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  1. Article ; Online: A novel dissociative steroid VBP15 reduces MUC5AC gene expression in airway epithelial cells but lacks the GRE mediated transcriptional properties of dexamethasone.

    Garvin, Lindsay M / Chen, Yajun / Damsker, Jesse M / Rose, Mary C

    Pulmonary pharmacology & therapeutics

    2016  Volume 38, Page(s) 17–26

    Abstract: Overproduction of secretory mucins contributes to morbidity/mortality in inflammatory lung diseases. Inflammatory mediators directly increase expression of mucin genes, but few drugs have been shown to directly repress mucin gene expression. IL-1β ... ...

    Abstract Overproduction of secretory mucins contributes to morbidity/mortality in inflammatory lung diseases. Inflammatory mediators directly increase expression of mucin genes, but few drugs have been shown to directly repress mucin gene expression. IL-1β upregulates the MUC5AC mucin gene in part via the transcription factors NFκB while the glucocorticoid Dexamethasone (Dex) transcriptionally represses MUC5AC expression by Dex-activated GR binding to two GRE cis-sites in the MUC5AC promoter in lung epithelial cells. VBP compounds (ReveraGen BioPharma) maintain anti-inflammatory activity through inhibition of NFκB but exhibit reduced GRE-mediated transcriptional properties associated with adverse side-effects and thus have potential to minimize harmful side effects of long-term steroid therapy in inflammatory lung diseases. We investigated VBP15 efficacy as an anti-mucin agent in two types of airway epithelial cells and analyzed the transcription factor activity and promoter binding associated with VBP15-induced MUC5AC repression. VBP15 reduced MUC5AC mRNA abundance in a dose- and time-dependent manner similar to Dex in the presence or absence of IL-1β in A549 and differentiated human bronchial epithelial cells. Repression was abrogated in the presence of RU486, demonstrating a requirement for GR in the VBP15-induced repression of MUC5AC. Inhibition of NFκB activity resulted in reduced baseline expression of MUC5AC indicating that constitutive activity maintains MUC5AC production. Chromatin immunoprecipitation analysis demonstrated lack of GR and of p65 (NFκB) binding to composite GRE domains in the MUC5AC promoter following VBP15 exposure of cells, in contrast to Dex. These data demonstrate that VBP15 is a novel anti-mucin agent that mediates the reduction of MUC5AC gene expression differently than the classical glucocorticoid, Dex.
    MeSH term(s) A549 Cells ; Anti-Inflammatory Agents/administration & dosage ; Anti-Inflammatory Agents/pharmacology ; Bronchi/cytology ; Bronchi/drug effects ; Cell Line ; Dexamethasone/administration & dosage ; Dexamethasone/pharmacology ; Dose-Response Relationship, Drug ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Gene Expression Regulation/drug effects ; Glucocorticoids/administration & dosage ; Glucocorticoids/pharmacology ; Humans ; Inflammation Mediators/metabolism ; Interleukin-1beta/metabolism ; Mucin 5AC/genetics ; Mucins/antagonists & inhibitors ; Mucins/metabolism ; Pregnadienediols/administration & dosage ; Pregnadienediols/pharmacology ; RNA, Messenger/metabolism ; Time Factors
    Chemical Substances Anti-Inflammatory Agents ; Glucocorticoids ; Inflammation Mediators ; Interleukin-1beta ; MUC5AC protein, human ; Mucin 5AC ; Mucins ; Pregnadienediols ; RNA, Messenger ; VBP15 compound ; Dexamethasone (7S5I7G3JQL)
    Language English
    Publishing date 2016-06
    Publishing country England
    Document type Comparative Study ; Journal Article
    ZDB-ID 1399707-5
    ISSN 1522-9629 ; 1094-5539
    ISSN (online) 1522-9629
    ISSN 1094-5539
    DOI 10.1016/j.pupt.2016.04.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2389: Show issues Location:
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  2. Article ; Online: Quantitative proteomics reveals an altered cystic fibrosis in vitro bronchial epithelial secretome.

    Peters-Hall, Jennifer R / Brown, Kristy J / Pillai, Dinesh K / Tomney, Amarel / Garvin, Lindsay M / Wu, Xiaofang / Rose, Mary C

    American journal of respiratory cell and molecular biology

    2015  Volume 53, Issue 1, Page(s) 22–32

    Abstract: Alterations in epithelial secretions and mucociliary clearance contribute to chronic bacterial infection in cystic fibrosis (CF) lung disease, but whether CF lungs are unchanged in the absence of infection remains controversial. A proteomic comparison of ...

    Abstract Alterations in epithelial secretions and mucociliary clearance contribute to chronic bacterial infection in cystic fibrosis (CF) lung disease, but whether CF lungs are unchanged in the absence of infection remains controversial. A proteomic comparison of airway secretions from subjects with CF and control subjects shows alterations in key biological processes, including immune response and proteolytic activity, but it is unclear if these are due to mutant CF transmembrane conductance regulator (CFTR) and/or chronic infection. We hypothesized that the CF lung apical secretome is altered under constitutive conditions in the absence of inflammatory cells and pathogens. To test this, we performed quantitative proteomics of in vitro apical secretions from air-liquid interface cultures of three life-extended CF (ΔF508/ΔF508) and three non-CF human bronchial epithelial cells after labeling of CF cells by stable isotope labeling with amino acids in cell culture. Mass spectrometry analysis identified and quantitated 666 proteins across samples, of which 70 exhibited differential enrichment or depletion in CF secretions (±1.5-fold change; P < 0.05). The key molecular functions were innate immunity (24%), cytoskeleton/extracellular matrix organization (24%), and protease/antiprotease activity (17%). Oxidative proteins and classical complement pathway proteins that are altered in CF secretions in vivo were not altered in vitro. Specific differentially increased proteins-MUC5AC and MUC5B mucins, fibronectin, and matrix metalloproteinase-9-were validated by antibody-based assays. Overall, the in vitro CF secretome data are indicative of a constitutive airway epithelium with altered innate immunity, suggesting that downstream consequences of mutant CFTR set the stage for chronic inflammation and infection in CF airways.
    MeSH term(s) Bronchi/metabolism ; Bronchi/pathology ; Cell Line ; Chronic Disease ; Cystic Fibrosis/genetics ; Cystic Fibrosis/metabolism ; Cystic Fibrosis/pathology ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Proteome/genetics ; Proteome/metabolism ; Proteomics ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology
    Chemical Substances Proteome
    Language English
    Publishing date 2015-02-18
    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.2014-0256RC
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    Zs.A 2851: Show issues Location:
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  3. Article ; Online: IL-1β induction of MUC5AC gene expression is mediated by CREB and NF-κB and repressed by dexamethasone.

    Chen, Yajun / Garvin, Lindsay M / Nickola, Tracey J / Watson, Alan M / Colberg-Poley, Anamaris M / Rose, Mary C

    American journal of physiology. Lung cellular and molecular physiology

    2014  Volume 306, Issue 8, Page(s) L797–807

    Abstract: Chronic airway diseases are characterized by inflammation and mucus overproduction. The MUC5AC mucin gene is upregulated by the proinflammatory cytokine interleukin-1 β (IL-1β) via activation of cAMP response element-binding protein (CREB) in the NCI- ... ...

    Abstract Chronic airway diseases are characterized by inflammation and mucus overproduction. The MUC5AC mucin gene is upregulated by the proinflammatory cytokine interleukin-1 β (IL-1β) via activation of cAMP response element-binding protein (CREB) in the NCI-H292 cancer cell line and nuclear factor-κB (NF-κB) in the HBE1 transformed cell line, with each transcription factor binding to a cognate cis site in the proximal or distal region, respectively, of the MUC5AC promoter. We utilized primary differentiated human bronchial epithelial (HBE) and A549 lung adenocarcinoma cells to further investigate the contributions of CREB and NF-κB subunits to the IL-1β-induced upregulation of MUC5AC. Data show that ligand binding of IL-1β to the IL-1β receptor is required to increase MUC5AC mRNA abundance. Chromatin immunoprecipitation analyses show direct binding of CREB to the previously identified cAMP response element site and binding of p65 and p50 subunits to a novel NF-κB site in a mucin-regulatory domain in the proximal promoter and to a previously identified NF-κB site in the distal promoter. P50 binds to both NF-κB sites at 1 h following IL-1β exposure, but is replaced at 2 h by p65 in A549 cells and by a p50/p65 heterodimer in HBE cells. Thus IL-1β activates multiple domains in the MUC5AC promoter but exhibits some cell-specific responses, highlighting the complexity of MUC5AC transcriptional regulation. Data show that dexamethasone, a glucocorticoid that transcriptionally represses MUC5AC gene expression under constitutive conditions, also represses IL-1β-mediated upregulation of MUC5AC gene expression. A further understanding of mechanisms mediating MUC5AC regulation should lead to a honing of therapeutic approaches for the treatment of mucus overproduction in inflammatory lung diseases.
    MeSH term(s) Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Anti-Inflammatory Agents/pharmacology ; Bronchi/drug effects ; Bronchi/metabolism ; Cells, Cultured ; Chromatin Immunoprecipitation ; Cyclic AMP Response Element-Binding Protein/genetics ; Cyclic AMP Response Element-Binding Protein/metabolism ; DNA-Directed RNA Polymerases/genetics ; DNA-Directed RNA Polymerases/metabolism ; Dexamethasone/pharmacology ; Electrophoretic Mobility Shift Assay ; Gene Expression Regulation ; Humans ; Interleukin-1beta/pharmacology ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Mucin 5AC/genetics ; Mucin 5AC/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptors, Interleukin-1/genetics ; Receptors, Interleukin-1/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances Anti-Inflammatory Agents ; CREB1 protein, human ; Cyclic AMP Response Element-Binding Protein ; Interleukin-1beta ; MUC5AC protein, human ; Mucin 5AC ; NF-kappa B ; RNA, Messenger ; Receptors, Interleukin-1 ; Dexamethasone (7S5I7G3JQL) ; DNA-Directed RNA Polymerases (EC 2.7.7.6)
    Language English
    Publishing date 2014-01-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00347.2013
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    Uc I Zs.89: Show issues Location:
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    Zs.A 2749: Show issues Location:
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  4. Article ; Online: Platelets induce apoptosis during sepsis in a contact-dependent manner that is inhibited by GPIIb/IIIa blockade.

    Sharron, Matthew / Hoptay, Claire E / Wiles, Andrew A / Garvin, Lindsay M / Geha, Mayya / Benton, Angela S / Nagaraju, Kanneboyina / Freishtat, Robert J

    PloS one

    2012  Volume 7, Issue 7, Page(s) e41549

    Abstract: Purpose: End-organ apoptosis is well-described in progressive sepsis and Multiple Organ Dysfunction Syndrome (MODS), especially where platelets accumulate (e.g. spleen and lung). We previously reported an acute sepsis-induced cytotoxic platelet ... ...

    Abstract Purpose: End-organ apoptosis is well-described in progressive sepsis and Multiple Organ Dysfunction Syndrome (MODS), especially where platelets accumulate (e.g. spleen and lung). We previously reported an acute sepsis-induced cytotoxic platelet phenotype expressing serine protease granzyme B. We now aim to define the site(s) of and mechanism(s) by which platelet granzyme B induces end-organ apoptosis in sepsis.
    Methods: End-organ apoptosis in murine sepsis (i.e. polymicrobial peritonitis) was analyzed by immunohistochemistry. Platelet cytotoxicity was measured by flow cytometry following 90 minute ex vivo co-incubation with healthy murine splenocytes. Sepsis progression was measured via validated preclinical murine sepsis score.
    Measurements and main results: There was evident apoptosis in spleen, lung, and kidney sections from septic wild type mice. In contrast, there was a lack of TUNEL staining in spleens and lungs from septic granzyme B null mice and these mice survived longer following induction of sepsis than wild type mice. In co-incubation experiments, physical separation of septic platelets from splenocytes by a semi-permeable membrane reduced splenocyte apoptosis to a rate indistinguishable from negative controls. Chemical separation by the platelet GPIIb/IIIa receptor inhibitor eptifibatide decreased apoptosis by 66.6±10.6% (p = 0.008). Mice treated with eptifibatide in vivo survived longer following induction of sepsis than vehicle control mice.
    Conclusions: In sepsis, platelet granzyme B-mediated apoptosis occurs in spleen and lung, and absence of granzyme B slows sepsis progression. This process proceeds in a contact-dependent manner that is inhibited ex vivo and in vivo by the platelet GPIIb/IIIa receptor inhibitor eptifibatide. The GPIIb/IIIa inhibitors and other classes of anti-platelet drugs may be protective in sepsis.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Blood Platelets/drug effects ; Blood Platelets/pathology ; Caspases/metabolism ; Disease Progression ; Eptifibatide ; Granzymes/metabolism ; Lung/drug effects ; Lung/immunology ; Lymphocytes/drug effects ; Male ; Mice ; Peptides/pharmacology ; Peptides/therapeutic use ; Perforin/metabolism ; Platelet Aggregation/drug effects ; Platelet Glycoprotein GPIIb-IIIa Complex/antagonists & inhibitors ; Platelet Glycoprotein GPIIb-IIIa Complex/metabolism ; Sepsis/blood ; Sepsis/drug therapy ; Sepsis/metabolism ; Sepsis/pathology ; Spleen/drug effects ; Spleen/immunology
    Chemical Substances Peptides ; Platelet Glycoprotein GPIIb-IIIa Complex ; Perforin (126465-35-8) ; Granzymes (EC 3.4.21.-) ; Caspases (EC 3.4.22.-) ; Eptifibatide (NA8320J834)
    Language English
    Publishing date 2012-07-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0041549
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  5. Article ; Online: Δ-9,11 modification of glucocorticoids dissociates nuclear factor-κB inhibitory efficacy from glucocorticoid response element-associated side effects.

    Baudy, Andreas R / Reeves, Erica K M / Damsker, Jesse M / Heier, Christopher / Garvin, Lindsay M / Dillingham, Blythe C / McCall, John / Rayavarapu, Sree / Wang, Zuyi / Vandermeulen, Jack H / Sali, Arpana / Jahnke, Vanessa / Duguez, Stephanie / DuBois, Debra / Rose, Mary C / Nagaraju, Kanneboyina / Hoffman, Eric P

    The Journal of pharmacology and experimental therapeutics

    2012  Volume 343, Issue 1, Page(s) 225–232

    Abstract: Glucocorticoids are standard of care for many inflammatory conditions, but chronic use is associated with a broad array of side effects. This has led to a search for dissociative glucocorticoids--drugs able to retain or improve efficacy associated with ... ...

    Abstract Glucocorticoids are standard of care for many inflammatory conditions, but chronic use is associated with a broad array of side effects. This has led to a search for dissociative glucocorticoids--drugs able to retain or improve efficacy associated with transrepression [nuclear factor-κB (NF-κB) inhibition] but with the loss of side effects associated with transactivation (receptor-mediated transcriptional activation through glucocorticoid response element gene promoter elements). We investigated a glucocorticoid derivative with a Δ-9,11 modification as a dissociative steroid. The Δ-9,11 analog showed potent inhibition of tumor necrosis factor-α-induced NF-κB signaling in cell reporter assays, and this transrepression activity was blocked by 17β-hydroxy-11β-[4-dimethylamino phenyl]-17α-[1-propynyl]estra-4,9-dien-3-one (RU-486), showing the requirement for the glucocorticoid receptor (GR). The Δ-9,11 analog induced the nuclear translocation of GR but showed the loss of transactivation as assayed by GR-luciferase constructs as well as mRNA profiles of treated cells. The Δ-9,11 analog was tested for efficacy and side effects in two mouse models of muscular dystrophy: mdx (dystrophin deficiency), and SJL (dysferlin deficiency). Daily oral delivery of the Δ-9,11 analog showed a reduction of muscle inflammation and improvements in multiple muscle function assays yet no reductions in body weight or spleen size, suggesting the loss of key side effects. Our data demonstrate that a Δ-9,11 analog dissociates the GR-mediated transcriptional activities from anti-inflammatory activities. Accordingly, Δ-9,11 analogs may hold promise as a source of safer therapeutic agents for chronic inflammatory disorders.
    MeSH term(s) Animals ; Dose-Response Relationship, Drug ; Dronabinol/analogs & derivatives ; Dronabinol/chemistry ; Dronabinol/pharmacology ; Female ; Glucocorticoids/adverse effects ; Glucocorticoids/pharmacology ; HEK293 Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Inbred mdx ; Mice, Knockout ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/metabolism ; Response Elements/drug effects ; Response Elements/physiology ; Spleen/drug effects ; Spleen/metabolism ; Treatment Outcome
    Chemical Substances Glucocorticoids ; NF-kappa B ; 11-nor-delta(9)-tetrahydrocannabinol-9-carboxylic acid (4TPC9E4A32) ; Dronabinol (7J8897W37S)
    Language English
    Publishing date 2012-06-28
    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 3106-9
    ISSN 1521-0103 ; 0022-3565
    ISSN (online) 1521-0103
    ISSN 0022-3565
    DOI 10.1124/jpet.112.194340
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uf I Zs.40: Show issues Location:
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  6. Article ; Online: Wnt signaling arrests effector T cell differentiation and generates CD8+ memory stem cells.

    Gattinoni, Luca / Zhong, Xiao-Song / Palmer, Douglas C / Ji, Yun / Hinrichs, Christian S / Yu, Zhiya / Wrzesinski, Claudia / Boni, Andrea / Cassard, Lydie / Garvin, Lindsay M / Paulos, Chrystal M / Muranski, Pawel / Restifo, Nicholas P

    Nature medicine

    2009  Volume 15, Issue 7, Page(s) 808–813

    Abstract: Self-renewing cell populations such as hematopoietic stem cells and memory B and T lymphocytes might be regulated by shared signaling pathways. The Wnt-beta-catenin pathway is an evolutionarily conserved pathway that promotes hematopoietic stem cell self- ...

    Abstract Self-renewing cell populations such as hematopoietic stem cells and memory B and T lymphocytes might be regulated by shared signaling pathways. The Wnt-beta-catenin pathway is an evolutionarily conserved pathway that promotes hematopoietic stem cell self-renewal and multipotency by limiting stem cell proliferation and differentiation, but its role in the generation and maintenance of memory T cells is unknown. We found that induction of Wnt-beta-catenin signaling by inhibitors of glycogen sythase kinase-3beta or the Wnt protein family member Wnt3a arrested CD8(+) T cell development into effector cells. By blocking T cell differentiation, Wnt signaling promoted the generation of CD44(low)CD62L(high)Sca-1(high)CD122(high)Bcl-2(high) self-renewing multipotent CD8(+) memory stem cells with proliferative and antitumor capacities exceeding those of central and effector memory T cell subsets. These findings reveal a key role for Wnt signaling in the maintenance of 'stemness' in mature memory CD8(+) T cells and have major implications for the design of new vaccination strategies and adoptive immunotherapies.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/physiology ; Cell Differentiation ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3 beta ; Hematopoietic Stem Cells/physiology ; Hepatocyte Nuclear Factor 1-alpha ; Hyaluronan Receptors/analysis ; Immunologic Memory ; L-Selectin/analysis ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Signal Transduction/physiology ; T Cell Transcription Factor 1/physiology ; Wnt Proteins/physiology ; beta Catenin/physiology
    Chemical Substances Cd44 protein, mouse ; Hepatocyte Nuclear Factor 1-alpha ; Hnf1a protein, mouse ; Hyaluronan Receptors ; T Cell Transcription Factor 1 ; Wnt Proteins ; beta Catenin ; L-Selectin (126880-86-2) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
    Language English
    Publishing date 2009-06-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm.1982
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