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  1. Book ; Online ; Thesis: Funktionelle Studie der NO-cGMP-Signalkaskade in Niere und Thrombozyten

    Schinner, Elisabeth [Verfasser]

    2010  

    Author's details vorgelegt von Elisabeth Schinner
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language German
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  2. Article ; Online: Differences in the renal antifibrotic cGMP/cGKI-dependent signaling of serelaxin, zaprinast, and their combination.

    Wetzl, Veronika / Schinner, Elisabeth / Kees, Frieder / Faerber, Lothar / Schlossmann, Jens

    Naunyn-Schmiedeberg's archives of pharmacology

    2017  Volume 390, Issue 9, Page(s) 939–948

    Abstract: Renal fibrosis is an important factor for end-stage renal failure. However, only few therapeutic options for its treatment are established. Zaprinast, a phosphodiesterase 5 inhibitor, and serelaxin, the recombinant form of the naturally occurring hormone ...

    Abstract Renal fibrosis is an important factor for end-stage renal failure. However, only few therapeutic options for its treatment are established. Zaprinast, a phosphodiesterase 5 inhibitor, and serelaxin, the recombinant form of the naturally occurring hormone relaxin, are differently acting modulators of cyclic guanosine monophosphate (cGMP) signaling. Both agents enhance cGMP availability in kidney tissue. These substances alone or in combination might interfere with the development of kidney fibrosis. Therefore, we compared the effects of combination therapy with the effects of monotherapy on renal fibrosis. Renal fibrosis was induced by unilateral ureteral obstruction (UUO) for 7 days in wild-type (WT) and cGKI knockout (KO) mice. Renal antifibrotic effects were assessed after 7 days. In WT, zaprinast and the combination of zaprinast and serelaxin significantly reduced renal interstitial fibrosis assessed by α-SMA, fibronectin, collagen1A1, and gelatinases (MMP2 and MMP9). Intriguingly in cGKI-KO, mRNA and protein expression of fibronectin and collagen1A1 were reduced by zaprinast, in contrast to serelaxin. Gelatinases are not regulated by zaprinast. Although both substances showed similar antifibrotic properties in WT, they distinguished in their effect mechanisms. In contrast to serelaxin which acts both on Smad2 and Erk1, zaprinast did not significantly diminish Erk1/2 phosphorylation. Interestingly, the combination of serelaxin/zaprinast achieved no additive antifibrotic effects compared to the monotherapy. Due to antifibrotic effects of zaprinast in cGKI-KO, we hypothesize that additional cGKI-independent mechanisms are supposed for antifibrotic signaling of zaprinast.
    MeSH term(s) Animals ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type I/genetics ; Cyclic GMP-Dependent Protein Kinase Type I/metabolism ; Drug Therapy, Combination ; Fibrosis ; Kidney/drug effects ; Kidney/pathology ; Kidney Diseases/pathology ; Kidney Diseases/prevention & control ; Mice ; Mice, Knockout ; Phosphodiesterase 5 Inhibitors/administration & dosage ; Phosphodiesterase 5 Inhibitors/pharmacology ; Purinones/administration & dosage ; Purinones/pharmacology ; Recombinant Proteins/administration & dosage ; Recombinant Proteins/pharmacology ; Relaxin/administration & dosage ; Relaxin/pharmacology ; Signal Transduction/drug effects ; Ureteral Obstruction/complications
    Chemical Substances Phosphodiesterase 5 Inhibitors ; Purinones ; Recombinant Proteins ; serelaxin protein, human ; Relaxin (9002-69-1) ; Cyclic GMP-Dependent Protein Kinase Type I (EC 2.7.11.12) ; zaprinast (GXT25D5DS0) ; Cyclic GMP (H2D2X058MU)
    Language English
    Publishing date 2017-09
    Publishing country Germany
    Document type Comparative Study ; Journal Article
    ZDB-ID 121471-8
    ISSN 1432-1912 ; 0028-1298
    ISSN (online) 1432-1912
    ISSN 0028-1298
    DOI 10.1007/s00210-017-1394-z
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  3. Article ; Online: cGMP becomes a drug target.

    Schlossmann, Jens / Schinner, Elisabeth

    Naunyn-Schmiedeberg's archives of pharmacology

    2012  Volume 385, Issue 3, Page(s) 243–252

    Abstract: Cyclic guanosine 3',5'-monophosphate (cGMP) serves as a second messenger molecule, which regulates pleiotropic cellular functions in health and disease. cGMP is generated by particulate or soluble guanylyl cyclases upon stimulation with natriuretic ... ...

    Abstract Cyclic guanosine 3',5'-monophosphate (cGMP) serves as a second messenger molecule, which regulates pleiotropic cellular functions in health and disease. cGMP is generated by particulate or soluble guanylyl cyclases upon stimulation with natriuretic peptides or nitric oxide, respectively. Furthermore, the cGMP concentration is modulated by cGMP-degrading phosphodiesterases. Several targets of cGMP are utilized to effect its various cellular functions. These effector molecules comprise cGMP-dependent protein kinases, ion channels, and phosphodiesterases. During the last decade, it emerged that cGMP is a novel drug target for the treatment of pulmonary and cardiovascular disorders. In this respect, several drugs were developed, which are now in clinical phase studies for, e.g., pulmonary hypertension or cardiovascular diseases. These new drugs act NO-independently with/without heme on soluble guanylyl cyclases or induce subtypes of particular guanylyl cyclases and thereby lead to new therapeutic concepts and horizons. In this regard, the fifth cGMP meeting held in June 2011 in Halle, Germany, comprised the new therapeutic challenges with the novel functional and structural concepts of cGMP generating and effector molecules. This report summarizes the new data on molecular mechanisms, (patho)physiological relevance, and therapeutic potentials of the cGMP signaling system that were presented at this meeting.
    MeSH term(s) Animals ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/physiopathology ; Cyclic GMP/metabolism ; Drug Design ; Guanylate Cyclase/metabolism ; Humans ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/physiopathology ; Molecular Targeted Therapy ; Receptors, Cytoplasmic and Nuclear/metabolism ; Signal Transduction/drug effects ; Soluble Guanylyl Cyclase
    Chemical Substances Receptors, Cytoplasmic and Nuclear ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
    Language English
    Publishing date 2012-01-24
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 121471-8
    ISSN 1432-1912 ; 0028-1298
    ISSN (online) 1432-1912
    ISSN 0028-1298
    DOI 10.1007/s00210-012-0730-6
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    In stock of ZB MED Cologne/Königswinter

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  4. Article: Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris.

    Schlögl, Elisabeth / Radeva, Mariya Y / Vielmuth, Franziska / Schinner, Camilla / Waschke, Jens / Spindler, Volker

    Frontiers in immunology

    2018  Volume 9, Page(s) 858

    Abstract: Pemphigus ... ...

    Abstract Pemphigus vulgaris
    MeSH term(s) Autoantibodies/blood ; Autoantibodies/immunology ; Autoantigens/immunology ; Cell Adhesion/immunology ; Cell Line ; Desmoglein 1/immunology ; Desmoglein 3/immunology ; Desmoglein 3/metabolism ; Endocytosis/immunology ; Humans ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Intermediate Filaments/immunology ; Intermediate Filaments/metabolism ; Keratinocytes ; Keratins/immunology ; Keratins/metabolism ; Pemphigus/blood ; Pemphigus/immunology ; Pemphigus/pathology ; Skin/cytology ; Skin/immunology ; Skin/pathology
    Chemical Substances Autoantibodies ; Autoantigens ; DSG1 protein, human ; DSG3 protein, human ; Desmoglein 1 ; Desmoglein 3 ; Immunoglobulin G ; Keratins (68238-35-7)
    Language English
    Publishing date 2018-04-25
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.00858
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  5. Article ; Online: Cyclic nucleotide signalling in kidney fibrosis.

    Schinner, Elisabeth / Wetzl, Veronika / Schlossmann, Jens

    International journal of molecular sciences

    2015  Volume 16, Issue 2, Page(s) 2320–2351

    Abstract: Kidney fibrosis is an important factor for the progression of kidney diseases, e.g., diabetes mellitus induced kidney failure, glomerulosclerosis and nephritis resulting in chronic kidney disease or end-stage renal disease. Cyclic adenosine monophosphate ...

    Abstract Kidney fibrosis is an important factor for the progression of kidney diseases, e.g., diabetes mellitus induced kidney failure, glomerulosclerosis and nephritis resulting in chronic kidney disease or end-stage renal disease. Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were implicated to suppress several of the above mentioned renal diseases. In this review article, identified effects and mechanisms of cGMP and cAMP regarding renal fibrosis are summarized. These mechanisms include several signalling pathways of nitric oxide/ANP/guanylyl cyclases/cGMP-dependent protein kinase and cAMP/Epac/adenylyl cyclases/cAMP-dependent protein kinase. Furthermore, diverse possible drugs activating these pathways are discussed. From these diverse mechanisms it is expected that new pharmacological treatments will evolve for the therapy or even prevention of kidney failure.
    MeSH term(s) Adenylyl Cyclases/metabolism ; Animals ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic GMP/metabolism ; Fibrosis ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Nitric Oxide/metabolism ; Phosphoric Diester Hydrolases/metabolism ; Signal Transduction
    Chemical Substances Cyclic AMP Response Element-Binding Protein ; Guanine Nucleotide Exchange Factors ; Nitric Oxide (31C4KY9ESH) ; Cyclic AMP (E0399OZS9N) ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; Adenylyl Cyclases (EC 4.6.1.1) ; Cyclic GMP (H2D2X058MU)
    Language English
    Publishing date 2015-01-22
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms16022320
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  6. Article ; Online: Cyclic Nucleotide Signalling in Kidney Fibrosis

    Elisabeth Schinner / Veronika Wetzl / Jens Schlossmann

    International Journal of Molecular Sciences, Vol 16, Iss 2, Pp 2320-

    2015  Volume 2351

    Abstract: Kidney fibrosis is an important factor for the progression of kidney diseases, e.g., diabetes mellitus induced kidney failure, glomerulosclerosis and nephritis resulting in chronic kidney disease or end-stage renal disease. Cyclic adenosine monophosphate ...

    Abstract Kidney fibrosis is an important factor for the progression of kidney diseases, e.g., diabetes mellitus induced kidney failure, glomerulosclerosis and nephritis resulting in chronic kidney disease or end-stage renal disease. Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were implicated to suppress several of the above mentioned renal diseases. In this review article, identified effects and mechanisms of cGMP and cAMP regarding renal fibrosis are summarized. These mechanisms include several signalling pathways of nitric oxide/ANP/guanylyl cyclases/cGMP-dependent protein kinase and cAMP/Epac/adenylyl cyclases/cAMP-dependent protein kinase. Furthermore, diverse possible drugs activating these pathways are discussed. From these diverse mechanisms it is expected that new pharmacological treatments will evolve for the therapy or even prevention of kidney failure.
    Keywords signalling ; cyclic nucleotides ; cyclic guanosine monophosphate ; cyclic adenosine monophosphate ; kidney fibrosis ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2015-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Publisher Correction: Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro.

    Fischer, Carola / Milting, Hendrik / Fein, Evelyn / Reiser, Elisabeth / Lu, Kun / Seidel, Thomas / Schinner, Camilla / Schwarzmayr, Thomas / Schramm, Rene / Tomasi, Roland / Husse, Britta / Cao-Ehlker, Xiaochun / Pohl, Ulrich / Dendorfer, Andreas

    Nature communications

    2019  Volume 10, Issue 1, Page(s) 532

    Abstract: The original version of this Article incorrectly acknowledged Elisabeth Reiser and Rene Schramm ...

    Abstract The original version of this Article incorrectly acknowledged Elisabeth Reiser and Rene Schramm as a corresponding author. This has now been corrected in both the PDF and HTML versions of the Article.
    Language English
    Publishing date 2019-01-28
    Publishing country England
    Document type Journal Article ; Published Erratum
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/s41467-019-08510-9
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  8. Article: Involvement of Cyclic Guanosine Monophosphate-Dependent Protein Kinase I in Renal Antifibrotic Effects of Serelaxin.

    Wetzl, Veronika / Schinner, Elisabeth / Kees, Frieder / Hofmann, Franz / Faerber, Lothar / Schlossmann, Jens

    Frontiers in pharmacology

    2016  Volume 7, Page(s) 195

    Abstract: Introduction: Kidney fibrosis has shown to be ameliorated through the involvement of cyclic guanosine monophosphate (cGMP) and its dependent protein kinase I (cGKI). Serelaxin, the recombinant form of human relaxin-II, increases cGMP levels and has ... ...

    Abstract Introduction: Kidney fibrosis has shown to be ameliorated through the involvement of cyclic guanosine monophosphate (cGMP) and its dependent protein kinase I (cGKI). Serelaxin, the recombinant form of human relaxin-II, increases cGMP levels and has shown beneficial effects on kidney function in acute heart failure patients. Antifibrotic properties of serelaxin are supposed to be mediated via relaxin family peptide receptor 1 and subsequently enhanced nitric oxide/cGMP to inhibit transforming growth factor-β (TGF-β) signaling. This study examines the involvement of cGKI in the antifibrotic signaling of serelaxin.
    Methods and results: Kidney fibrosis was induced by unilateral ureteral obstruction in wildtype (WT) and cGKI knock-out (KO) mice. After 7 days, renal antifibrotic effects of serelaxin were assessed. Serelaxin treatment for 7 days significantly increased cGMP in the kidney of WT and cGKI-KO. In WT, renal fibrosis was reduced through decreased accumulation of collagen1A1, total collagen, and fibronectin. The profibrotic connective tissue growth factor as well as myofibroblast differentiation were reduced and matrix metalloproteinases-2 and -9 were positively modulated after treatment. Moreover, Smad2 as well as extracellular signal-regulated kinase 1 (ERK1) phosphorylation were decreased, whereas phosphodiesterase (PDE) 5a phosphorylation was increased. However, these effects were not observed in cGKI-KO.
    Conclusion: Antifibrotic renal effects of serelaxin are mediated via cGMP/cGKI to inhibit Smad2- and ERK1-dependent TGF-β signaling and increased PDE5a phosphorylation.
    Language English
    Publishing date 2016-07-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2016.00195
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  9. Article ; Online: NO/cGMP signalling in platelets

    Schinner Elisabeth / Schlossmann Jens

    BMC Pharmacology, Vol 9, Iss Suppl 1, p P

    2009  Volume 62

    Keywords Therapeutics. Pharmacology ; RM1-950 ; Medicine ; R ; DOAJ:Therapeutics ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2009-08-01T00:00:00Z
    Publisher BioMed Central
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article: Inhibition of the TGFβ signalling pathway by cGMP and cGMP‐dependent kinase I in renal fibrosis

    Schinner, Elisabeth / Wetzl, Veronika / Schramm, Andrea / Kees, Frieder / Sandner, Peter / Stasch, Johannes‐Peter / Hofmann, Franz / Schlossmann, Jens

    FEBS Open Bio. 2017 Apr., v. 7, no. 4

    2017  

    Abstract: Agents that enhance production of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) ameliorate the progression of renal fibrosis. However, the molecular mechanism of this process is not fully understood. We hypothesize that the antifibrotic ... ...

    Abstract Agents that enhance production of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) ameliorate the progression of renal fibrosis. However, the molecular mechanism of this process is not fully understood. We hypothesize that the antifibrotic effects of cGMP and cGMP‐dependent kinase I (cGKI) are mediated via regulation of the TGFβ signalling pathway, both via ERK and the Smad‐dependent route. Kidney fibrosis was induced by unilateral ureter obstruction (UUO) in wild‐type and cGKI‐deficient (cGKI‐KO) mice. The cGMP/cGKI signalling pathway was activated by application of the soluble guanylate cyclase (sGC) stimulator BAY 41‐8543 (BAY), beginning 1 day after UUO. After 7 days, the antifibrotic effects of BAY were analysed by measuring mRNA and protein expression of characteristic fibrotic biomarkers. The effects of cGMP/TGFβ on cultured fibroblasts were also analysed in vitro. BAY application influenced the activity of the extracellular matrix (ECM)‐degrading matrix metalloproteases (MMP2 and MMP9) and their inhibitor tissue inhibitors of metalloproteinase‐1, the secretion of cytokines (e.g. IL‐6) and the expression pattern of ECM proteins (e.g. collagen, fibronectin) and profibrotic mediators (e.g. connective tissue growth factors and plasminogen‐activator inhibitor‐1). Activation of the cGMP/cGKI signalling pathway showed protective effects against fibrosis which were mediated by inhibition of P‐Erk1/2 and translocation of P‐smad3. The elucidation of these signalling mechanisms might support the development of new therapeutic options regarding cGMP/cGKI‐mediated antifibrotic actions.
    Keywords biomarkers ; collagen ; cyclic GMP ; extracellular matrix ; fibroblasts ; fibronectins ; fibrosis ; guanylate cyclase ; interleukin-6 ; kidneys ; metalloproteinases ; nitric oxide ; plasminogen activator inhibitors ; protein synthesis ; secretion ; therapeutics ; ureter
    Language English
    Dates of publication 2017-04
    Size p. 550-561.
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note JOURNAL ARTICLE
    ZDB-ID 2651702-4
    ISSN 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.12202
    Database NAL-Catalogue (AGRICOLA)

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