Fatty acid metabolism and cell proliferation. III. Effect of prostaglandin biosynthesis either from exogenous fatty acid or endogenous fatty acid release with hydralazine

Lipids ◽  
1983 ◽  
Vol 18 (5) ◽  
pp. 349-352 ◽  
Author(s):  
N. Morisaki ◽  
J. A. Lindsey ◽  
G. E. Milo ◽  
D. G. Cornwell
Keyword(s):  
Cell Proliferation ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Endogenous Fatty Acid ◽  
Exogenous Fatty Acid ◽  
Prostaglandin Biosynthesis ◽  
Fatty Acid Release ◽  
Acid Release

Fatty acid metabolism and cell proliferation: IV. Effect of prostanoid biosynthesis from endogenous fatty acid release with cyclosporin-A

Lipids ◽  
1983 ◽  
Vol 18 (8) ◽  
pp. 566-569 ◽  
Author(s):  
Jenifer A. Lindsey ◽  
Nobuhiro Morisaki ◽  
Judith M. Stitts ◽  
Richard A. Zager ◽  
David G. Cornwell
Keyword(s):  
Cell Proliferation ◽  
Fatty Acid ◽  
Cyclosporin A ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Endogenous Fatty Acid ◽  
Fatty Acid Release ◽  
Acid Release

scholarly journals PCB11 Metabolite, 3,3’-Dichlorobiphenyl-4-ol, Exposure Alters the Expression of Genes Governing Fatty Acid Metabolism in the Absence of Functional Sirtuin 3: Examining the Contribution of MnSOD

Antioxidants ◽  
2018 ◽  
Vol 7 (9) ◽  
pp. 121 ◽  
Author(s):  
Sinthia Alam ◽  
Gwendolyn Carter ◽  
Kimberly Krager ◽  
Xueshu Li ◽  
Hans-Joachim Lehmler ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Mitochondrial Respiration ◽  
Mammalian Cells ◽  
Acid Metabolism ◽  
Cellular Growth ◽  
Acid Oxidation ◽  
Sirtuin 3 ◽  
Endogenous Fatty Acid ◽  
Mnsod Activity

Although the production of polychlorinated biphenyls (PCBs) is prohibited, the inadvertent production of certain lower-chlorinated PCB congeners still threatens human health. We and others have identified 3,3’-dichlorobiphenyl (PCB11) and its metabolite, 3,3’-dichlorobiphenyl-4-ol (4OH-PCB11), in human blood, and there is a correlation between exposure to this metabolite and mitochondrial oxidative stress in mammalian cells. Here, we evaluated the downstream effects of 4OH-PCB11 on mitochondrial metabolism and function in the presence and absence of functional Sirtuin 3 (SIRT3), a mitochondrial fidelity protein that protects redox homeostasis. A 24 h exposure to 3 μM 4OH-PCB11 significantly decreased the cellular growth and mitochondrial membrane potential of SIRT3-knockout mouse embryonic fibroblasts (MEFs). Only wild-type cells demonstrated an increase in Manganese superoxide dismutase (MnSOD) activity in response to 4OH-PCB11–induced oxidative injury. This suggests the presence of a SIRT3-mediated post-translational modification to MnSOD, which was impaired in SIRT3-knockout MEFs, which counters the PCB insult. We found that 4OH-PCB11 increased mitochondrial respiration and endogenous fatty-acid oxidation-associated oxygen consumption in SIRT3-knockout MEFs; this appeared to occur because the cells exhausted their reserve respiratory capacity. To determine whether these changes in mitochondrial respiration were accompanied by similar changes in the regulation of fatty acid metabolism, we performed quantitative real-time polymerase chain reaction (qRT-PCR) after a 24 h treatment with 4OH-PCB11. In SIRT3-knockout MEFs, 4OH-PCB11 significantly increased the expression of ten genes controlling fatty acid biosynthesis, metabolism, and transport. When we overexpressed MnSOD in these cells, the expression of six of these genes returned to the baseline level, suggesting that the protective role of SIRT3 against 4OH-PCB11 is partially governed by MnSOD activity.

scholarly journals Global Gene Expression Profiling in PPAR-γAgonist-Treated Kidneys in an Orthologous Rat Model of Human Autosomal Recessive Polycystic Kidney Disease

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Daisuke Yoshihara ◽  
Masanori Kugita ◽  
Tamio Yamaguchi ◽  
Harold M. Aukema ◽  
Hiroki Kurahashi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Fatty Acid ◽  
Kidney Disease ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Interstitial Fibrosis ◽  
Global Gene Expression ◽  
Polycystic Kidney

Kidneys are enlarged by aberrant proliferation of tubule epithelial cells leading to the formation of numerous cysts, nephron loss, and interstitial fibrosis in polycystic kidney disease (PKD). Pioglitazone (PIO), a PPAR-γagonist, decreased cell proliferation, interstitial fibrosis, and inflammation, and ameliorated PKD progression in PCK rats (Am. J. Physiol.-Renal, 2011). To explore genetic mechanisms involved, changes in global gene expression were analyzed. By Gene Set Enrichment Analysis of 30655 genes, 13 of the top 20 downregulated gene ontology biological process gene sets and six of the top 20 curated gene set canonical pathways identified to be downregulated by PIOtreatment were related to cell cycle and proliferation, including EGF, PDGF and JNK pathways. Their relevant pathways were identified using the Kyoto Encyclopedia of Gene and Genomes database. Stearoyl-coenzyme A desaturase 1 is a key enzyme in fatty acid metabolism found in the top 5 genes downregulated by PIO treatment. Immunohistochemical analysis revealed that the gene product of this enzyme was highly expressed in PCK kidneys and decreased by PIO. These data show that PIO alters the expression of genes involved in cell cycle progression, cell proliferation, and fatty acid metabolism.

scholarly journals 4-1BB signaling activates glucose and fatty acid metabolism to enhance CD8+ T cell proliferation

2016 ◽  
Vol 14 (9) ◽  
pp. 748-757 ◽  
Author(s):  
Beom K Choi ◽  
Do Y Lee ◽  
Don G Lee ◽  
Young H Kim ◽  
Seon-Hee Kim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Fatty Acid ◽  
T Cell ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Cd8 T Cell ◽  
T Cell Proliferation

scholarly journals The Mutual Inhibition of FoxO1 and SREBP-1c Regulated the Progression of Hepatoblastoma by Regulating Fatty Acid Metabolism

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Yu Hu ◽  
Hongyan Zai ◽  
Wei Jiang ◽  
Zhenglin Ou ◽  
Yuanbing Yao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Tumor Tissue ◽  
Acid Metabolism ◽  
Migration And Invasion ◽  
Mouse Tumor ◽  
Liver Malignancy ◽  
Foxo1 Gene

Background. Hepatoblastoma (HB) is the most common liver malignancy in pediatrics, but the treatment for this disease is minimal. This study is aimed at exploring the effect of FoxO1 and SREBP-1c on HB and their mechanism. Methods. FoxO1, SREBP-1c, FASN, ACLY, ACC, and MAGL expressions in tissue samples were detected by RT-qPCR and WB. IHC was utilized to measure FASN content. Overexpression and knockdown of FoxO1 and sSREBP-1c were performed on Huh-6 cells. Cell proliferation, migration, and invasion were examined by CCK8, scratch, and transwell assay. ELISA was performed to test the ATP, FAO, NEFA, and Acetyl-CoA contents. ChIP was used to detect the interaction between SREBP-1c protein and the FoxO1 gene. In vivo tumorigenesis was conducted on mice. The morphology of tumor tissue sections was observed by HE staining. Results. FoxO1 expression was downregulated in HB tissue, while the expressions of SREBP-1c, FASN, ACLY, ACC, and MAGL were upregulated. In Huh-6 cells and mouse tumor tissues, FoxO1 knockdown resulted in increased cell proliferation, migration, and invasion and active fatty acid metabolism. On the contrary, after the knockdown of SREBP-1c, cell proliferation, migration, and invasion were weakened, and fatty acid metabolism was significantly reduced. SREBP-1c interacted with the promoter of the FoxO1 gene. When FoxO1 was knocked down, the tumor tissue was more closely packed. After the knockdown of the SREBP-1c gene, the structure of tumor cells was deformed. Conclusion. FoxO1 and SREBP-1c inhibited each other in HB, leading to the increase of intracellular fatty acid metabolism, and ultimately facilitated the development of HB.

Eicosapentaenoic and dihomo gamma linolenic acid metabolism by cultured rat mesangial cells

1989 ◽  
Vol 256 (1) ◽  
pp. C101-C108 ◽  
Author(s):  
L. A. Scharschmidt ◽  
N. B. Gibbons ◽  
R. Neuwirth
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Acid Metabolism ◽  
Mesangial Cells ◽  
Gamma Linolenic Acid ◽  
Significant Extent ◽  
Glomerular Function ◽  
Fatty Acid Release ◽  
Acid Release ◽  
Stimulation Of

To better understand the effects of dietary fatty acid manipulations on glomerular function, we compared mesangial incorporation, release, and metabolism of arachidonic (AA), eicosapentaenoic (EPA), and dihomo gamma linolenic (DHG) acids. We found marked differences in mesangial handling of these fatty acids. AA was incorporated into lipids of mesangial cells much more rapidly than EPA or DHG. Ionophore-induced stimulation of fatty acid release from mesangial cells prelabeled with [14C]AA, [14C]EPA, or [14C]DHG caused a release of labeled AA greater than DHG much less than EPA, respectively. Preloading mesangial cells with DHG or EPA for 24 h reduced subsequent basal, ionophore-, and hormone-stimulated prostaglandin E2 (PGE2) synthesis. Finally, unlike AA, neither EPA nor DHG was converted to a significant extent by mesangial cyclooxygenase or lipoxygenase. Thus the mesangial metabolism of DHG and EPA differs both quantitatively and qualitatively from that of AA. Furthermore, EPA and DHG inhibit metabolism of AA at the level of mesangial cyclooxygenase.

scholarly journals The Effect of MicroRNA-331-3p on Preadipocytes Proliferation and Differentiation and Fatty Acid Accumulation in Laiwu Pigs

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Tao Chen ◽  
Jingxiang Cui ◽  
Lixia Ma ◽  
Yongqing Zeng ◽  
Wei Chen
Keyword(s):  
Fatty Acids ◽  
Cell Proliferation ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Cellular Differentiation ◽  
Target Gene ◽  
Acid Metabolism ◽  
Fatty Acid Accumulation ◽  
Proliferation And Differentiation ◽  
Acid Accumulation

Objective. The proliferation and differentiation of preadipocytes are regulated by microRNAs (miRNAs), hormones, and other factors. This study aimed to investigate the effects of miR-331-3p on the proliferation and differentiation of preadipocytes in addition to fatty acid metabolism. Methods. Preadipocytes were transfected with miR-331-3p mimics, miR-NC, or miR-331-3p inhibitor to explore its effect on cell proliferation and fatty acid accumulation. Furthermore, preadipocytes were transfected with pre-miR-331-3p, pcDNA3.1(+), or miR-331-3p inhibitor to explore its effect on differentiation. Results. It was observed that miR-331-3p could inhibit preadipocytes proliferation. Furthermore, miR-331-3p was highly expressed during cellular differentiation and appeared to promote the process. In addition, dual fluorescein analysis showed that dihydrolipoamide S-succinyltransferase (DLST) is a target gene of miR-331-3p, and overexpression of miR-331-3p could regulate the metabolism of fatty acids in the citrate pyruvate cycle by targeting DLST expression. Conclusion. In summary, these findings indicated that miR-331-3p exerts contrasting effects on the processes of fat deposition.

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