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  1. Article ; Online: The anti-inflammatory and vasoprotective properties of mPGES-1 inhibition offer promising therapeutic potential.

    Steinmetz-Späh, Julia / Jakobsson, Per-Johan

    Expert opinion on therapeutic targets

    2023  Volume 27, Issue 11, Page(s) 1115–1123

    Abstract: Introduction: Prostaglandin E: Areas covered: The article briefly describes prostanoid history and metabolism with a strong focus on the vascular effects of prostanoids. Recent advances in mPGES-1 inhibitor development and results from pre-clinical ... ...

    Abstract Introduction: Prostaglandin E
    Areas covered: The article briefly describes prostanoid history and metabolism with a strong focus on the vascular effects of prostanoids. Recent advances in mPGES-1 inhibitor development and results from pre-clinical and clinical studies are presented. Prostanoid shunting after mPGES-1 inhibition is highlighted and particularly discussed in the context of cardiovascular diseases.
    Expert opinion: The newest research demonstrates that inhibition of mPGES-1 is a potent anti-inflammatory treatment strategy and beneficial and safer regarding cardiovascular side effects compared to NSAIDs. Inhibitors of mPGES-1 hold great potential to advance to the clinic and there are ongoing phase-II trials in endometriosis.
    MeSH term(s) Female ; Humans ; Prostaglandin-E Synthases/metabolism ; Prostaglandins/metabolism ; Anti-Inflammatory Agents/pharmacology ; Dinoprostone/metabolism ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Cyclooxygenase 2/metabolism
    Chemical Substances Prostaglandin-E Synthases (EC 5.3.99.3) ; Prostaglandins ; Anti-Inflammatory Agents ; Dinoprostone (K7Q1JQR04M) ; Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase 2 (EC 1.14.99.1)
    Language English
    Publishing date 2023-12-07
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2023.2285785
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5244: Show issues Location:
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  2. 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

    Prostaglandins & other lipid mediators

    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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 815: Show issues Location:
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  3. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6637: Show issues Location:
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  4. 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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  5. Article ; Online: Effects of microsomal prostaglandin E synthase-1 inhibition on resistance artery tone in patients with end stage kidney disease.

    Steinmetz-Späh, Julia / Arefin, Samsul / Larsson, Karin / Jahan, Jabin / Mudrovcic, Neja / Wennberg, Lars / Stenvinkel, Peter / Korotkova, Marina / Kublickiene, Karolina / Jakobsson, Per-Johan

    British journal of pharmacology

    2022  Volume 179, Issue 7, Page(s) 1433–1449

    Abstract: Background: The microvasculature is a target organ for the early manifestations of cardiovascular disease. Therefore, a better understanding of the prostaglandin system and characterising the effects of mPGES-1 inhibition and concomitant reduction of ... ...

    Abstract Background: The microvasculature is a target organ for the early manifestations of cardiovascular disease. Therefore, a better understanding of the prostaglandin system and characterising the effects of mPGES-1 inhibition and concomitant reduction of PGE
    Experimental approach: The effects of mPGES-1 inhibition on constriction and relaxation of resistance arteries (diameter: 100-400 μm) from patients with end stage kidney disease (ESKD) and controls (Non-ESKD) were studied using wire-myography in combination with immunological and mass-spectrometry based analyses.
    Key results: Inhibition of mPGES-1 in arteries from ESKD patients and Non-ESKD controls significantly reduced adrenergic vasoconstriction, which was unaffected by the COX-2 inhibitors NS-398 and Etoricoxib, or by the COX-1/COX-2 inhibitor Indomethacin tested in Non-ESKD controls. However, a significant increase of acetylcholine-induced dilatation was observed for mPGES-1 inhibition. In IL-1β treated arteries, inhibition of mPGES-1 significantly reduced PGE
    Conclusion: Our study demonstrates vasodilating effects following mPGES-1 inhibition in human microvasculature and suggests that several pathways besides shunting to PGI
    MeSH term(s) Adrenergic Agents ; Arteries/metabolism ; Arteries/physiology ; Cyclooxygenase 1/metabolism ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2 Inhibitors/pharmacology ; Etoricoxib ; Humans ; Kidney Failure, Chronic/complications ; Microvessels/metabolism ; Microvessels/physiology ; Nitrobenzenes ; Prostaglandin-E Synthases/antagonists & inhibitors ; Prostaglandins ; Sulfonamides
    Chemical Substances Adrenergic Agents ; Cyclooxygenase 2 Inhibitors ; Nitrobenzenes ; Prostaglandins ; Sulfonamides ; N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide (123653-11-2) ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Prostaglandin-E Synthases (EC 5.3.99.3) ; Etoricoxib (WRX4NFY03R)
    Language English
    Publishing date 2022-02-12
    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.15729
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  6. Article ; Online: Biosynthesis of prostaglandin 15dPGJ

    Steinmetz-Späh, Julia / Liu, Jianyang / Singh, Rajkumar / Ekoff, Maria / Boddul, Sanjaykumar / Tang, Xiao / Bergqvist, Filip / Idborg, Helena / Heitel, Pascal / Rönnberg, Elin / Merk, Daniel / Wermeling, Fredrik / Haeggström, Jesper Z / Nilsson, Gunnar / Steinhilber, Dieter / Larsson, Karin / Korotkova, Marina / Jakobsson, Per-Johan

    Journal of lipid research

    2022  , Page(s) 100310

    Abstract: Inhibition of microsomal prostaglandin E synthase-1 (mPGES-1) results in decreased production of pro-inflammatory ... ...

    Abstract Inhibition of microsomal prostaglandin E synthase-1 (mPGES-1) results in decreased production of pro-inflammatory PGE
    Language English
    Publishing date 2022-11-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1016/j.jlr.2022.100310
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    Zs.A 175: Show issues Location:
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  7. Article ; Online: Disruption of Prostaglandin E2 Signaling in Cancer-Associated Fibroblasts Limits Mammary Carcinoma Growth but Promotes Metastasis.

    Elwakeel, Eiman / Brüggemann, Mirko / Wagih, Jessica / Lityagina, Olga / Elewa, Mohammed A F / Han, Yingying / Frömel, Timo / Popp, Rüdiger / Nicolas, Adele M / Schreiber, Yannick / Gradhand, Elise / Thomas, Dominique / Nüsing, Rolf / Steinmetz-Späh, Julia / Savai, Rajkumar / Fokas, Emmanouil / Fleming, Ingrid / Greten, Florian R / Zarnack, Kathi /
    Brüne, Bernhard / Weigert, Andreas

    Cancer research

    2022  Volume 82, Issue 7, Page(s) 1380–1395

    Abstract: The activation and differentiation of cancer-associated fibroblasts (CAF) are involved in tumor progression. Here, we show that the tumor-promoting lipid mediator prostaglandin E2 (PGE2) plays a paradoxical role in CAF activation and tumor progression. ... ...

    Abstract The activation and differentiation of cancer-associated fibroblasts (CAF) are involved in tumor progression. Here, we show that the tumor-promoting lipid mediator prostaglandin E2 (PGE2) plays a paradoxical role in CAF activation and tumor progression. Restricting PGE2 signaling via knockout of microsomal prostaglandin E synthase-1 (mPGES-1) in PyMT mice or of the prostanoid E receptor 3 (EP3) in CAFs stunted mammary carcinoma growth associated with strong CAF proliferation. CAF proliferation upon EP3 inhibition required p38 MAPK signaling. Mechanistically, TGFβ-activated kinase-like protein (TAK1L), which was identified as a negative regulator of p38 MAPK activation, was decreased following ablation of mPGES-1 or EP3. In contrast with its effects on primary tumor growth, disruption of PGE2 signaling in CAFs induced epithelial-to-mesenchymal transition in cancer organoids and promoted metastasis in mice. Moreover, TAK1L expression in CAFs was associated with decreased CAF activation, reduced metastasis, and prolonged survival in human breast cancer. These data characterize a new pathway of regulating inflammatory CAF activation, which affects breast cancer progression.
    Significance: The inflammatory lipid prostaglandin E2 suppresses cancer-associated fibroblast expansion and activation to limit primary mammary tumor growth while promoting metastasis.
    MeSH term(s) Animals ; Breast Neoplasms/pathology ; Cancer-Associated Fibroblasts/metabolism ; Carcinoma/pathology ; Dinoprostone/metabolism ; Female ; Fibroblasts/metabolism ; Humans ; Mice ; Prostaglandin-E Synthases/genetics ; Prostaglandin-E Synthases/metabolism ; Prostaglandin-E Synthases/pharmacology
    Chemical Substances Prostaglandin-E Synthases (EC 5.3.99.3) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2022-01-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-21-2116
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