1KO) ...

    Abstract The proton-sensing receptor, ovarian cancer G protein-coupled receptor (OGR1), has been shown to be expressed in airway smooth muscle (ASM) cells and is capable of promoting ASM contraction in response to decreased extracellular pH. OGR1 knockout (OGR1KO) mice are reported to be resistant to the asthma features induced by inhaled allergen. We recently described certain benzodiazepines as OGR1 activators capable of mediating both procontractile and prorelaxant signaling in ASM cells. Here we assess the effect of treatment with the benzodiazepines lorazepam or sulazepam on the asthma phenotype in wild-type (WT) and OGR1KO mice subjected to inhaled house dust mite (HDM;
    MeSH term(s) Allergens/toxicity ; Animals ; Anti-Anxiety Agents/pharmacology ; Asthma/etiology ; Asthma/metabolism ; Asthma/pathology ; Benzodiazepines/pharmacology ; Bronchial Hyperreactivity/etiology ; Bronchial Hyperreactivity/metabolism ; Bronchial Hyperreactivity/pathology ; Bronchoconstriction ; Cytokines/metabolism ; Female ; Lorazepam/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phenotype ; Pneumonia/etiology ; Pneumonia/metabolism ; Pneumonia/pathology ; Pyroglyphidae ; Receptors, G-Protein-Coupled/physiology
    Chemical Substances Allergens ; Anti-Anxiety Agents ; Cytokines ; GPR68 protein, mouse ; Receptors, G-Protein-Coupled ; Benzodiazepines (12794-10-4) ; Lorazepam (O26FZP769L)
    Language English
    Publishing date 2021-10-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00200.2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: α-Catenin-dependent cytoskeletal tension controls Yap activity in the heart.

    Vite, Alexia / Zhang, Caimei / Yi, Roslyn / Emms, Sabrina / Radice, Glenn L

    Development (Cambridge, England)

    2018  Volume 145, Issue 5

    Abstract: Shortly after birth, muscle cells of the mammalian heart lose their ability to divide. At the same time, the N-cadherin/catenin cell adhesion complex accumulates at the cell termini, creating a specialized type of cell-cell contact called the ... ...

    Abstract Shortly after birth, muscle cells of the mammalian heart lose their ability to divide. At the same time, the N-cadherin/catenin cell adhesion complex accumulates at the cell termini, creating a specialized type of cell-cell contact called the intercalated disc (ICD). To investigate the relationship between ICD maturation and proliferation, αE-catenin (
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Signal Transducing/physiology ; Animals ; Animals, Newborn ; Cell Communication/genetics ; Cell Cycle Proteins ; Cells, Cultured ; Cytoskeleton/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; Phosphoproteins/metabolism ; Phosphoproteins/physiology ; YAP-Signaling Proteins ; alpha Catenin/genetics ; alpha Catenin/physiology
    Chemical Substances Adaptor Proteins, Signal Transducing ; CTNNA3 protein, mouse ; Cell Cycle Proteins ; Ctnna1 protein, mouse ; Phosphoproteins ; YAP-Signaling Proteins ; Yap1 protein, mouse ; alpha Catenin
    Language English
    Publishing date 2018-03-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.149823
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Engineered red blood cells (activating antigen carriers) drive potent T cell responses and tumor regression in mice.

    Blagovic, Katarina / Smith, Carolyne K / Ramakrishnan, Amritha / Moore, Lindsay / Soto, David R / Thompson, Zachary / Stockmann, Adam P / Kruszelnicki, Sonia / Thakkar, Akshi / Murray, Jason / Torres, Sebastian / Wondimagegnhu, Bersabel / Yi, Roslyn / Dadgar, Maisam / Paracha, Abdul M / Page, Claire / Clear, Louise / Chaudhry, Omer A / Myint, Melissa /
    Bridgen, Devin T / Gilbert, Jonathan B / Seidl, Katherine J / Sharei, Armon / Loughhead, Scott / Bernstein, Howard / Yarar, Defne

    Frontiers in immunology

    2022  Volume 13, Page(s) 1015585

    Abstract: Activation of T cell responses is essential for effective tumor clearance; however, inducing targeted, potent antigen presentation to stimulate T cell responses remains challenging. We generated Activating Antigen Carriers (AACs) by engineering red blood ...

    Abstract Activation of T cell responses is essential for effective tumor clearance; however, inducing targeted, potent antigen presentation to stimulate T cell responses remains challenging. We generated Activating Antigen Carriers (AACs) by engineering red blood cells (RBCs) to encapsulate relevant tumor antigens and the adjuvant polyinosinic-polycytidylic acid (poly I:C), for use as a tumor-specific cancer vaccine. The processing method and conditions used to create the AACs promote phosphatidylserine exposure on RBCs and thus harness the natural process of aged RBC clearance to enable targeting of the AACs to endogenous professional antigen presenting cells (APCs) without the use of chemicals or viral vectors. AAC uptake, antigen processing, and presentation by APCs drive antigen-specific activation of T cells, both in mouse
    MeSH term(s) Mice ; Humans ; Animals ; Aged ; Cancer Vaccines ; Poly I-C ; Phosphatidylserines ; Cisplatin ; Antigens, Neoplasm ; Erythrocytes
    Chemical Substances Cancer Vaccines ; Poly I-C (O84C90HH2L) ; Phosphatidylserines ; Cisplatin (Q20Q21Q62J) ; Antigens, Neoplasm
    Language English
    Publishing date 2022-10-03
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.1015585
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Bitter Taste Receptor Agonists Mitigate Features of Allergic Asthma in Mice.

    Sharma, Pawan / Yi, Roslyn / Nayak, Ajay P / Wang, Nadan / Tang, Francesca / Knight, Morgan J / Pan, Shi / Oliver, Brian / Deshpande, Deepak A

    Scientific reports

    2017  Volume 7, Page(s) 46166

    Abstract: Asthma is characterized by airway inflammation, mucus secretion, remodeling and hyperresponsiveness (AHR). Recent research has established the bronchodilatory effect of bitter taste receptor (TAS2R) agonists in various models. Comprehensive pre-clinical ... ...

    Abstract Asthma is characterized by airway inflammation, mucus secretion, remodeling and hyperresponsiveness (AHR). Recent research has established the bronchodilatory effect of bitter taste receptor (TAS2R) agonists in various models. Comprehensive pre-clinical studies aimed at establishing effectiveness of TAS2R agonists in disease models are lacking. Here we aimed to determine the effect of TAS2R agonists on features of asthma. Further, we elucidated a mechanism by which TAS2R agonists mitigate features of asthma. Asthma was induced in mice using intranasal house dust mite or aerosol ova-albumin challenge, and chloroquine or quinine were tested in both prophylactic and treatment models. Allergen challenge resulted in airway inflammation as evidenced by increased immune cells infiltration and release of cytokines and chemokines in the lungs, which were significantly attenuated in TAS2R agonists treated mice. TAS2R agonists attenuated features of airway remodeling including smooth muscle mass, extracellular matrix deposition and pro-fibrotic signaling, and also prevented mucus accumulation and development of AHR in mice. Mechanistic studies using human neutrophils demonstrated that inhibition of immune cell chemotaxis is a key mechanism by which TAS2R agonists blocked allergic airway inflammation and exerted anti-asthma effects. Our comprehensive studies establish the effectiveness of TAS2R agonists in mitigating multiple features of allergic asthma.
    MeSH term(s) Airway Remodeling/drug effects ; Allergens/immunology ; Animals ; Asthma/drug therapy ; Asthma/immunology ; Asthma/physiopathology ; Asthma/prevention & control ; Bronchial Hyperreactivity/complications ; Bronchial Hyperreactivity/immunology ; Bronchial Hyperreactivity/pathology ; Bronchial Hyperreactivity/physiopathology ; Bronchoalveolar Lavage Fluid/cytology ; Cell Count ; Chemotaxis/drug effects ; Chloroquine/therapeutic use ; Cytokines/metabolism ; Disease Models, Animal ; Female ; Humans ; Hypersensitivity/drug therapy ; Hypersensitivity/immunology ; Hypersensitivity/physiopathology ; Hypersensitivity/prevention & control ; Immunization ; Inflammation/complications ; Inflammation/pathology ; Lung/immunology ; Lung/parasitology ; Lung/pathology ; Lung/physiopathology ; Matrix Metalloproteinases/metabolism ; Mice, Inbred BALB C ; Mucus/metabolism ; Muscle, Smooth/drug effects ; Muscle, Smooth/pathology ; Neutrophils/drug effects ; Pyroglyphidae/drug effects ; Quinine/therapeutic use ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/metabolism ; Taste
    Chemical Substances Allergens ; Cytokines ; Receptors, G-Protein-Coupled ; Chloroquine (886U3H6UFF) ; Quinine (A7V27PHC7A) ; Matrix Metalloproteinases (EC 3.4.24.-)
    Language English
    Publishing date 2017-04-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep46166
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Regulation of ovarian cancer G protein-coupled receptor-1 expression and signaling.

    Nayak, Ajay P / Pera, Tonio / Deshpande, Deepak A / Michael, James V / Liberato, Jennifer R / Pan, Shi / Tompkins, Eric / Morelli, Henry P / Yi, Roslyn / Wang, Nadan / Penn, Raymond B

    American journal of physiology. Lung cellular and molecular physiology

    2019  Volume 316, Issue 5, Page(s) L894–L902

    Abstract: Ovarian cancer G protein-coupled receptor 1 (OGR1) is a recently deorphanized G protein-coupled receptor shown to signal in response to low extracellular pH (↓ ... ...

    Abstract Ovarian cancer G protein-coupled receptor 1 (OGR1) is a recently deorphanized G protein-coupled receptor shown to signal in response to low extracellular pH (↓pH
    MeSH term(s) Animals ; Cell Adhesion Molecules/metabolism ; Female ; HEK293 Cells ; Humans ; Hydrogen-Ion Concentration ; Lorazepam/pharmacology ; MAP Kinase Signaling System ; Mice ; Mice, Knockout ; Microfilament Proteins/metabolism ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Phosphoproteins/metabolism ; Receptors, G-Protein-Coupled/biosynthesis ; Respiratory System/metabolism ; Respiratory System/pathology ; Up-Regulation
    Chemical Substances Cell Adhesion Molecules ; GPR68 protein, mouse ; Microfilament Proteins ; Phosphoproteins ; Receptors, G-Protein-Coupled ; vasodilator-stimulated phosphoprotein ; Lorazepam (O26FZP769L)
    Language English
    Publishing date 2019-02-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00426.2018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Alpha-catenins control cardiomyocyte proliferation by regulating Yap activity.

    Li, Jifen / Gao, Erhe / Vite, Alexia / Yi, Roslyn / Gomez, Ludovic / Goossens, Steven / van Roy, Frans / Radice, Glenn L

    Circulation research

    2014  Volume 116, Issue 1, Page(s) 70–79

    Abstract: Rationale: Shortly after birth, muscle cells of the mammalian heart lose their ability to divide. Thus, they are unable to effectively replace dying cells in the injured heart. The recent discovery that the transcriptional coactivator Yes-associated ... ...

    Abstract Rationale: Shortly after birth, muscle cells of the mammalian heart lose their ability to divide. Thus, they are unable to effectively replace dying cells in the injured heart. The recent discovery that the transcriptional coactivator Yes-associated protein (Yap) is necessary and sufficient for cardiomyocyte proliferation has gained considerable attention. However, the upstream regulators and signaling pathways that control Yap activity in the heart are poorly understood.
    Objective: To investigate the role of α-catenins in the heart using cardiac-specific αE- and αT-catenin double knockout mice.
    Methods and results: We used 2 cardiac-specific Cre transgenes to delete both αE-catenin (Ctnna1) and αT-catenin (Ctnna3) genes either in the perinatal or in the adult heart. Perinatal depletion of α-catenins increased cardiomyocyte number in the postnatal heart. Increased nuclear Yap and the cell cycle regulator cyclin D1 accompanied cardiomyocyte proliferation in the α-catenin double knockout hearts. Fetal genes were increased in the α-catenin double knockout hearts indicating a less mature cardiac gene expression profile. Knockdown of α-catenins in neonatal rat cardiomyocytes also resulted in increased proliferation, which could be blocked by knockdown of Yap. Finally, inactivation of α-catenins in the adult heart using an inducible Cre led to increased nuclear Yap and cardiomyocyte proliferation and improved contractility after myocardial infarction.
    Conclusions: These studies demonstrate that α-catenins are critical regulators of Yap, a transcriptional coactivator essential for cardiomyocyte proliferation. Furthermore, we provide proof of concept that inhibiting α-catenins might be a useful strategy to promote myocardial regeneration after injury.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Animals, Newborn ; Cell Cycle Proteins ; Cell Proliferation/physiology ; Cells, Cultured ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac/metabolism ; Phosphoproteins/metabolism ; Rats ; alpha Catenin/physiology
    Chemical Substances Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Phosphoproteins ; Yap1 protein, mouse ; alpha Catenin
    Language English
    Publishing date 2014-10-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.116.304472
    Database MEDical Literature Analysis and Retrieval System OnLINE

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