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Article ; Online: Soluble guanylate cyclase stimulation prevents fibrotic tissue remodeling and improves survival in salt-sensitive Dahl rats.

Geschka, Sandra / Kretschmer, Axel / Sharkovska, Yuliya / Evgenov, Oleg V / Lawrenz, Bettina / Hucke, Andreas / Hocher, Berthold / Stasch, Johannes-Peter

PloS one

2011 Volume 6, Issue 7, Page(s) e21853

Abstract: Background: A direct pharmacological stimulation of soluble guanylate cyclase (sGC) is an emerging therapeutic approach to the management of various cardiovascular disorders associated with endothelial dysfunction. Novel sGC stimulators, including ... ...

Abstract	Background: A direct pharmacological stimulation of soluble guanylate cyclase (sGC) is an emerging therapeutic approach to the management of various cardiovascular disorders associated with endothelial dysfunction. Novel sGC stimulators, including riociguat (BAY 63-2521), have a dual mode of action: They sensitize sGC to endogenously produced nitric oxide (NO) and also directly stimulate sGC independently of NO. Little is known about their effects on tissue remodeling and degeneration and survival in experimental malignant hypertension. Methods and results: Mortality, hemodynamics and biomarkers of tissue remodeling and degeneration were assessed in Dahl salt-sensitive rats maintained on a high salt diet and treated with riociguat (3 or 10 mg/kg/d) for 14 weeks. Riociguat markedly attenuated systemic hypertension, improved systolic heart function and increased survival from 33% to 85%. Histological examination of the heart and kidneys revealed that riociguat significantly ameliorated fibrotic tissue remodeling and degeneration. Correspondingly, mRNA expression of the pro-fibrotic biomarkers osteopontin (OPN), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and plasminogen activator inhibitor-1 (PAI-1) in the myocardium and the renal cortex was attenuated by riociguat. In addition, riociguat reduced plasma and urinary levels of OPN, TIMP-1, and PAI-1. Conclusions: Stimulation of sGC by riociguat markedly improves survival and attenuates systemic hypertension and systolic dysfunction, as well as fibrotic tissue remodeling in the myocardium and the renal cortex in a rodent model of pressure and volume overload. These findings suggest a therapeutic potential of sGC stimulators in diseases associated with impaired cardiovascular and renal functions.
MeSH term(s)	Animals ; Biomarkers/blood ; Biomarkers/urine ; Blood Pressure/drug effects ; Body Weight/drug effects ; Echocardiography ; Fibrosis ; Gene Expression Regulation/drug effects ; Guanylate Cyclase/metabolism ; Heart Rate/drug effects ; Hemodynamics/drug effects ; Kidney/drug effects ; Kidney/pathology ; Kidney/physiopathology ; Kidney Function Tests ; Myocardium/pathology ; Organ Size/drug effects ; Organ Specificity/drug effects ; Pyrazoles/pharmacology ; Pyrimidines/pharmacology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats ; Rats, Inbred Dahl ; Receptors, Cytoplasmic and Nuclear/metabolism ; Soluble Guanylyl Cyclase ; Survival Analysis ; Systole/drug effects
Chemical Substances	Biomarkers ; Pyrazoles ; Pyrimidines ; RNA, Messenger ; Receptors, Cytoplasmic and Nuclear ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; riociguat (RU3FE2Y4XI)
Language	English
Publishing date	2011-07-18
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0021853
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Riociguat prevents fibrotic tissue remodelling and improves survival in salt-sensitive Dahl rats

Hucke Andreas / Lawrenz Bettina / Evgenov Oleg V / Sharkovska Yuliya / Kretschmer Axel / Geschka Sandra / Hocher Berthold / Stasch Johannes-Peter

BMC Pharmacology, Vol 11, Iss Suppl 1, p P

2011 Volume 28

Keywords	Therapeutics. Pharmacology ; RM1-950 ; Medicine ; R ; DOAJ:Therapeutics ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	English
Publishing date	2011-08-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cardiovascular and pharmacological implications of haem-deficient NO-unresponsive soluble guanylate cyclase knock-in mice.

Thoonen, Robrecht / Cauwels, Anje / Decaluwe, Kelly / Geschka, Sandra / Tainsh, Robert E / Delanghe, Joris / Hochepied, Tino / De Cauwer, Lode / Rogge, Elke / Voet, Sofie / Sips, Patrick / Karas, Richard H / Bloch, Kenneth D / Vuylsteke, Marnik / Stasch, Johannes-Peter / Van de Voorde, Johan / Buys, Emmanuel S / Brouckaert, Peter

Nature communications

2015 Volume 6, Page(s) 8482

Abstract: Oxidative stress, a central mediator of cardiovascular disease, results in loss of the prosthetic haem group of soluble guanylate cyclase (sGC), preventing its activation by nitric oxide (NO). Here we introduce Apo-sGC mice expressing haem-free sGC. Apo- ... ...

Abstract	Oxidative stress, a central mediator of cardiovascular disease, results in loss of the prosthetic haem group of soluble guanylate cyclase (sGC), preventing its activation by nitric oxide (NO). Here we introduce Apo-sGC mice expressing haem-free sGC. Apo-sGC mice are viable and develop hypertension. The haemodynamic effects of NO are abolished, but those of the sGC activator cinaciguat are enhanced in apo-sGC mice, suggesting that the effects of NO on smooth muscle relaxation, blood pressure regulation and inhibition of platelet aggregation require sGC activation by NO. Tumour necrosis factor (TNF)-induced hypotension and mortality are preserved in apo-sGC mice, indicating that pathways other than sGC signalling mediate the cardiovascular collapse in shock. Apo-sGC mice allow for differentiation between sGC-dependent and -independent NO effects and between haem-dependent and -independent sGC effects. Apo-sGC mice represent a unique experimental platform to study the in vivo consequences of sGC oxidation and the therapeutic potential of sGC activators.
MeSH term(s)	Animals ; Benzoates/pharmacology ; Blood Pressure/drug effects ; Cardiovascular System/drug effects ; Cardiovascular System/metabolism ; Gene Knock-In Techniques ; Guanylate Cyclase/genetics ; Heme/genetics ; Hypertension/genetics ; Hypotension/chemically induced ; Hypotension/genetics ; Mice ; Mice, Transgenic ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Nitric Oxide/metabolism ; Oxidative Stress/drug effects ; Platelet Aggregation/drug effects ; Receptors, Cytoplasmic and Nuclear/genetics ; Soluble Guanylyl Cyclase ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Benzoates ; Receptors, Cytoplasmic and Nuclear ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH) ; BAY 58-2667 (329773-35-5) ; Heme (42VZT0U6YR) ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2)
Language	English
Publishing date	2015-10-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms9482
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Article ; Online: Soluble guanylate cyclase stimulation prevents fibrotic tissue remodeling and improves survival in salt-sensitive Dahl rats.

Sandra Geschka / Axel Kretschmer / Yuliya Sharkovska / Oleg V Evgenov / Bettina Lawrenz / Andreas Hucke / Berthold Hocher / Johannes-Peter Stasch

PLoS ONE, Vol 6, Iss 7, p e

2011 Volume 21853

Abstract: A direct pharmacological stimulation of soluble guanylate cyclase (sGC) is an emerging therapeutic approach to the management of various cardiovascular disorders associated with endothelial dysfunction. Novel sGC stimulators, including riociguat (BAY 63- ... ...

Abstract	A direct pharmacological stimulation of soluble guanylate cyclase (sGC) is an emerging therapeutic approach to the management of various cardiovascular disorders associated with endothelial dysfunction. Novel sGC stimulators, including riociguat (BAY 63-2521), have a dual mode of action: They sensitize sGC to endogenously produced nitric oxide (NO) and also directly stimulate sGC independently of NO. Little is known about their effects on tissue remodeling and degeneration and survival in experimental malignant hypertension.Mortality, hemodynamics and biomarkers of tissue remodeling and degeneration were assessed in Dahl salt-sensitive rats maintained on a high salt diet and treated with riociguat (3 or 10 mg/kg/d) for 14 weeks. Riociguat markedly attenuated systemic hypertension, improved systolic heart function and increased survival from 33% to 85%. Histological examination of the heart and kidneys revealed that riociguat significantly ameliorated fibrotic tissue remodeling and degeneration. Correspondingly, mRNA expression of the pro-fibrotic biomarkers osteopontin (OPN), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and plasminogen activator inhibitor-1 (PAI-1) in the myocardium and the renal cortex was attenuated by riociguat. In addition, riociguat reduced plasma and urinary levels of OPN, TIMP-1, and PAI-1.Stimulation of sGC by riociguat markedly improves survival and attenuates systemic hypertension and systolic dysfunction, as well as fibrotic tissue remodeling in the myocardium and the renal cortex in a rodent model of pressure and volume overload. These findings suggest a therapeutic potential of sGC stimulators in diseases associated with impaired cardiovascular and renal functions.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Nitric oxide-independent stimulation of soluble guanylate cyclase reduces organ damage in experimental low-renin and high-renin models.

Sharkovska, Yuliya / Kalk, Philipp / Lawrenz, Bettina / Godes, Michael / Hoffmann, Linda Sarah / Wellkisch, Kathrin / Geschka, Sandra / Relle, Katharina / Hocher, Berthold / Stasch, Johannes-Peter

Journal of hypertension

2010 Volume 28, Issue 8, Page(s) 1666–1675

Abstract: Objectives: The nitric oxide-soluble guanylate cyclase (sGC)-cGMP signal transduction pathway is impaired in different cardiovascular diseases, including pulmonary hypertension, heart failure and arterial hypertension. Riociguat is a novel stimulator of ...

Abstract	Objectives: The nitric oxide-soluble guanylate cyclase (sGC)-cGMP signal transduction pathway is impaired in different cardiovascular diseases, including pulmonary hypertension, heart failure and arterial hypertension. Riociguat is a novel stimulator of soluble guanylate cyclase (sGC). However, little is known about the effects of sGC stimulators in experimental models of hypertension. We thus investigated the cardio-renal protective effects of riociguat in low-renin and high-renin rat models of hypertension. Methods: The vasorelaxant effect of riociguat was tested in vitro on isolated saphenous artery rings of normal and nitrate tolerant rabbits. The cardiovascular in-vivo effects of sGC stimulation were evaluated in hypertensive renin-transgenic rats treated with the nitric oxide-synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) (high-renin model) and in rats with 5/6 nephrectomy (low-renin model). Results: In both animal models, riociguat treatment improved survival and normalized blood pressure. Moreover, in the L-NAME study part, riociguat reduced cardiac target organ damage as indicated by lower plasma ANP, lower relative left ventricular weight and lower cardiac interstitial fibrosis, and reduced renal target organ damage as indicated by lower plasma creatinine and urea, less glomerulosclerosis and less renal interstitial fibrosis. In the 5/6 nephrectomy study part, riociguat reduced cardiac target organ damage as indicated by lower plasma ANP, lower relative left ventricular weight, lower myocyte diameter and lower arterial media/lumen ratio, and reduced renal target organ damage as indicated by improved creatinine clearance and less renal interstitial fibrosis. Conclusion: We demonstrate for the first time that the novel sGC stimulator riociguat shows in two independent models of hypertension a potent protection against cardiac and renal target organ damage.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Antihypertensive Agents/pharmacology ; Disease Models, Animal ; Disease Progression ; Dose-Response Relationship, Drug ; Guanylate Cyclase/antagonists & inhibitors ; Guanylate Cyclase/metabolism ; Heart/drug effects ; Hypertension/chemically induced ; Hypertension/enzymology ; Hypertension/prevention & control ; Kidney/drug effects ; Kidney/pathology ; Longevity/drug effects ; Male ; Muscle Contraction/drug effects ; Muscle, Smooth, Vascular/drug effects ; Myocardium/pathology ; NG-Nitroarginine Methyl Ester/toxicity ; Nephrectomy ; Nephritis, Interstitial/chemically induced ; Nephritis, Interstitial/pathology ; Nephritis, Interstitial/prevention & control ; Nitric Oxide/metabolism ; Pyrazoles/pharmacology ; Pyrimidines/pharmacology ; Rabbits ; Rats ; Rats, Wistar ; Renin/drug effects ; Renin/physiology ; Signal Transduction
Chemical Substances	Antihypertensive Agents ; Pyrazoles ; Pyrimidines ; Nitric Oxide (31C4KY9ESH) ; Renin (EC 3.4.23.15) ; Guanylate Cyclase (EC 4.6.1.2) ; riociguat (RU3FE2Y4XI) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2010-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605532-1
ISSN	1473-5598 ; 0263-6352 ; 0952-1178
ISSN (online)	1473-5598
ISSN	0263-6352 ; 0952-1178
DOI	10.1097/HJH.0b013e32833b558c
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Article ; Online: α1-A680T variant in GUCY1A3 as a candidate conferring protection from pulmonary hypertension among Kyrgyz highlanders.

Wilkins, Martin R / Aldashev, Almaz A / Wharton, John / Rhodes, Christopher J / Vandrovcova, Jana / Kasperaviciute, Dalia / Bhosle, Shriram G / Mueller, Michael / Geschka, Sandra / Rison, Stuart / Kojonazarov, Baktybek / Morrell, Nicholas W / Neidhardt, Inga / Surmeli, Nur Basak / Surmeli, Nur Basek / Aitman, Tim J / Stasch, Johannes-Peter / Behrends, Soenke / Marletta, Michael A

Circulation. Cardiovascular genetics

2014 Volume 7, Issue 6, Page(s) 920–929

Abstract: Background: Human variation in susceptibility to hypoxia-induced pulmonary hypertension is well recognized. High-altitude residents who do not develop pulmonary hypertension may host protective gene mutations.: Methods and results: Exome sequencing ... ...

Abstract	Background: Human variation in susceptibility to hypoxia-induced pulmonary hypertension is well recognized. High-altitude residents who do not develop pulmonary hypertension may host protective gene mutations. Methods and results: Exome sequencing was conducted on 24 unrelated Kyrgyz highlanders living 2400 to 3800 m above sea level, 12 (10 men; mean age, 54 years) with an elevated mean pulmonary artery pressure (mean±SD, 38.7±2.7 mm Hg) and 12 (11 men; mean age, 52 years) with a normal mean pulmonary artery pressure (19.2±0.6 mm Hg) to identify candidate genes that may influence the pulmonary vascular response to hypoxia. A total of 140 789 exomic variants were identified and 26 116 (18.5%) were classified as novel or rare. Thirty-three novel or rare potential pathogenic variants (frameshift, essential splice-site, and nonsynonymous) were found exclusively in either ≥3 subjects with high-altitude pulmonary hypertension or ≥3 highlanders with a normal mean pulmonary artery pressure. A novel missense mutation in GUCY1A3 in 3 subjects with a normal mean pulmonary artery pressure encodes an α1-A680T soluble guanylate cyclase (sGC) variant. Expression of the α1-A680T sGC variant in reporter cells resulted in higher cyclic guanosine monophosphate production compared with the wild-type enzyme and the purified α1-A680T sGC exhibited enhanced sensitivity to nitric oxide in vitro. Conclusions: The α1-A680T sGC variant may contribute to protection against high-altitude pulmonary hypertension and supports sGC as a pharmacological target for reducing pulmonary artery pressure in humans at altitude.
MeSH term(s)	Alleles ; Altitude Sickness/genetics ; Altitude Sickness/pathology ; Amino Acid Sequence ; Animals ; Cyclic GMP/metabolism ; Female ; Genotype ; Guanylate Cyclase/genetics ; Guanylate Cyclase/metabolism ; HEK293 Cells ; High-Throughput Nucleotide Sequencing ; Humans ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/pathology ; Male ; Middle Aged ; Molecular Sequence Data ; Nitric Oxide/metabolism ; Phylogeny ; Polymorphism, Single Nucleotide ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Sequence Alignment ; Sequence Analysis, DNA ; Signal Transduction ; Soluble Guanylyl Cyclase
Chemical Substances	GUCY1A2 protein, human ; Receptors, Cytoplasmic and Nuclear ; Nitric Oxide (31C4KY9ESH) ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2014-11-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2477394-3
ISSN	1942-3268 ; 1942-325X
ISSN (online)	1942-3268
ISSN	1942-325X
DOI	10.1161/CIRCGENETICS.114.000763
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Article ; Online: Nitric oxide-independent vasodilator rescues heme-oxidized soluble guanylate cyclase from proteasomal degradation.

Meurer, Sabine / Pioch, Sylke / Pabst, Tatjana / Opitz, Nils / Schmidt, Peter M / Beckhaus, Tobias / Wagner, Kristina / Matt, Simone / Gegenbauer, Kristina / Geschka, Sandra / Karas, Michael / Stasch, Johannes-Peter / Schmidt, Harald H H W / Müller-Esterl, Werner

Circulation research

2009 Volume 105, Issue 1, Page(s) 33–41

Abstract: Nitric oxide (NO) is an essential vasodilator. In vascular diseases, oxidative stress attenuates NO signaling by both chemical scavenging of free NO and oxidation and downregulation of its major intracellular receptor, the alphabeta heterodimeric heme- ... ...

Abstract	Nitric oxide (NO) is an essential vasodilator. In vascular diseases, oxidative stress attenuates NO signaling by both chemical scavenging of free NO and oxidation and downregulation of its major intracellular receptor, the alphabeta heterodimeric heme-containing soluble guanylate cyclase (sGC). Oxidation can also induce loss of the heme of sGC, as well as the responsiveness of sGC to NO. sGC activators such as BAY 58-2667 bind to oxidized/heme-free sGC and reactivate the enzyme to exert disease-specific vasodilation. Here, we show that oxidation-induced downregulation of sGC protein extends to isolated blood vessels. Mechanistically, degradation was triggered through sGC ubiquitination and proteasomal degradation. The heme-binding site ligand BAY 58-2667 prevented sGC ubiquitination and stabilized both alpha and beta subunits. Collectively, our data establish oxidation-ubiquitination of sGC as a modulator of NO/cGMP signaling and point to a new mechanism of action for sGC activating vasodilators by stabilizing their receptor, oxidized/heme-free sGC.
MeSH term(s)	Blood Vessels ; Cell Line ; Cyclic GMP/metabolism ; Guanylate Cyclase/metabolism ; Heme/metabolism ; Humans ; Nitric Oxide/pharmacology ; Oxidation-Reduction ; Proteasome Endopeptidase Complex/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Soluble Guanylyl Cyclase ; Ubiquitination ; Vasodilator Agents/pharmacology
Chemical Substances	Receptors, Cytoplasmic and Nuclear ; Vasodilator Agents ; Nitric Oxide (31C4KY9ESH) ; Heme (42VZT0U6YR) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2009-07-02
Publishing country	United States
Document type	Journal Article ; 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.109.198234
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Article ; Online: Cardio-renal protection of riociguat (BAY 63-2521) in low- and high-renin models of hypertension

Geschka Sandra / Wellkisch Kathrin / Hoffmann Linda / Godes Michael / Lawrenz Bettina / Sharkovska Yuliya / Kalk Philipp / Relle Katharina / Hocher Berthold / Stasch Johannes-Peter

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

2009 Volume 30

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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Article ; Online: Nitric oxide-independent vasodilator rescues heme-oxidized soluble guanylate cyclase from proteosomal degradation

Gegenbauer Kristina / Matt Simone / Wagner Kristina / Beckhaus Tobias / Schmidt Peter M / Opitz Nils / Pabst Tatjana / Pioch Sylke / Meurer Sabine / Geschka Sandra / Karas Michael / Stasch Johannes-Peter / Schmidt Harald HHW / Müller-Esterl Werner

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

2009 Volume 49

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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