Prostaglandins & other lipid mediators最新文献

{"title":"Prostaglandin E2 is a crucial intermediator of 17β-estradiol-induced growth factor expression in bovine endometrial cells and explants","authors":"Wenhui Bao ,&nbsp;Shuangyi Zhang ,&nbsp;Jiamin Zhao ,&nbsp;Zhiguo Gong ,&nbsp;Yunjie Bai ,&nbsp;Yanqin Dong ,&nbsp;Wei Mao ,&nbsp;Bo Liu","doi":"10.1016/j.prostaglandins.2025.107041","DOIUrl":"10.1016/j.prostaglandins.2025.107041","url":null,"abstract":"<div><div>Estradiol is a critical hormone that regulates morphological and functional changes in the bovine endometrium throughout the estrous cycle. Prostaglandin E₂ (PGE₂), a well-established inflammatory mediator, also plays an essential role in endometrial physiology. Whether PGE₂ acts as an intermediary in estradiol-related activities within the bovine endometrium remains unclear. The results revealed that 17β-estradiol at 10⁻¹⁰ M and 10⁻⁹ M induced PGE₂ secretion in endometrial explants, whereas a higher concentration (10⁻⁷ M) downregulated PGE₂ secretion. In endometrial epithelial cells, 17β-estradiol at concentrations ranging from 10⁻¹⁰ to 10⁻⁸ M stimulated PGE₂ secretion. In endometrial stromal cells, 17β-estradiol at 10⁻¹⁰ to 10⁻⁷ M concentrations promoted PGE₂ production. PGE₂ synthesis was inhibited by the mPGES-1 inhibitor MF63 [2-(6-chloro-1H-phenanthro[9,10-<em>d</em>]imidazol-2-yl) isophthalonitrile] in the presence of 17β-estradiol (10⁻⁹ M), highlighting mPGES-1 as a key enzyme in 17β-estradiol-induced PGE₂ production in the bovine endometrium. Furthermore, both the mRNA and protein levels of endometrial growth factors, including fibroblast growth factor 2 (FGF-2), vascular endothelial growth factor A (VEGFA), matrix metalloproteinase-2 (MMP-2), and MMP-9, were increased by 17β-estradiol (10⁻⁹ M). This effect was reversed by pretreatment with the mPGES-1 inhibitor MF63 in endometrial cells and explants. Notably, supplementation with exogenous PGE₂ restored the expression of these growth factors in the presence of both 17β-estradiol (10⁻⁹ M) and MF63. In conclusion, mPGES-1-derived PGE₂ serves as a crucial mediator of the 17β-estradiol-induced expression of FGF-2, VEGFA, MMP-2, and MMP-9 in the bovine endometrium, underscoring its significant role in regulating endometrial function.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"181 ","pages":"Article 107041"},"PeriodicalIF":2.5,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145204482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Understanding the possible role of endocannabinoid system in obesity\" [Prostaglandins Other Lipid Mediat. 152 (2021) 106520]","authors":"Tapan Behl ,&nbsp;Swati Chadha ,&nbsp;Monika Sachdeva ,&nbsp;Aayush Sehgal ,&nbsp;Arun Kumar ,&nbsp;Dhruv ,&nbsp;Thangavel Venkatachalam ,&nbsp;Abdul Hafeez ,&nbsp;Lotfi Aleya ,&nbsp;Sandeep Arora ,&nbsp;Gaber El-Saber Batiha ,&nbsp;Priya Nijhawan ,&nbsp;Simona Bungau","doi":"10.1016/j.prostaglandins.2025.107027","DOIUrl":"10.1016/j.prostaglandins.2025.107027","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107027"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of lysophosphatidic acid in the regulation of immune cells and hematological malignancies","authors":"Vishal Kumar Gupta ,&nbsp;Kriti Gupta ,&nbsp;Pratishtha Sonker ,&nbsp;Manoj Mishra ,&nbsp;Ajay Kumar","doi":"10.1016/j.prostaglandins.2025.107028","DOIUrl":"10.1016/j.prostaglandins.2025.107028","url":null,"abstract":"<div><div>Lysophosphatidic acid (LPA), a small bioactive glycerophospholipid, has been reported to play an indispensable role in the regulation of a wide range of cellular processes, including cell proliferation, morphology, differentiation, invasion, migration, and apoptosis. Besides, it has a diverse role in the development, differentiation, migration, and trafficking of immune cells. The role of LPA in the functioning of immune cells, such as macrophages, natural killer cells, T cells, and B cells has been poorly understood and is still a major thrust area for immunological research. Further, accumulating experimental evidence indicates the pro-tumoral action of LPA in various cancers, including hematological malignancies. Hematological malignancies or blood cancers are a group of neoplastic conditions derived from the cells of hematopoietic tissues. LPA is reported to promote the development and progression of cancers of hematological origin through altering apoptosis, invasion and migration, metabolism, and anti-tumor immune response. But still, the mechanistic pathways by which LPA supports the development and progression of hematological malignancies are not well explored. The present review aims to provide an elaborate survey on the role of LPA in the functioning of immune cells and its implication in hematological malignancies.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107028"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144922990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “The association between vitamin D deficiency and childhood obesity and its impact on children’s serum calcium, alkaline phosphatase, and bone age” [Prostaglandins Other Lipid Mediat. 176 (2024) 106920]","authors":"Juanjuan Zhu ,&nbsp;Bingbing Wang ,&nbsp;Sanaz Asemani ,&nbsp;Shiwei Bao ,&nbsp;Niannian Tian","doi":"10.1016/j.prostaglandins.2025.107025","DOIUrl":"10.1016/j.prostaglandins.2025.107025","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107025"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of IRGM in acute lung injury: Inducing mitophagy and inactivating cGAS-STING signaling to improve lipopolysaccharide-induced alveolar epithelial barrier dysfunction","authors":"Yanqiong Shi,&nbsp;Yang Liang,&nbsp;Yang Chen,&nbsp;Zhenghuan Li","doi":"10.1016/j.prostaglandins.2025.107026","DOIUrl":"10.1016/j.prostaglandins.2025.107026","url":null,"abstract":"<div><div>Acute lung injury (ALI) is a common disorder of the respiratory system with high mortality. Inducing mitophagy is generally considered to be an effective target for alleviating ALI. We aimed to elucidate the role of immunity related GTPase M (IRGM) in ALI by using a lipopolysaccharide (LPS)-induced alveolar epithelial cell model. Firstly, IRGM expression in A549 cells under LPS conditions was evaluated. Then, IRGM was upregulated and oxidative stress was evaluated by measuring intracellular reactive oxygen species (ROS) using 2′, 7′-Dichlorofluorescin diacetate (DCFH-DA) staining. The permeability of A549 cells was determined by detecting transepithelial electrical resistance (TEER) value and fluorescein isothiocyanate-dextran 4 (FITC-FD4) fluorescence. Proteins related to epithelial barrier, mitophagy and mitochondrial function were assessed. Further Mdivi-1 (an inhibitor of mitophagy) addition or cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling overexpression was conducted to investigate the potential mechanism. Results suggested that IRGM was downregulated in LPS-treated A549 cells and IRGM upregulation alleviated LPS-induced oxidative stress, inflammation and barrier dysfunction in A549 cells. IRGM upregulation induced mitophagy and maintains mitochondrial function in LPS-treated A549 cells. Particularly, Mdivi-1 treatment or cGAS overexpression abrogated the impacts of IRGM upregulation on oxidative stress, inflammation and barrier dysfunction in LPS-treated A549 cells. Collectively, IRGM attenuates LPS-triggered alveolar epithelial cell damage by enhancing mitophagy to inactivate cGAS/STING signaling.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107026"},"PeriodicalIF":2.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the diverse signaling mechanisms of 17β-estradiol deficiency and replacement: Impacts on cognitive dysfunction in a post-menopausal experimental model","authors":"Mona A. El-Bana ,&nbsp;Jihan Hussein ,&nbsp;Sherien M. El-Daly ,&nbsp;Heba H. Metwaly ,&nbsp;Mahmoud A. Abdel-Monem ,&nbsp;Enayat A. Omara ,&nbsp;Dalia Medhat","doi":"10.1016/j.prostaglandins.2025.107024","DOIUrl":"10.1016/j.prostaglandins.2025.107024","url":null,"abstract":"<div><div>This study aimed to investigate brain signaling mechanisms affected by estradiol deficiency during menopause and how these pathways are modified with 17β-estradiol replacement to mitigate menopause-related changes, particularly in cognitive function and neuroinflammation, which are linked to the risk of dementia. Forty female white albino rats were divided into four groups: control, sham, ovariectomized (OVX), and OVX rats treated with 17β-estradiol. Cognitive tests using the Morris Water Maze assessed spatial learning and memory, while neurotransmitter levels were analyzed via HPLC. Serum levels of estrogen, Nerve Growth Factor (NGF), amyloid precursor protein(Aβ), and Postsynaptic Density Protein 95 (PSD-95) were measured using ELISA. Additionally, RT-PCR was used to evaluate the expression of gap junction protein connexin-43 (Cx43), Lipoprotein receptor-related protein (LRP1), and receptor for advanced glycation end products (RAGE), and aromatase expression was assessed via immunohistochemistry. Results showed that estrogen deficiency in OVX rats led to significant impairments in cognition, neurotransmitter signaling, and neurotrophic factors. Reduced NGF and altered PSD-95 levels indicated compromised neuronal health and synaptic plasticity. Increased aromatase expression reflected reduced local estrogen synthesis, potentially contributing to cognitive deficits. Upregulated RAGE and altered LRP1 expression suggested inflammatory and neurodegenerative processes, while decreased Cx43 expression and modified Aβ processing indicated impaired intercellular communication. Overall, the findings highlight the detrimental effects of estrogen deficiency on brain function and suggest that 17β-estradiol replacement may mitigate menopause-related cognitive decline and neuroinflammation.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107024"},"PeriodicalIF":2.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144660066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic profiling of bioactive components from Schizophyllum commune Fries in hypercholesterolemic Wistar-Kyoto rats using LC-QTOF-MS analysis","authors":"Rushitha Sadasevevam,&nbsp;Norhaniza Aminudin,&nbsp;Noorlidah Abdullah","doi":"10.1016/j.prostaglandins.2025.107011","DOIUrl":"10.1016/j.prostaglandins.2025.107011","url":null,"abstract":"<div><div>Atherosclerosis is an inflammatory condition that contributes to myocardial infarction, cardiac arrest and stroke. Current knowledge of mushroom metabolomics in the context of atherosclerosis remains inadequate. Hence, further investigation into the underlying pathways and characterization of metabolites is necessary to establish a significant network for early-stage diagnosis of atherosclerosis. Therefore, the standard phytopreparation of <em>Schizophyllum commune</em> (SPPSC) was administered in hypercholesterolemic-induced rats. Sera were evaluated for lipid profile parameters; hepatic marker enzymes and the metabolic profile characterization was determined via liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (LC-QTOF-MS). SPPSC suppressed the elevation of cholesterol, LDL, triglyceride and atherogenic coefficient levels while increased HDL concentration and restored the function of hepatic antioxidant enzymes. The predictive accuracies and partial least square discriminant analysis (PLS-DA) revealed clear separation in metabolic features between normal, untreated, olive oil and SPPSC treated groups. Pathway analysis of the most significant metabolites targeted towards anti-atherosclerotic and cardio-protective activities were tryptophan metabolism, sphingolipid metabolism, β-alanine metabolism, taurine and hypotaurine metabolism, glutathione metabolism, phenylalanine metabolism, primary bile acid biosynthesis, histidine metabolism, pantothenate and CoA biosynthesis and cysteine and methionine metabolism. Identified metabolites indicate that <em>S. commune</em> is novel in preventing atherosclerosis and enhancing endogenous antioxidant system, protecting the cardiovascular system, minimalizing inflammation and regulating endothelial dysfunction.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"179 ","pages":"Article 107011"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144596727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phagocytosis is differentially regulated by LPS in M1- and M2-like macrophages via PGE2 formation and EP4 signaling","authors":"Rebecca Kirchhoff,&nbsp;Michel André Chromik,&nbsp;Nils Helge Schebb","doi":"10.1016/j.prostaglandins.2025.106998","DOIUrl":"10.1016/j.prostaglandins.2025.106998","url":null,"abstract":"<div><div>Phagocytosis is a key process in human innate immune response. Human macrophages are important phagocytes engulfing and neutralizing pathogens and cell debris. In addition, they modulate the inflammatory process by releasing cytokines and lipid mediators. However, the link between oxylipins and phagocytosis in different macrophage phenotypes remains poorly understood. In order to better understand the link between phagocytosis and the arachidonic acid (ARA) cascade, we established a phagocytosis assay in primary human ‘inflammatory’ M1- and ‘anti-inflammatory’ M2-like macrophages from peripheral blood mononuclear cells (PBMC), representing extremes of macrophage phenotypes. The branches of the ARA cascade were investigated by quantitative targeted proteomics and metabolomics. M1-like macrophages show a higher abundance of cyclooxygenase (COX)-2 and its products particularly after LPS stimulus compared to M2-like macrophages. LPS increased phagocytosis in M2-like, but not in M1-like macrophages. We demonstrate that the COX product prostaglandin E2 (PGE₂) modulates the differential effects of LPS on phagocytosis: Via the EP4 receptor PGE₂ signaling suppresses phagocytosis in primary human macrophages. Thus, blockage of COX, e.g. by non-steroidal anti-inflammatory drugs (NSAID), leads to an increase of phagocytosis also in ‘inflammatory’ M1-like macrophages. This supports the well-described anti-inflammatory effects of these drugs and underscores the importance of the link between the COX branch of the ARA cascade and the regulation of phagocytosis in human macrophages.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106998"},"PeriodicalIF":2.5,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnoflorine alleviates nonalcoholic fatty liver disease by modulating lipid metabolism, mitophagy and inflammation","authors":"Liming Wang,&nbsp;Yan Yang,&nbsp;Haibing Sun,&nbsp;Mengxue Fei","doi":"10.1016/j.prostaglandins.2025.106997","DOIUrl":"10.1016/j.prostaglandins.2025.106997","url":null,"abstract":"<div><h3>Background</h3><div>Nonalcoholic fatty liver disease (NAFLD) is a prevalent liver condition associated with metabolic syndrome, often aggravated by inflammation and mitochondrial dysfunction. This study aims to explore the therapeutic potential of magnoflorine, an alkaloid with known anti-inflammatory properties, in ameliorating NAFLD by modulating mitochondrial autophagy and inhibiting the NLRP3 inflammasome.</div></div><div><h3>Methods</h3><div>Male C57BL/6 J mice were fed a high-fat diet (HFD) for 16 weeks to induce NAFLD. Magnoflorine (5 and 10 mg/kg) was administered by gavage daily for 16 weeks. Liver and serum samples were analyzed for lipid profiles, inflammation markers, and autophagy-related proteins, and liver histology was examined to assess changes.</div></div><div><h3>Results</h3><div>Magnoflorine treatment improved dyslipidemia in NAFLD mice, shown by decreased serum triglycerides, total cholesterol, and LDL-C, and increased HDL-C. Histological analysis showed reduced hepatic steatosis and inflammation, with less lipid droplet accumulation and hepatocyte ballooning. Western blot results indicated upregulation of Parkin and PINK1, and downregulation of NLRP3, ASC, and caspase-1, with lower serum IL-1β levels, reflecting reduced inflammation.</div></div><div><h3>Conclusions</h3><div>Magnoflorine offers a promising approach for mitigating NAFLD progression through modulating mitochondrial autophagy and inhibiting inflammation.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106997"},"PeriodicalIF":2.5,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances and challenges in lipid droplet isolation from animal tissues and cells","authors":"Yangli Pei,&nbsp;Siyu Wu,&nbsp;Zheng Feng","doi":"10.1016/j.prostaglandins.2025.106996","DOIUrl":"10.1016/j.prostaglandins.2025.106996","url":null,"abstract":"<div><div>Lipid droplets (LDs) are essential intracellular organelles involved in lipid storage and metabolism, playing critical roles in various cellular processes and diseases. Researchers require efficiently isolate and analyze LDs to understand lipid metabolism and related pathologies. This review summarizes recent advances in LD isolation methods, including traditional techniques such as centrifugation and density gradient centrifugation, as well as emerging technologies like automated and high-throughput approaches. We explore the applications of these methods in lipid metabolism research and discuss the challenges faced by current isolation techniques. Future directions, including automation, single-cell analysis, and integration with advanced analytical tools, are also highlighted to provide insights for the next generation of LD research.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106996"},"PeriodicalIF":2.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}