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Results: 11 to 19 of 19

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Open-label pilot study of combination therapy with rosiglitazone and bexarotene in the treatment of cutaneous T-cell lymphoma.
Sepmeyer JA, Greer JP, Koyama T, Zic JA
(2007) J Am Acad Dermatol 56: 584-7
MeSH Terms: Aged, Anticarcinogenic Agents, Bexarotene, Biopsy, Needle, Dose-Response Relationship, Drug, Drug Administration Schedule, Drug Therapy, Combination, Female, Follow-Up Studies, Humans, Immunohistochemistry, Lymphoma, T-Cell, Cutaneous, Male, Maximum Tolerated Dose, Middle Aged, Neoplasm Staging, Pilot Projects, Risk Assessment, Rosiglitazone, Single-Blind Method, Survival Analysis, Tetrahydronaphthalenes, Thiazolidinediones, Treatment Outcome
Show Abstract · Added March 20, 2014
Four patients with stable or progressive cutaneous T-cell lymphoma treated with oral bexarotene received oral rosiglitazone. After 16 weeks of combination therapy, skin score decreased in two patients. Pruritus was alleviated in 3 of 4 patients, whereas quality of life was unchanged. Adverse events included hyperlipidemia, anemia, neutropenia, and lymphopenia.
0 Communities
1 Members
0 Resources
24 MeSH Terms
Rosiglitazone promotes development of a novel adipocyte population from bone marrow-derived circulating progenitor cells.
Crossno JT, Majka SM, Grazia T, Gill RG, Klemm DJ
(2006) J Clin Invest 116: 3220-8
MeSH Terms: Adipocytes, Adiponectin, Animals, Blotting, Western, Bone Marrow Cells, Bone Marrow Transplantation, CD11 Antigens, Carrier Proteins, Cell Differentiation, Collagenases, Dietary Fats, Female, Flow Cytometry, Green Fluorescent Proteins, Hypoglycemic Agents, Leptin, Leukocyte Common Antigens, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Phase-Contrast, PPAR gamma, Perilipin-1, Phosphoproteins, Reverse Transcriptase Polymerase Chain Reaction, Rosiglitazone, Stem Cells, Thiazolidinediones
Show Abstract · Added August 4, 2015
Obesity and weight gain are characterized by increased adipose tissue mass due to an increase in the size of individual adipocytes and the generation of new adipocytes. New adipocytes are believed to arise from resident adipose tissue preadipocytes and mesenchymal progenitor cells. However, it is possible that progenitor cells from other tissues, in particular BM, could also contribute to development of new adipocytes in adipose tissue. We tested this hypothesis by transplanting whole BM cells from GFP-expressing transgenic mice into wild-type C57BL/6 mice and subjecting them to a high-fat diet or treatment with the thiazolidinedione (TZD) rosiglitazone (ROSI) for several weeks. Histological examination of adipose tissue or FACS of adipocytes revealed the presence of GFP(+) multilocular (ML) adipocytes, whose number was significantly increased by ROSI treatment or high-fat feeding. These ML adipocytes expressed adiponectin, perilipin, fatty acid-binding protein (FABP), leptin, C/EBPalpha, and PPARgamma but not uncoupling protein-1 (UCP-1), the CD45 hematopoietic lineage marker, or the CDllb monocyte marker. They also exhibited increased mitochondrial content. Appearance of GFP(+) ML adipocytes was contemporaneous with an increase in circulating levels of mesenchymal and hematopoietic progenitor cells in ROSI-treated animals. We conclude that TZDs and high-fat feeding promote the trafficking of BM-derived circulating progenitor cells to adipose tissue and their differentiation into ML adipocytes.
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28 MeSH Terms
Altered PPARgamma expression and activation after transient focal ischemia in rats.
Victor NA, Wanderi EW, Gamboa J, Zhao X, Aronowski J, Deininger K, Lust WD, Landreth GE, Sundararajan S
(2006) Eur J Neurosci 24: 1653-63
MeSH Terms: Animals, Benzamides, Enzyme Activation, Gene Expression Regulation, Immunohistochemistry, Ischemic Attack, Transient, Male, PPAR gamma, Protein Binding, Pyridines, RNA, Messenger, Rats, Rats, Wistar, Reverse Transcriptase Polymerase Chain Reaction, Rosiglitazone, Thiazolidinediones, Time Factors
Show Abstract · Added May 26, 2016
Stroke is a devastating disease with limited treatment options. Recently, we found that the peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists troglitazone and pioglitazone reduce injury and inflammation in a rat model of transient cerebral ischemia. The mechanism of this protection is unclear, as these agents can act through PPAR-gamma activation or through PPAR-gamma-independent mechanisms. Therefore, we examined PPAR-gamma expression, DNA binding and transcriptional activity following stroke. In addition, we used a PPAR-gamma antagonist, T0070907, to determine the role of PPAR-gamma during ischemia. Using immunohistochemical techniques and real-time PCR, we found low levels of PPAR-gamma mRNA and PPAR-gamma immunoreactivity in nonischemic brain; however, PPAR-gamma expression dramatically increased in ischemic neurons, peaking 24 h following middle cerebral artery occlusion. Interestingly, we found that in both vehicle- and agonist-treated brains, DNA binding was reduced in the ischemic hemisphere relative to the contralateral hemisphere. Expression of a PPAR-gamma target gene, lipoprotein lipase, was also reduced in ischemic relative to nonischemic brain. Both DNA binding and lipoprotein lipase expression were increased by the addition of the PPAR-gamma agonist rosiglitazone. Finally, we found that rosiglitazone-mediated protection after stroke was reversed by the PPAR-gamma antagonist T0070907. Interestingly, infarction size was also increased by T0070907 in the absence of PPAR-gamma agonist, suggesting that endogenous PPAR-gamma ligands may mitigate the effects of cerebral ischemia.
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1 Members
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17 MeSH Terms
Collecting duct-specific deletion of peroxisome proliferator-activated receptor gamma blocks thiazolidinedione-induced fluid retention.
Zhang H, Zhang A, Kohan DE, Nelson RD, Gonzalez FJ, Yang T
(2005) Proc Natl Acad Sci U S A 102: 9406-11
MeSH Terms: Aldosterone, Animals, Biological Transport, Body Weight, Coloring Agents, Diabetes Mellitus, Type 2, Evans Blue, Gene Deletion, Genotype, Heterozygote, Hypoglycemic Agents, Immunohistochemistry, Integrases, Kidney, Kidney Tubules, Collecting, Mice, Mice, Knockout, Mice, Transgenic, Microscopy, Fluorescence, Microscopy, Phase-Contrast, Nephrons, PPAR gamma, Promoter Regions, Genetic, Radioimmunoassay, Rosiglitazone, Sodium, Thiazolidinediones
Show Abstract · Added September 9, 2013
The peroxisome proliferator-activated receptor subtype gamma (PPARgamma) ligands, namely the synthetic insulin-sensitizing thiazolidinedione (TZD) compounds, have demonstrated great potential in the treatment of type II diabetes. However, their clinical applicability is limited by a common and serious side effect of edema. To address the mechanism of TZD-induced edema, we generated mice with collecting duct (CD)-specific disruption of the PPARgamma gene. We found that mice with CD knockout of this receptor were resistant to the rosiglitazone- (RGZ) induced increases in body weight and plasma volume expansion found in control mice expressing PPARgamma in the CD. RGZ reduced urinary sodium excretion in control and not in conditional knockout mice. Furthermore, RGZ stimulated sodium transport in primary cultures of CD cells expressing PPARgamma and not in cells lacking this receptor. These findings demonstrate a PPARgamma-dependent pathway in regulation of sodium transport in the CD that underlies TZD-induced fluid retention.
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27 MeSH Terms
Hepatic glucocorticoid receptor antagonism is sufficient to reduce elevated hepatic glucose output and improve glucose control in animal models of type 2 diabetes.
Jacobson PB, von Geldern TW, Ohman L, Osterland M, Wang J, Zinker B, Wilcox D, Nguyen PT, Mika A, Fung S, Fey T, Goos-Nilsson A, Grynfarb M, Barkhem T, Marsh K, Beno DW, Nga-Nguyen B, Kym PR, Link JT, Tu N, Edgerton DS, Cherrington A, Efendic S, Lane BC, Opgenorth TJ
(2005) J Pharmacol Exp Ther 314: 191-200
MeSH Terms: 3T3 Cells, Adipocytes, Animals, Biotransformation, Blood Glucose, Cell Differentiation, Cholic Acids, Diabetes Mellitus, Type 2, Dogs, Drug Synergism, Estrone, Glucocorticoids, Glucose, Glutamate-Ammonia Ligase, Hypoglycemic Agents, Liver, Male, Mice, Obesity, Prednisolone, Rats, Rats, Zucker, Receptors, Glucocorticoid, Reverse Transcriptase Polymerase Chain Reaction, Rosiglitazone, Thiazolidinediones, Tyrosine Transaminase
Show Abstract · Added December 10, 2013
Glucocorticoids amplify endogenous glucose production in type 2 diabetes by increasing hepatic glucose output. Systemic glucocorticoid blockade lowers glucose levels in type 2 diabetes, but with several adverse consequences. It has been proposed, but never demonstrated, that a liver-selective glucocorticoid receptor antagonist (LSGRA) would be sufficient to reduce hepatic glucose output (HGO) and restore glucose control to type 2 diabetic patients with minimal systemic side effects. A-348441 [(3b,5b,7a,12a)-7,12-dihydroxy-3-{2-[{4-[(11b,17b)-17-hydroxy-3-oxo-17-prop-1-ynylestra-4,9-dien-11-yl] phenyl}(methyl)amino]ethoxy}cholan-24-oic acid] represents the first LSGRA with significant antidiabetic activity. A-348441 antagonizes glucocorticoid-up-regulated hepatic genes, normalizes postprandial glucose in diabetic mice, and demonstrates synergistic effects on blood glucose in these animals when coadministered with an insulin sensitizer. In insulin-resistant Zucker fa/fa rats and fasted conscious normal dogs, A-348441 reduces HGO with no acute effect on peripheral glucose uptake. A-348441 has no effect on the hypothalamic pituitary adrenal axis or on other measured glucocorticoid-induced extrahepatic responses. Overall, A-348441 demonstrates that an LSGRA is sufficient to reduce elevated HGO and normalize blood glucose and may provide a new therapeutic approach for the treatment of type 2 diabetes.
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2 Members
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27 MeSH Terms
Activation of peroxisome proliferator-activated receptor gamma suppresses nuclear factor kappa B-mediated apoptosis induced by Helicobacter pylori in gastric epithelial cells.
Gupta RA, Polk DB, Krishna U, Israel DA, Yan F, DuBois RN, Peek RM
(2001) J Biol Chem 276: 31059-66
MeSH Terms: Apoptosis, Cell Line, Cyclooxygenase 2, Gastric Mucosa, Helicobacter pylori, Humans, Isoenzymes, Membrane Proteins, NF-kappa B, Prostaglandin-Endoperoxide Synthases, Receptors, Cytoplasmic and Nuclear, Rosiglitazone, Species Specificity, Thiazoles, Thiazolidinediones, Transcription Factors
Show Abstract · Added March 5, 2014
Helicobacter pylori colonization leads to epithelial cell hyperproliferation within inflamed mucosa, but levels of apoptosis vary, suggesting that imbalances between rates of cell production and loss may contribute to differences in gastric cancer risk among infected populations. Peroxisome proliferator-activated receptor gamma (PPARgamma) regulates inflammatory and growth responses of intestinal epithelial cells. We determined whether activation of PPARgamma modified H. pylori-induced apoptosis in gastric epithelial cells. PPARgamma was expressed and functionally active in gastric epithelial cell lines sensitive to H. pylori-induced apoptosis. PPARgamma ligands 15d-PGJ(2) and BRL-49653 significantly attenuated H. pylomicronri-induced apoptosis, effects that could be reversed by co-treatment with a specific PPARgamma antagonist. Cyclopentanone prostaglandins that do not bind and activate PPARgamma had no effects on H. pylori-induced apoptosis. The ability of H. pylori to activate nuclear factor (NF)-kappaB and increase levels of the NF-kappaB target IL-8 was blocked by co-treatment with PPARgamma agonists, and direct inhibition of NF-kappaB also abolished H. pylori-stimulated apoptosis. These results suggest that activation of the PPARgamma pathway attenuates the ability of H. pylori to induce NF-kappaB-mediated apoptosis in gastric epithelial cells. Because PPARgamma regulates a multitude of host responses, activation of this receptor may contribute to varying levels of cellular turnover as well as the diverse pathologic outcomes associated with chronic H. pylori colonization.
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2 Members
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16 MeSH Terms
Oxidized alkyl phospholipids are specific, high affinity peroxisome proliferator-activated receptor gamma ligands and agonists.
Davies SS, Pontsler AV, Marathe GK, Harrison KA, Murphy RC, Hinshaw JC, Prestwich GD, Hilaire AS, Prescott SM, Zimmerman GA, McIntyre TM
(2001) J Biol Chem 276: 16015-23
MeSH Terms: Animals, Binding Sites, Binding, Competitive, CD36 Antigens, Cell Line, DNA-Binding Proteins, Genes, Reporter, Humans, In Vitro Techniques, Kinetics, Ligands, Lipoproteins, LDL, Monocytes, Oxidation-Reduction, Phosphatidylcholines, Receptors, Cytoplasmic and Nuclear, Recombinant Fusion Proteins, Rosiglitazone, Thiazoles, Thiazolidinediones, Transcription Factors, Transfection
Show Abstract · Added June 1, 2013
Synthetic high affinity peroxisome proliferator-activated receptor (PPAR) agonists are known, but biologic ligands are of low affinity. Oxidized low density lipoprotein (oxLDL) is inflammatory and signals through PPARs. We showed, by phospholipase A(1) digestion, that PPARgamma agonists in oxLDL arise from the small pool of alkyl phosphatidylcholines in LDL. We identified an abundant oxidatively fragmented alkyl phospholipid in oxLDL, hexadecyl azelaoyl phosphatidylcholine (azPC), as a high affinity ligand and agonist for PPARgamma. [(3)H]azPC bound recombinant PPARgamma with an affinity (K(d)((app)) approximately 40 nm) that was equivalent to rosiglitazone (BRL49653), and competition with rosiglitazone showed that binding occurred in the ligand-binding pocket. azPC induced PPRE reporter gene expression, as did rosiglitazone, with a half-maximal effect at 100 nm. Overexpression of PPARalpha or PPARgamma revealed that azPC was a specific PPARgamma agonist. The scavenger receptor CD36 is encoded by a PPRE-responsive gene, and azPC enhanced expression of CD36 in primary human monocytes. We found that anti-CD36 inhibited azPC uptake, and it inhibited PPRE reporter induction. Results with a small molecule phospholipid flippase mimetic suggest azPC acts intracellularly and that cellular azPC accumulation was efficient. Thus, certain alkyl phospholipid oxidation products in oxLDL are specific, high affinity extracellular ligands and agonists for PPARgamma that induce PPAR-responsive genes.
1 Communities
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22 MeSH Terms
15S-Hydroxyeicosatetraenoic acid activates peroxisome proliferator-activated receptor gamma and inhibits proliferation in PC3 prostate carcinoma cells.
Shappell SB, Gupta RA, Manning S, Whitehead R, Boeglin WE, Schneider C, Case T, Price J, Jack GS, Wheeler TM, Matusik RJ, Brash AR, Dubois RN
(2001) Cancer Res 61: 497-503
MeSH Terms: Agar, Arachidonate 15-Lipoxygenase, Blotting, Northern, Catalysis, Cell Division, Culture Media, Dose-Response Relationship, Drug, Gene Expression Regulation, Neoplastic, Humans, Hydroxyeicosatetraenoic Acids, Isoenzymes, Luciferases, Male, Prostatic Neoplasms, RNA, Messenger, Receptors, Cytoplasmic and Nuclear, Recombinant Fusion Proteins, Rosiglitazone, Thiazoles, Thiazolidinediones, Transcription Factors, Transcription, Genetic, Tumor Cells, Cultured
Show Abstract · Added December 10, 2013
15-Lipoxygenase (15-LOX)-2 is expressed in benign prostate secretory cells and benign prostate produces 15S-hydroxyeicosatetraenoic acid (15S-HETE) from exogenous arachidonic acid (AA). In contrast, 15S-LOX-2 and 15S-HETE formation are reduced in prostate carcinoma (Pca). The mechanisms whereby reduced 15-LOX-2 may contribute to Pca development or progression are not known. We investigated the expression of peroxisome proliferator-activated receptor (PPAR) gamma in benign and malignant prostate tissues and the ability of 15S-HETE to activate PPARgamma-dependent transcription and modulate proliferation of the Pca cell line PC3. In contrast to benign prostate and similar to most Pca tissues, 15-LOX-2 mRNA was not detected in PC3 cells, and they did not produce detectable 15-HETE from [14C]AA. By reverse transcription-PCR, PPARgamma mRNA was present in 18 of 18 benign and 9 of 9 tumor specimens. The PPARgamma ligand BRL 49653 and 15S-HETE caused a dose-dependent inhibition of PC3 proliferation in a 14-day soft agar colony-forming assay (IC50 of 3 and 30 microM, respectively). 15S-HETE (10 microM) caused greater inhibition than 10 microM 15R-HETE. At 3 days, BRL 49653 and 15S-HETE caused a slight increase in cells in G0-G1 and a corresponding decrease in cells in S phase. In PC3 cells transiently transfected with a luciferase reporter linked to a PPAR response element, 1 microM BRL 49653 and 10 microM 15S-HETE caused approximately threefold and greater than twofold induction of PPAR-dependent transcription, respectively. By quantitative real-time reverse transcription-PCR and Northern analysis, 3-day treatment with BRL 49653 and 15S-HETE caused a reduction of PPARgamma expression but a marked up-regulation of the PPAR response element containing adipocyte type fatty acid binding protein. These results support the hypothesis that 15-LOX-2-derived 15S-HETE may constitute an endogenous ligand for PPARgamma in the prostate and that loss of this pathway by reduced expression of 15-LOX-2 may contribute to increased proliferation and reduced differentiation in prostate carcinoma.
1 Communities
3 Members
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23 MeSH Terms
Isolated elevation of alkaline phosphatase level associated with rosiglitazone.
Hachey DM, O'Neil MP, Force RW
(2000) Ann Intern Med 133: 752
MeSH Terms: Alkaline Phosphatase, Chemical and Drug Induced Liver Injury, Female, Humans, Hypoglycemic Agents, Middle Aged, Risk Factors, Rosiglitazone, Thiazoles, Thiazolidinediones
Added March 20, 2014
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1 Members
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10 MeSH Terms