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Article ; Online: Supplemental Fibrinogen Restores Platelet Inhibitor-Induced Reduction in Thrombus Formation without Altering Platelet Function: An In Vitro Study.

Bärnthaler, Thomas / Mahla, Elisabeth / Toth, Gabor G / Schuligoi, Rufina / Prüller, Florian / Buschmann, Eva / Heinemann, Akos

Thrombosis and haemostasis

2020 Volume 120, Issue 11, Page(s) 1548–1556

Abstract: Background: For patients treated with dual antiplatelet therapy, standardized drug-specific 3-to-7 day cessation is recommended prior to major surgery to reach sufficient platelet function recovery. Here we investigated the hypothesis that supplemental ...

Abstract	Background: For patients treated with dual antiplatelet therapy, standardized drug-specific 3-to-7 day cessation is recommended prior to major surgery to reach sufficient platelet function recovery. Here we investigated the hypothesis that supplemental fibrinogen might mitigate the inhibitory effects of antiplatelet therapy. Methods and results: To this end blood from healthy donors was treated in vitro with platelet inhibitors, and in vitro thrombus formation and platelet activation were assessed. Ticagrelor, acetylsalicylic acid, the combination of both, and tirofiban all markedly attenuated the formation of adherent thrombi, when whole blood was perfused through collagen-coated microchannels at physiological shear rates. Addition of fibrinogen restored in vitro thrombus formation in the presence of antiplatelet drugs and heparin. However, platelet activation, as investigated in assays of P-selectin expression and calcium flux, was not altered by fibrinogen supplementation. Most importantly, fibrinogen was able to restore in vitro thrombogenesis in patients on maintenance dual antiplatelet therapy after percutaneous coronary intervention. Conclusion: Thus, our in vitro data support the notion that supplementation of fibrinogen influences the perioperative hemostasis in patients undergoing surgery during antiplatelet therapy by promoting thrombogenesis without significantly interfering with platelet activation.
MeSH term(s)	Aged ; Aspirin/pharmacology ; Calcium Signaling/drug effects ; Female ; Fibrinogen/pharmacology ; Hemorheology ; Heparin/pharmacology ; Hirudins/pharmacology ; Humans ; In Vitro Techniques ; Male ; Middle Aged ; P-Selectin/biosynthesis ; P-Selectin/genetics ; Platelet Activation/drug effects ; Platelet Aggregation Inhibitors/pharmacology ; Thrombosis/prevention & control ; Ticagrelor/pharmacology ; Tirofiban/pharmacology
Chemical Substances	Hirudins ; P-Selectin ; Platelet Aggregation Inhibitors ; Fibrinogen (9001-32-5) ; Heparin (9005-49-6) ; Tirofiban (GGX234SI5H) ; Ticagrelor (GLH0314RVC) ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2020-08-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	518294-3
ISSN	2567-689X ; 0340-6245
ISSN (online)	2567-689X
ISSN	0340-6245
DOI	10.1055/s-0040-1715445
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Article ; Online: E-type prostanoid receptor 4 (EP4) in disease and therapy.

Konya, Viktoria / Marsche, Gunther / Schuligoi, Rufina / Heinemann, Akos

Pharmacology & therapeutics

2013 Volume 138, Issue 3, Page(s) 485–502

Abstract: The large variety of biological functions governed by prostaglandin (PG) E2 is mediated by signaling through four distinct E-type prostanoid (EP) receptors. The availability of mouse strains with genetic ablation of each EP receptor subtype and the ... ...

Abstract	The large variety of biological functions governed by prostaglandin (PG) E2 is mediated by signaling through four distinct E-type prostanoid (EP) receptors. The availability of mouse strains with genetic ablation of each EP receptor subtype and the development of selective EP agonists and antagonists have tremendously advanced our understanding of PGE2 as a physiologically and clinically relevant mediator. Moreover, studies using disease models revealed numerous conditions in which distinct EP receptors might be exploited therapeutically. In this context, the EP4 receptor is currently emerging as most versatile and promising among PGE2 receptors. Anti-inflammatory, anti-thrombotic and vasoprotective effects have been proposed for the EP4 receptor, along with its recently described unfavorable tumor-promoting and pro-angiogenic roles. A possible explanation for the diverse biological functions of EP4 might be the multiple signaling pathways switched on upon EP4 activation. The present review attempts to summarize the EP4 receptor-triggered signaling modules and the possible therapeutic applications of EP4-selective agonists and antagonists.
MeSH term(s)	Animals ; Bone Diseases/metabolism ; Cardiovascular Diseases/metabolism ; Dinoprostone/metabolism ; Gastrointestinal Diseases/metabolism ; Humans ; Immunologic Factors/metabolism ; Kidney Diseases/metabolism ; Lung Diseases/metabolism ; Neoplasms/metabolism ; Receptors, Prostaglandin E, EP4 Subtype/agonists ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & inhibitors ; Receptors, Prostaglandin E, EP4 Subtype/metabolism
Chemical Substances	Immunologic Factors ; Receptors, Prostaglandin E, EP4 Subtype ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2013-03-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2013.03.006
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Article: Supplemental Fibrinogen Restores Platelet Inhibitor-Induced Reduction in Thrombus Formation without Altering Platelet Function: An In Vitro Study

Bärnthaler, Thomas / Mahla, Elisabeth / Toth, Gabor G. / Schuligoi, Rufina / Prüller, Florian / Buschmann, Eva / Heinemann, Akos

Thrombosis and Haemostasis

2020 Volume 120, Issue 11, Page(s) 1548–1556

Abstract	Background: For patients treated with dual antiplatelet therapy, standardized drug-specific 3-to-7 day cessation is recommended prior to major surgery to reach sufficient platelet function recovery. Here we investigated the hypothesis that supplemental fibrinogen might mitigate the inhibitory effects of antiplatelet therapy. Methods and Results: To this end blood from healthy donors was treated in vitro with platelet inhibitors, and in vitro thrombus formation and platelet activation were assessed. Ticagrelor, acetylsalicylic acid, the combination of both, and tirofiban all markedly attenuated the formation of adherent thrombi, when whole blood was perfused through collagen-coated microchannels at physiological shear rates. Addition of fibrinogen restored in vitro thrombus formation in the presence of antiplatelet drugs and heparin. However, platelet activation, as investigated in assays of P-selectin expression and calcium flux, was not altered by fibrinogen supplementation. Most importantly, fibrinogen was able to restore in vitro thrombogenesis in patients on maintenance dual antiplatelet therapy after percutaneous coronary intervention. Conclusion: Thus, our in vitro data support the notion that supplementation of fibrinogen influences the perioperative hemostasis in patients undergoing surgery during antiplatelet therapy by promoting thrombogenesis without significantly interfering with platelet activation.
Keywords	fibrinogen ; platelet inhibitors ; platelets ; ticagrelor ; acetylsalicylic acid
Language	English
Publishing date	2020-08-09
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	518294-3
ISSN	2567-689X ; 0340-6245
ISSN (online)	2567-689X
ISSN	0340-6245
DOI	10.1055/s-0040-1715445
Database	Thieme publisher's database

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Uh III Zs.192: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Abnormal composition and function of high-density lipoproteins in atopic dermatitis patients.

Trieb, Markus / Wolf, Peter / Knuplez, Eva / Weger, Wolfgang / Schuster, Christian / Peinhaupt, Miriam / Holzer, Michael / Trakaki, Athina / Eichmann, Thomas / Lass, Achim / Wadsack, Christian / Schuligoi, Rufina / Heinemann, Akos / Marsche, Gunther

Allergy

2018 Volume 74, Issue 2, Page(s) 398–402

MeSH term(s)	Biomarkers ; Dermatitis, Atopic/diagnosis ; Dermatitis, Atopic/immunology ; Dermatitis, Atopic/metabolism ; Disease Susceptibility ; Humans ; Immunomodulation ; Lipid Metabolism ; Lipoproteins, HDL/blood ; Lipoproteins, HDL/metabolism
Chemical Substances	Biomarkers ; Lipoproteins, HDL
Language	English
Publishing date	2018-10-30
Publishing country	Denmark
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.13620
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Uh III Zs.150: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Dextran sulfate sodium-induced colitis alters stress-associated behaviour and neuropeptide gene expression in the amygdala-hippocampus network of mice.

Reichmann, Florian / Hassan, Ahmed Mostafa / Farzi, Aitak / Jain, Piyush / Schuligoi, Rufina / Holzer, Peter

Scientific reports

2015 Volume 5, Page(s) 9970

Abstract: Psychological stress causes disease exacerbation and relapses in inflammatory bowel disease (IBD) patients. Since studies on stress processing during visceral inflammation are lacking, we investigated the effects of experimental colitis as well as ... ...

Abstract	Psychological stress causes disease exacerbation and relapses in inflammatory bowel disease (IBD) patients. Since studies on stress processing during visceral inflammation are lacking, we investigated the effects of experimental colitis as well as psychological stress on neurochemical and neuroendocrine changes as well as behaviour in mice. Dextran sulfate sodium (DSS)-induced colitis and water avoidance stress (WAS) were used as mouse models of colitis and mild psychological stress, respectively. We measured WAS-associated behaviour, gene expression and proinflammatory cytokine levels within the amygdala, hippocampus and hypothalamus as well as plasma levels of cytokines and corticosterone in male C57BL/6N mice. Animals with DSS-induced colitis presented with prolonged immobility during the WAS session, which was associated with brain region-dependent alterations of neuropeptide Y (NPY), NPY receptor Y1, corticotropin-releasing hormone (CRH), CRH receptor 1, brain-derived neurotrophic factor and glucocorticoid receptor gene expression. Furthermore, the combination of DSS and WAS increased interleukin-6 and growth regulated oncogene-α levels in the brain. Altered gut-brain signalling in the course of DSS-induced colitis is thought to cause the observed distinct gene expression changes in the limbic system and the aberrant molecular and behavioural stress responses. These findings provide new insights into the effects of stress during IBD.
MeSH term(s)	Amygdala/metabolism ; Amygdala/pathology ; Animals ; Behavior, Animal/drug effects ; Colitis/chemically induced ; Colitis/metabolism ; Colitis/pathology ; Colitis/physiopathology ; Dextran Sulfate/toxicity ; Disease Models, Animal ; Gene Expression Regulation ; Hippocampus/metabolism ; Hippocampus/pathology ; Male ; Mice ; Neuropeptides/biosynthesis ; Stress, Physiological/drug effects
Chemical Substances	Neuropeptides ; Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2015-06-12
Publishing country	England
Document type	Journal Article ; 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/srep09970
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The EP3 Agonist Sulprostone Enhances Platelet Adhesion But Not Thrombus Formation Under Flow Conditions.

Pasterk, Lisa / Philipose, Sonia / Eller, Kathrin / Marsche, Gunther / Heinemann, Akos / Schuligoi, Rufina

Pharmacology

2015 Volume 96, Issue 3-4, Page(s) 137–143

Abstract: Platelets express the EP2, EP3 and EP4 receptors. Prostaglandin (PG) E2 has a biphasic effect on platelets. Low concentrations of PGE2 enhance platelet aggregation through the activation of the EP3 receptors, while at high concentrations it attenuates ... ...

Abstract	Platelets express the EP2, EP3 and EP4 receptors. Prostaglandin (PG) E2 has a biphasic effect on platelets. Low concentrations of PGE2 enhance platelet aggregation through the activation of the EP3 receptors, while at high concentrations it attenuates aggregation via the EP4 receptor. Consequently, EP3 receptor inhibition was shown to inhibit artherothrombosis, but had no influence on bleeding time in vivo. In this study, we investigated the role of the EP3 receptor in adhesion and thrombus formation under flow conditions in vitro. The EP3 agonist sulprostone caused an increase in the adhesion of washed platelets to fibrinogen as well as to collagen under low shear stress, an effect that was blocked by the EP3 antagonist L-798106. In contrast, when whole blood was perfused over collagen-coated surfaces, sulprostone did not enhance binding and thrombus formation of platelets on collagen; at high concentrations it even attenuated this response. We conclude that in more physiological models of thrombus formation, the role for EP3 receptors is limited, indirectly suggesting that the primary action of PGE2 in haemostasis might be an inhibitory one.
MeSH term(s)	Blood Platelets/drug effects ; Blood Platelets/metabolism ; Collagen/pharmacology ; Dinoprostone/analogs & derivatives ; Dinoprostone/pharmacology ; Fibrinogen/pharmacology ; Humans ; In Vitro Techniques ; Platelet Adhesiveness/drug effects ; Platelet Aggregation/drug effects ; Receptors, Prostaglandin E, EP3 Subtype/agonists ; Sulfonamides/pharmacology ; Thrombosis/blood ; Thrombosis/chemically induced
Chemical Substances	5-bromo-2-methoxy-N-(3-(naphthalen-2-yl-methylphenyl)acryloyl)benzenesulfonamide ; Receptors, Prostaglandin E, EP3 Subtype ; Sulfonamides ; sulprostone (501Q5EQ1GM) ; Fibrinogen (9001-32-5) ; Collagen (9007-34-5) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2015-07-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	206671-3
ISSN	1423-0313 ; 0031-7012
ISSN (online)	1423-0313
ISSN	0031-7012
DOI	10.1159/000437143
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Article ; Online: Inhibiting eicosanoid degradation exerts antifibrotic effects in a pulmonary fibrosis mouse model and human tissue.

Bärnthaler, Thomas / Theiler, Anna / Zabini, Diana / Trautmann, Sandra / Stacher-Priehse, Elvira / Lanz, Ilse / Klepetko, Walter / Sinn, Katharina / Flick, Holger / Scheidl, Stefan / Thomas, Dominique / Olschewski, Horst / Kwapiszewska, Grazyna / Schuligoi, Rufina / Heinemann, Akos

The Journal of allergy and clinical immunology

2019 Volume 145, Issue 3, Page(s) 818–833.e11

Abstract: Background: Idiopathic pulmonary fibrosis (IPF) is a disease with high 5-year mortality and few therapeutic options. Prostaglandin (PG) E: Objective: We sought to investigate the expression of 15-PGDH in IPF and the therapeutic potential of a ... ...

Abstract	Background: Idiopathic pulmonary fibrosis (IPF) is a disease with high 5-year mortality and few therapeutic options. Prostaglandin (PG) E Objective: We sought to investigate the expression of 15-PGDH in IPF and the therapeutic potential of a specific inhibitor of this enzyme in a mouse model and human tissue. Methods: In vitro studies, including fibrocyte differentiation, regulation of 15-PGDH, RT-PCR, and Western blot, were performed using peripheral blood from healthy donors and patients with IPF and A549 cells. Immunohistochemistry, immunofluorescence, 15-PGDH activity assays, and in situ hybridization as well as ex vivo IPF tissue culture experiments were done using healthy donor and IPF lungs. Therapeutic effects of 15-PGDH inhibition were studied in the bleomycin mouse model of pulmonary fibrosis. Results: We demonstrate that 15-PGDH shows areas of increased expression in patients with IPF. Inhibition of this enzyme increases PGE Conclusions: These findings highlight the role of 15-PGDH in IPF and suggest 15-PGDH inhibition as a promising therapeutic approach.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Cell Proliferation/drug effects ; Dinoprostone/metabolism ; Eicosanoids/metabolism ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation ; Humans ; Hydroxyprostaglandin Dehydrogenases/metabolism ; Idiopathic Pulmonary Fibrosis/enzymology ; Idiopathic Pulmonary Fibrosis/pathology ; Mice ; MicroRNAs/metabolism ; Pyridines/pharmacology ; Thiophenes/pharmacology
Chemical Substances	Eicosanoids ; Enzyme Inhibitors ; MIRN218 microRNA, human ; MicroRNAs ; Pyridines ; SW033291 ; Thiophenes ; Hydroxyprostaglandin Dehydrogenases (EC 1.1.1.-) ; 15-hydroxyprostaglandin dehydrogenase (EC 1.1.1.141) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2019-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2019.11.032
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Article: E-type prostanoid receptor 4 (EP4) in disease and therapy

Konya, Viktoria / Marsche, Gunther / Schuligoi, Rufina / Heinemann, Akos

Pharmacology and therapeutics. 2013 June, v. 138, no. 3

2013

Abstract	The large variety of biological functions governed by prostaglandin (PG) E2 is mediated by signaling through four distinct E-type prostanoid (EP) receptors. The availability of mouse strains with genetic ablation of each EP receptor subtype and the development of selective EP agonists and antagonists have tremendously advanced our understanding of PGE2 as a physiologically and clinically relevant mediator. Moreover, studies using disease models revealed numerous conditions in which distinct EP receptors might be exploited therapeutically. In this context, the EP4 receptor is currently emerging as most versatile and promising among PGE2 receptors. Anti-inflammatory, anti-thrombotic and vasoprotective effects have been proposed for the EP4 receptor, along with its recently described unfavorable tumor-promoting and pro-angiogenic roles. A possible explanation for the diverse biological functions of EP4 might be the multiple signaling pathways switched on upon EP4 activation. The present review attempts to summarize the EP4 receptor-triggered signaling modules and the possible therapeutic applications of EP4-selective agonists and antagonists.
Keywords	agonists ; antagonists ; anti-inflammatory activity ; disease models ; mice ; prostaglandins ; receptors ; signal transduction ; therapeutics
Language	English
Dates of publication	2013-06
Size	p. 485-502.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2013.03.006
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A biological target for antiplatelet therapy

Schuligoi Rufina / Heinemann Ákos / Ofner Martina / Philipose Sonia

BMC Pharmacology, Vol 10, Iss Suppl 1, p A

the prostaglandin E 2 receptor EP 4

2010 Volume 17

Keywords	Therapeutics. Pharmacology ; RM1-950 ; Medicine ; R ; DOAJ:Therapeutics ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	English
Publishing date	2010-11-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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Article ; Online: Butyrate ameliorates allergic airway inflammation by limiting eosinophil trafficking and survival.

Theiler, Anna / Bärnthaler, Thomas / Platzer, Wolfgang / Richtig, Georg / Peinhaupt, Miriam / Rittchen, Sonja / Kargl, Julia / Ulven, Trond / Marsh, Leigh M / Marsche, Gunther / Schuligoi, Rufina / Sturm, Eva M / Heinemann, Akos

The Journal of allergy and clinical immunology

2019 Volume 144, Issue 3, Page(s) 764–776

Abstract: Background: Lung eosinophilia is a hallmark of asthma, and eosinophils are believed to play a crucial role in the pathogenesis of allergic inflammatory diseases. Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, are produced in ...

Abstract	Background: Lung eosinophilia is a hallmark of asthma, and eosinophils are believed to play a crucial role in the pathogenesis of allergic inflammatory diseases. Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, are produced in high amounts in the gastrointestinal tract by commensal bacteria and can be absorbed into the bloodstream. Although there is recent evidence that SCFAs are beneficial in allergic asthma models, the effect on eosinophils has remained elusive. Objective: The role of SCFAs was investigated in human eosinophil function and a mouse model of allergic asthma. Methods: Eosinophils were purified from self-reported allergic or healthy donors. Migration, adhesion to the endothelium, and eosinophil survival were studied in vitro. Ca Results: For the first time, we observed that SCFAs were able to attenuate human eosinophils at several functional levels, including (1) adhesion to the endothelium, (2) migration, and (3) survival. These effects were independent from GPR41 and GPR43 but were accompanied by histone acetylation and mimicked by trichostatin A, a pan-histone deacetylase inhibitor. In vivo butyrate ameliorated allergen-induced airway and lung eosinophilia, reduced type 2 cytokine levels in bronchial fluid, and improved airway hyperresponsiveness in mice. Conclusion: These in vitro and in vivo findings highlight the importance of SCFAs, especially butyrate as a promising therapeutic agent in allergic inflammatory diseases.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Apoptosis/drug effects ; Asthma/drug therapy ; Asthma/genetics ; Asthma/immunology ; Butyrates/pharmacology ; Butyrates/therapeutic use ; Cell Movement/drug effects ; Eosinophils/drug effects ; Eosinophils/immunology ; Eosinophils/physiology ; Female ; Gene Expression Regulation/drug effects ; Humans ; Mice, Inbred BALB C ; Pulmonary Eosinophilia/drug therapy ; Pulmonary Eosinophilia/genetics ; Pulmonary Eosinophilia/immunology
Chemical Substances	Anti-Inflammatory Agents ; Butyrates
Language	English
Publishing date	2019-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2019.05.002
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