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Article: Microsomal prostaglandin E synthase-1 inhibition promotes shunting in arachidonic acid metabolism during inflammatory responses in vitro.

Liu, Jianyang / Peng, Bing / Steinmetz-Späh, Julia / Idborg, Helena / Korotkova, Marina / Jakobsson, Per-Johan

2023 Volume 167, Page(s) 106738

Abstract: Microsomal Prostaglandin E Synthase 1 (mPGES-1) is the key enzyme for the generation of the pro-inflammatory lipid mediator prostaglandin ... ...

Abstract	Microsomal Prostaglandin E Synthase 1 (mPGES-1) is the key enzyme for the generation of the pro-inflammatory lipid mediator prostaglandin E
MeSH term(s)	Mice ; Animals ; Prostaglandin-E Synthases/metabolism ; Cyclooxygenase 2/metabolism ; Arachidonic Acid ; Prostaglandins ; Inflammation/drug therapy ; Inflammation/metabolism ; Dinoprostone/metabolism ; Eicosanoids
Chemical Substances	Prostaglandin-E Synthases (EC 5.3.99.3) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Arachidonic Acid (27YG812J1I) ; Prostaglandins ; Dinoprostone (K7Q1JQR04M) ; Eicosanoids
Language	English
Publishing date	2023-04-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1426962-4
ISSN	2212-196X ; 1098-8823 ; 0090-6980
ISSN (online)	2212-196X
ISSN	1098-8823 ; 0090-6980
DOI	10.1016/j.prostaglandins.2023.106738
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Article ; Online: Urinary prostanoids are elevated by anti-TNF and anti-IL6 receptor disease-modifying antirheumatic drugs but are not predictive of response to treatment in early rheumatoid arthritis.

Liu, Jianyang / Idborg, Helena / Korotkova, Marina / Lend, Kristina / van Vollenhoven, Ronald / Lampa, Jon / Rudin, Anna / Nordström, Dan / Gudbjornsson, Bjorn / Gröndal, Gerdur / Uhlig, Till / Hørslev-Petersen, Kim / Lund Hetland, Merete / Østergaard, Mikkel / Nurmohamed, Michael / Jakobsson, Per-Johan

Arthritis research & therapy

2024 Volume 26, Issue 1, Page(s) 61

Abstract: Background: Disease-modifying antirheumatic drugs (DMARDs) are widely used for treating rheumatoid arthritis (RA). However, there are no established biomarkers to predict a patient's response to these therapies. Prostanoids, encompassing prostaglandins, ...

Abstract	Background: Disease-modifying antirheumatic drugs (DMARDs) are widely used for treating rheumatoid arthritis (RA). However, there are no established biomarkers to predict a patient's response to these therapies. Prostanoids, encompassing prostaglandins, prostacyclins, and thromboxanes, are potent lipid mediators implicated in RA progression. Nevertheless, the influence of DMARDs on prostanoid biosynthesis in RA patients remains poorly understood. This study aims to assess the impact of various DMARDs on urinary prostanoids levels and to explore whether urinary prostanoid profiles correlate with disease activity or response to therapy. Methods: This study included 152 Swedish female patients with early RA, all rheumatoid factor (RF) positive, enrolled in the NORD-STAR trial (registration number: NCT01491815). Participants were randomized into four therapeutic regimes: methotrexate (MTX) combined with (i) prednisolone (arm ACT), (ii) TNF-α blocker certolizumab pegol (arm CZP), (iii) CTLA-4Ig abatacept (arm ABA), or (iv) IL-6R blocker tocilizumab (arm TCZ). Urine samples, collected before start of treatment and at 24 weeks post-treatment, were analyzed for tetranor-prostaglandin E metabolite (tPGEM), tetranor-prostaglandin D metabolite (tPGDM), 2,3-dinor thromboxane B Results: Patients receiving MTX combined with CZP or TCZ exhibited significant elevations in urinary tPGEM and TXBM levels after 24 weeks of treatment. Other eicosanoids did not show significant alterations in response to any treatment. Baseline urinary eicosanoid levels did not correlate with baseline clinical disease activity index (CDAI) levels, nor with changes in CDAI from baseline to week 24. Their levels were also similar between patients who achieved CDAI remission and those with active disease at week 24. Conclusions: Treatment with anti-TNF or anti-IL6R agents in early RA patients leads to an increased systemic production of proinflammatory and prothrombotic prostanoids. However, urinary eicosanoid levels do not appear to be predictive of the response to DMARDs therapy.
MeSH term(s)	Humans ; Female ; Prostaglandins ; Antirheumatic Agents/therapeutic use ; Tumor Necrosis Factor Inhibitors ; Arthritis, Rheumatoid/drug therapy ; Methotrexate ; Certolizumab Pegol ; Dimaprit/analogs & derivatives
Chemical Substances	Prostaglandins ; Antirheumatic Agents ; Tumor Necrosis Factor Inhibitors ; S-(2-(N,N-diisopropylamino)ethyl)isothiourea (142620-95-9) ; Methotrexate (YL5FZ2Y5U1) ; Certolizumab Pegol (UMD07X179E) ; Dimaprit (ZZQ699148P)
Language	English
Publishing date	2024-03-05
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-024-03295-9
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Article ; Online: High-mannose glycans from

Almeida, Luís / van Roey, Ruthger / Patente, Thiago Andrade / Otto, Frank / Veldhuizen, Tom / Ghorasaini, Mohan / van Diepen, Angela / Schramm, Gabriele / Liu, Jianyang / Idborg, Helena / Korotkova, Marina / Jakobsson, Per-Johan / Giera, Martin / Hokke, Cornelis Hendrik / Everts, Bart

Frontiers in immunology

2024 Volume 15, Page(s) 1372927

Abstract: The parasitic ... ...

Abstract	The parasitic helminth
MeSH term(s)	Animals ; Schistosoma mansoni/immunology ; Dinoprostone/metabolism ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Lectins, C-Type/metabolism ; Lectins, C-Type/immunology ; Mannose/metabolism ; Mannose/immunology ; Mice ; Polysaccharides/immunology ; Polysaccharides/metabolism ; Antigens, Helminth/immunology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Schistosomiasis mansoni/immunology ; Schistosomiasis mansoni/metabolism ; Schistosomiasis mansoni/parasitology ; Ovum/immunology ; Ovum/metabolism ; Mice, Inbred C57BL ; OX40 Ligand/metabolism
Language	English
Publishing date	2024-04-29
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.2024.1372927
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Article ; Online: The skeletal muscle arachidonic acid cascade in health and inflammatory disease.

Korotkova, Marina / Lundberg, Ingrid E

Nature reviews. Rheumatology

2014 Volume 10, Issue 5, Page(s) 295–303

Abstract: Muscle atrophy and weakness are often observed in patients with chronic inflammatory diseases, and are the major clinical features of the autoimmune myopathies, polymyositis and dermatomyositis. A general understanding of the pathogenesis of muscle ... ...

Abstract	Muscle atrophy and weakness are often observed in patients with chronic inflammatory diseases, and are the major clinical features of the autoimmune myopathies, polymyositis and dermatomyositis. A general understanding of the pathogenesis of muscle atrophy and the impaired muscle function associated with chronic inflammatory diseases has not been clarified. In this context, arachidonic acid metabolites, such as the prostaglandin and leukotriene subfamilies, are of interest because they contribute to immune and nonimmune processes. Accumulating evidence suggests that prostaglandins and leukotrienes are involved in causing muscular pain and inflammation, and also in myogenesis and the repair of muscles. In this Review, we summarize novel findings that implicate prostaglandins and leukotrienes in the muscle atrophy and weakness that occur in inflammatory diseases of the muscles, with a focus on inflammatory myopathies. We discuss the role of the arachidonic acid cascade in skeletal muscle growth and function, and individual metabolites as potential therapeutic targets for the treatment of inflammatory muscle diseases.
MeSH term(s)	Arachidonic Acid/metabolism ; Humans ; Leukotrienes/metabolism ; Leukotrienes/physiology ; Muscle, Skeletal/metabolism ; Myositis/metabolism ; Prostaglandins/metabolism ; Prostaglandins/physiology
Chemical Substances	Leukotrienes ; Prostaglandins ; Arachidonic Acid (27YG812J1I)
Language	English
Publishing date	2014-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2491532-4
ISSN	1759-4804 ; 1759-4790
ISSN (online)	1759-4804
ISSN	1759-4790
DOI	10.1038/nrrheum.2014.2
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Article ; Online: Persisting eicosanoid pathways in rheumatic diseases.

Korotkova, Marina / Jakobsson, Per-Johan

Nature reviews. Rheumatology

2014 Volume 10, Issue 4, Page(s) 229–241

Abstract: An unmet clinical need exists for early treatment of rheumatic diseases and improved treatment strategies that can better maintain remission with reduced ongoing subclinical inflammation and bone destruction. Eicosanoids form one of the most complex ... ...

Abstract	An unmet clinical need exists for early treatment of rheumatic diseases and improved treatment strategies that can better maintain remission with reduced ongoing subclinical inflammation and bone destruction. Eicosanoids form one of the most complex networks in the body controlling many physiological and pathophysiological processes, including inflammation, autoimmunity and cancer. Persisting eicosanoid pathways are thought to be involved in the development of rheumatic diseases, and targeting this pathway might enable improved treatment strategies. Several enzymes of the arachidonic acid cascade as well as eicosanoid receptors (all part of the eicosanoid pathway) are today well-recognized targets for anti-inflammatory drugs that can reduce symptoms of inflammation in rheumatic diseases. In this Review, we outline the evidence supporting pivotal roles of eicosanoid signalling in the pathogenesis of rheumatic diseases and discuss findings from studies in animals and humans. We focus first on rheumatoid arthritis and discuss the upregulation of the cyclooxygenase and lipoxygenase pathways as most data are available in this condition. Research into the roles of eicosanoids in other rheumatic diseases (osteoarthritis, idiopathic inflammatory myopathies, systemic lupus erythematosus and gout) is also progressing rapidly and is discussed. Finally, we summarize the prospects of targeting eicosanoid pathways as anti-inflammatory treatment strategies for patients with rheumatic diseases.
MeSH term(s)	Animals ; Arthritis, Rheumatoid/enzymology ; Arthritis, Rheumatoid/etiology ; Arthritis, Rheumatoid/physiopathology ; Eicosanoids/metabolism ; Humans ; Lipoxygenase/metabolism ; Prostaglandin-Endoperoxide Synthases/metabolism ; Rheumatic Diseases/drug therapy ; Rheumatic Diseases/enzymology ; Rheumatic Diseases/physiopathology
Chemical Substances	Eicosanoids ; Lipoxygenase (EC 1.13.11.12) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	2014-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2491532-4
ISSN	1759-4804 ; 1759-4790
ISSN (online)	1759-4804
ISSN	1759-4790
DOI	10.1038/nrrheum.2014.1
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Article ; Online: Characterization of microsomal prostaglandin E synthase 1 inhibitors.

Korotkova, Marina / Jakobsson, Per-Johan

Basic & clinical pharmacology & toxicology

2014 Volume 114, Issue 1, Page(s) 64–69

Abstract: Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible terminal synthase in PGE2 biosynthesis by inflammatory and cancer cells. Clinical and experimental data emphasize that mPGES-1 might be a valuable target, with improved selectivity and ... ...

Abstract	Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible terminal synthase in PGE2 biosynthesis by inflammatory and cancer cells. Clinical and experimental data emphasize that mPGES-1 might be a valuable target, with improved selectivity and safety compared to traditional NSAIDs or selective COX-2 inhibitors, in the treatment of inflammatory diseases, different types of cancer as well as central symptoms elicited by peripheral inflammation. Since the first characterization of mPGES-1, the numbers of publications on mPGES-1 structure, pathogenic role and inhibitor development have increased exponentially; however, there are currently no selective mPGES-1 inhibitors available for clinical use. In this MiniReview, we focus on recent advances in the development of selective inhibitors of mPGES-1 activity, with the aim to discuss the effects of targeting mPGES-1 in different inflammatory models in vitro and in vivo.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Cyclooxygenase 2 Inhibitors/pharmacology ; Disease Models, Animal ; Down-Regulation ; Humans ; Inflammation/drug therapy ; Intramolecular Oxidoreductases/antagonists & inhibitors ; Intramolecular Oxidoreductases/metabolism ; Microsomes/drug effects ; Neoplasms/drug therapy ; Prostaglandin-E Synthases
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase 2 Inhibitors ; Intramolecular Oxidoreductases (EC 5.3.-) ; PTGES protein, human (EC 5.3.99.3) ; Prostaglandin-E Synthases (EC 5.3.99.3)
Language	English
Publishing date	2014-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2134679-3
ISSN	1742-7843 ; 1742-7835
ISSN (online)	1742-7843
ISSN	1742-7835
DOI	10.1111/bcpt.12162
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Article ; Online: High-content screening of drug combinations of an mPGES-1 inhibitor in multicellular tumor spheroids leads to mechanistic insights into neuroblastoma chemoresistance.

Zaghmi, Ahlem / Aybay, Erdem / Jiang, Long / Shang, Mingmei / Steinmetz-Späh, Julia / Wermeling, Fredrik / Kogner, Per / Korotkova, Marina / Östling, Päivi / Jakobsson, Per-Johan / Seashore-Ludlow, Brinton / Larsson, Karin

Molecular oncology

2023 Volume 18, Issue 2, Page(s) 317–335

Abstract: High-throughput drug screening enables the discovery of new anticancer drugs. Although monolayer cell cultures are commonly used for screening, their limited complexity and translational efficiency require alternative models. Three-dimensional cell ... ...

Abstract	High-throughput drug screening enables the discovery of new anticancer drugs. Although monolayer cell cultures are commonly used for screening, their limited complexity and translational efficiency require alternative models. Three-dimensional cell cultures, such as multicellular tumor spheroids (MCTS), mimic tumor architecture and offer promising opportunities for drug discovery. In this study, we developed a neuroblastoma MCTS model for high-content drug screening. We also aimed to decipher the mechanisms underlying synergistic drug combinations in this disease model. Several agents from different therapeutic categories and with different mechanisms of action were tested alone or in combination with selective inhibition of prostaglandin E
MeSH term(s)	Humans ; Prostaglandin-E Synthases ; Drug Resistance, Neoplasm ; Spheroids, Cellular ; Neuroblastoma/drug therapy ; Drug Discovery/methods
Chemical Substances	Prostaglandin-E Synthases (EC 5.3.99.3)
Language	English
Publishing date	2023-08-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13502
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Article ; Online: Microsomal prostaglandin E synthase-1 inhibition prevents adverse cardiac remodelling after myocardial infarction in mice.

Zhang, Yuze / Steinmetz-Späh, Julia / Idborg, Helena / Zhu, Liyuan / Li, Huihui / Rao, Haojie / Chen, Zengrong / Guo, Ziyi / Hu, Lejia / Xu, Chuansheng / Chen, Hong / Korotkova, Marina / Jakobsson, Per-Johan / Wang, Miao

British journal of pharmacology

2023 Volume 180, Issue 15, Page(s) 1981–1998

Abstract: Background and purpose: Heart failure with reduced ejection fraction (HFrEF) is a major consequence of myocardial infarction (MI). The microsomal prostaglandin E synthase-1 (mPGES-1)/PGE: Experimental approach: Mice were subjected to left anterior ... ...

Abstract	Background and purpose: Heart failure with reduced ejection fraction (HFrEF) is a major consequence of myocardial infarction (MI). The microsomal prostaglandin E synthase-1 (mPGES-1)/PGE Experimental approach: Mice were subjected to left anterior descending coronary artery ligation, followed by intraperitoneal treatment with the mPGES-1 inhibitor compound III (CIII) or 118, celecoxib (cyclooxygenase-2 inhibitor) or vehicle, once daily for 28 days. Urinary prostanoid metabolites were measured by liquid chromatography-tandem mass spectrometry. Key results: Chronic administration of CIII improved cardiac function in mice after MI compared with vehicle or celecoxib. CIII did not affect thrombogenesis or blood pressure. In addition, CIII reduced infarct area, augmented scar thickness, decreased collagen I/III ratio, decreased the expression of fibrosis-related genes and increased capillary density in the ischaemic area. Shunting to urinary metabolites of PGI Conclusion and implications: Inhibition of mPGES-1 prevented chronic adverse cardiac remodelling via an augmented PGI
MeSH term(s)	Animals ; Mice ; Prostaglandin-E Synthases/metabolism ; Celecoxib/pharmacology ; Heart Failure ; Cicatrix ; Ventricular Remodeling ; Stroke Volume ; Myocardial Infarction/genetics ; Cyclooxygenase 2 Inhibitors
Chemical Substances	Prostaglandin-E Synthases (EC 5.3.99.3) ; Celecoxib (JCX84Q7J1L) ; Cyclooxygenase 2 Inhibitors
Language	English
Publishing date	2023-03-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.16061
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Article ; Online: Exploring inflammatory signatures in arthritic joint biopsies with Spatial Transcriptomics.

Carlberg, Konstantin / Korotkova, Marina / Larsson, Ludvig / Catrina, Anca I / Ståhl, Patrik L / Malmström, Vivianne

Scientific reports

2019 Volume 9, Issue 1, Page(s) 18975

Abstract: Lately it has become possible to analyze transcriptomic profiles in tissue sections with retained cellular context. We aimed to explore synovial biopsies from rheumatoid arthritis (RA) and spondyloarthritis (SpA) patients, using Spatial Transcriptomics ( ... ...

Abstract	Lately it has become possible to analyze transcriptomic profiles in tissue sections with retained cellular context. We aimed to explore synovial biopsies from rheumatoid arthritis (RA) and spondyloarthritis (SpA) patients, using Spatial Transcriptomics (ST) as a proof of principle approach for unbiased mRNA studies at the site of inflammation in these chronic inflammatory diseases. Synovial tissue biopsies from affected joints were studied with ST. The transcriptome data was subjected to differential gene expression analysis (DEA), pathway analysis, immune cell type identification using Xcell analysis and validation with immunohistochemistry (IHC). The ST technology allows selective analyses on areas of interest, thus we analyzed morphologically distinct areas of mononuclear cell infiltrates. The top differentially expressed genes revealed an adaptive immune response profile and T-B cell interactions in RA, while in SpA, the profiles implicate functions associated with tissue repair. With spatially resolved gene expression data, overlaid on high-resolution histological images, we digitally portrayed pre-selected cell types in silico. The RA displayed an overrepresentation of central memory T cells, while in SpA effector memory T cells were most prominent. Consequently, ST allows for deeper understanding of cellular mechanisms and diversity in tissues from chronic inflammatory diseases.
MeSH term(s)	Adult ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/pathology ; Biopsy ; Female ; Gene Expression Profiling ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Male ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; Spondylarthritis/immunology ; Spondylarthritis/pathology ; Synovial Membrane/immunology ; Synovial Membrane/pathology ; Transcriptome/immunology
Language	English
Publishing date	2019-12-12
Publishing country	England
Document type	Clinical Trial ; 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/s41598-019-55441-y
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Article ; Online: Three-dimensional spatial transcriptomics uncovers cell type localizations in the human rheumatoid arthritis synovium.

Vickovic, Sanja / Schapiro, Denis / Carlberg, Konstantin / Lötstedt, Britta / Larsson, Ludvig / Hildebrandt, Franziska / Korotkova, Marina / Hensvold, Aase H / Catrina, Anca I / Sorger, Peter K / Malmström, Vivianne / Regev, Aviv / Ståhl, Patrik L

Communications biology

2022 Volume 5, Issue 1, Page(s) 129

Abstract: The inflamed rheumatic joint is a highly heterogeneous and complex tissue with dynamic recruitment and expansion of multiple cell types that interact in multifaceted ways within a localized area. Rheumatoid arthritis synovium has primarily been studied ... ...

Abstract	The inflamed rheumatic joint is a highly heterogeneous and complex tissue with dynamic recruitment and expansion of multiple cell types that interact in multifaceted ways within a localized area. Rheumatoid arthritis synovium has primarily been studied either by immunostaining or by molecular profiling after tissue homogenization. Here, we use Spatial Transcriptomics, where tissue-resident RNA is spatially labeled in situ with barcodes in a transcriptome-wide fashion, to study local tissue interactions at the site of chronic synovial inflammation. We report comprehensive spatial RNA-Seq data coupled to cell type-specific localization patterns at and around organized structures of infiltrating leukocyte cells in the synovium. Combining morphological features and high-throughput spatially resolved transcriptomics may be able to provide higher statistical power and more insights into monitoring disease severity and treatment-specific responses in seropositive and seronegative rheumatoid arthritis.
MeSH term(s)	Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/metabolism ; Humans ; Synovial Membrane/metabolism ; Transcriptome
Language	English
Publishing date	2022-02-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-03050-3
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