scholarly journals Large-Scale Screening of Natural Products Transactivating Peroxisome Proliferator-Activated Receptor α Identifies 9S-Hydroxy-10E,12Z,15Z-Octadecatrienoic Acid and Cymarin as Potential Compounds Capable of Increasing Apolipoprotein A-I Transcription in Hum

Lipids ◽  
2018 ◽  
Vol 53 (11-12) ◽  
pp. 1021-1030 ◽  
Author(s):  
Sophie E. van der Krieken ◽  
Herman E. Popeijus ◽  
Igor Bendik ◽  
Bettina Böhlendorf ◽  
Maurice C. J. M. Konings ◽  
...  
Keyword(s):  
Natural Products ◽  
Large Scale ◽  
Octadecatrienoic Acid ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Apolipoprotein A ◽  
Large Scale Screening

scholarly journals Pparg may Promote Chemosensitivity of Hypopharyngeal Squamous Cell Carcinoma

PPAR Research ◽  
2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Meng Lian ◽  
Jiaming Chen ◽  
Xixi Shen ◽  
Lizhen Hou ◽  
Jugao Fang
Keyword(s):  
Gene Expression ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Large Scale ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Regulatory Pathways ◽  
Hypopharyngeal Squamous Cell Carcinoma ◽  
Expression Levels

The upregulation of peroxisome proliferator-activated receptor gamma (PPARG) has been shown to increase the chemosensitivity of several human cancers. This study is aimed at studying if PPARG sensitizes hypopharyngeal squamous cell carcinoma (HSCC) in chemotherapeutic treatments and at dissecting possible mechanisms of observed effects. We integrated large-scale literature data and HSCC gene expression data to identify regulatory pathways that link PPARG and chemosensitivity in HSCC. Expression levels of molecules within the PPARG regulatory pathways were compared in 21 patients that underwent chemotherapy for primary HSCC, including 12 chemotherapy-sensitive patients (CSP) and 9 chemotherapy-nonsensitive patients (CNSP). In the CPS group, expression levels of PPARG were higher than that in the CNSP group (log‐fold‐change=0.50). Structured text mining identified two chemosensitivity-related regulatory pathways driven by PPARG. In the CSP group, expression levels for 7 chemosensitivity-promoting genes were increased, while for 13 chemosensitivity suppressing the gene expression levels were decreased. Our results support the chemosensitivity-promoting role of PPARG in HSCC tumor cells, most likely by affecting both cell proliferation and cell motility pathways.

scholarly journals Pemafibrate Prevents Retinal Pathological Neovascularization by Increasing FGF21 Level in a Murine Oxygen-Induced Retinopathy Model

2019 ◽  
Vol 20 (23) ◽  
pp. 5878 ◽  
Author(s):  
Yohei Tomita ◽  
Nobuhiro Ozawa ◽  
Yukihiro Miwa ◽  
Ayako Ishida ◽  
Masayuki Ohta ◽  
...  
Keyword(s):  
Growth Factor ◽  
Large Scale ◽  
Luciferase Assay ◽  
Fibroblast Growth Factor 21 ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fatty Acid Binding ◽  
Pathological Angiogenesis ◽  
Oxygen Induced Retinopathy

Large-scale clinical trials, such as the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) and the Action to Control Cardiovascular Risk in Diabetes (ACCORD) studies, have shown that the administration of fenofibrate, a peroxisome proliferator-activated receptor alpha (PPARα) agonist, suppresses the progression of diabetic retinopathy. In this paper, we reveal a therapeutic effect of a selective PPARα modulator (SPPARMα), pemafibrate, against pathological angiogenesis in murine models of retinopathy. Oxygen-induced retinopathy (OIR) was induced in C57BL/6J mice by exposure to 85% oxygen from postnatal day eight (P8) for 72 h. Vehicle, pemafibrate or fenofibrate was administrated by oral gavage from P12 to P16 daily. Administration of pemafibrate, but not fenofibrate, significantly reduced pathological angiogenesis in OIR. After oral pemafibrate administration, expression levels of downstream PPARα targets such as acyl-CoA oxidase 1 (Acox1), fatty acid binding protein 4 (Fabp4), and fibroblast growth factor 21 (Fgf21) were significantly increased in the liver but not in the retina. A significant increase in plasma FGF21 and reduced retinal hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor A (Vegfa) were also observed after this treatment. In an in vitro HIF-luciferase assay, a long-acting FGF21 analogue, but not pemafibrate, suppressed HIF activity. These data indicate that SPPARMα pemafibrate administration may prevent retinal pathological neovascularization by upregulating FGF21 in the liver.

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