Peroxisome proliferator-activated receptor ?/? activation inhibits hypertrophy in neonatal rat cardiomyocytes

Planavila, Anna; Rodríguez-Calvo, Ricardo; Jové, Mireia; Michalik, Liliane; Wahli, Walter; Laguna, Juan C.; Vázquez‐Carrera, Manuel

doi:10.1016/j.cardiores.2004.11.011

Cited by 166 publications

(135 citation statements)

References 40 publications

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“…These observations are consistent with recent findings made in other human cancer cell lines (Hollingshead et al 2007a), as well as numerous reports linking PPARβ/δ with inducing terminal differentiation and/or inhibiting cell growth (Ali et al 2005;Aung et al 2006;Burdick et al 2007;Fukumoto et al 2005;Hollingshead et al 2007a;Kim et al 2004;Kim et al 2006;Kim et al 2005;Man et al 2007;Marin et al 2006;Martinasso et al 2006;Matthiessen et al 2005;Michalik et al 2001;Müller-Brüsselbach et al 2007;Nadra et al 2006;Ou et al 2007;Peters et al 2000;Planavila et al 2005;Schmuth et al 2004;Tan et al 2001;Teunissen et al 2007;Varnat et al 2006;Westergaard et al 2001). The relatively modest activation of PPARβ/δ in both UACC903 and MCF7 cells as shown by increased mRNA encoding ANGPTL4 shows that these cells are not highly responsive to PPARβ/δ ligands as compared to other cells such as keratinocytes.…”

Section: Discussionsupporting

confidence: 91%

“…There is also strong evidence that ligand activation of PPARβ/δ promotes terminal differentiation in intestinal epithelium, breast and colon cancer cell lines, trophoblasts and primary keratinocytes (Aung et al 2006;Burdick et al 2007;Kim et al 2006;Marin et al 2006;Nadra et al 2006;Schmuth et al 2004;Tan et al 2001;Varnat et al 2006;Westergaard et al 2001). Evidence from a large number of independent laboratories also shows that cell growth is inhibited by PPARβ/δ and its ligands in colonocytes, keratincytes, cardiomyocytes, fibroblasts, endothelial cells and a variety of cancer cell lines (Ali et al 2005;Aung et al 2006;Burdick et al 2007;Fukumoto et al 2005;Hollingshead et al 2007a;Kim et al 2004;Kim et al 2006;Kim et al 2005;Man et al 2007;Marin et al 2006;Martinasso et al 2006;Matthiessen et al 2005;Michalik et al 2001;Müller-Brüsselbach et al 2007;Nadra et al 2006;Ou et al 2007;Peters et al 2000;Planavila et al 2005;Schmuth et al 2004;Tan et al 2001;Teunissen et al 2007;Varnat et al 2006;Westergaard et al 2001). Given the potential of PPARβ/δ ligands as therapeutic agents, it is of great importance to determine the effect of ligand activation of PPARβ/δ on cell growth in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

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Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) ligands inhibit growth of UACC903 and MCF7 human cancer cell lines

et al. 2008

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The development of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) ligands for the treatment of diseases including metabolic syndrome, diabetes and obesity has been hampered due to contradictory findings on their potential safety. For example, while some reports show that ligand activation of PPARβ/δ promotes the induction of terminal differentiation and inhibition of cell growth, other reports suggest that PPARβ/δ ligands potentiate tumorigenesis by increasing cell proliferation. Some of the contradictory findings could be due in part to differences in the ligand examined, the presence or absence of serum in cell cultures, differences in cell lines, or differences in the method used to quantify cell growth. For these reasons, this study examined the effect of ligand activation of PPARβ/δ on cell growth of two human cancer cell lines, MCF7 (breast cancer) and UACC903 (melanoma) in the presence or absence of serum using two highly specific PPARβ/δ ligands, GW0742 or GW501516. Culturing cells in the presence of either GW0742 or GW501516 caused upregulation of the known PPARβ/δ target gene angiopoetin-like protein 4 (ANGPTL4). Inhibition of cell growth was observed in both cell lines cultured in the presence of either GW0742 or GW501516, and the presence or absence of serum had little influence on this inhibition. Results from the present studies demonstrate that ligand activation of PPARβ/δ inhibits the growth of both MCF7 and UACC903 cell lines and provide further evidence that PPARβ/δ ligands are not mitogenic in human cancer cell lines.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) ligands inhibit growth of UACC903 and MCF7 human cancer cell lines

et al. 2008

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“…This is consistent with evidence from other laboratories showing that PPARs can inhibit NF-B signaling by protein-protein interactions. [38][39][40][41] The current findings strongly suggest that PPAR␤/␦ can modulate NF-B signaling and by doing so, attenuate chemically induced liver toxicity. Because this was not examined in response to AOM or other chemicals, whether this occurs in response to all hepatotoxicants remains to be determined.…”

Section: Discussionsupporting

confidence: 51%

“…[9][10][11]21,24,35,41,[52][53][54][55][56][57][58][59][60][61][62] It is possible that PPAR␤/␦-dependent regulation of kinase signaling as found in skin cells, 24 is also critical in liver cells, and thus protects against enhanced cell proliferation. This putative PPAR␤/␦-dependent process could ultimately contribute to preventing liver cancer, as PPAR␤/␦-dependent regulation of cell proliferation is known to influence skin and colon cancer.…”

Section: Discussionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor-β/δ protects against chemically induced liver toxicity in mice

et al. 2008

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Potential functional roles for the peroxisome proliferator-activated receptor-␤/␦ (PPAR␤/␦) in skeletal muscle fatty acid catabolism and epithelial carcinogenesis have recently been described. Whereas PPAR␤/␦ is expressed in liver, its function in this tissue is less clear. To determine the role of PPAR␤/␦ in chemically induced liver toxicity, wild-type and PPAR␤/␦-null mice were treated with azoxymethane (AOM) and markers of liver toxicity examined. Bile duct hyperplasia, regenerative hyperplasia, and increased serum alanine aminotransferase (ALT) were found in AOM-treated PPAR␤/␦-null mice, and these effects were not observed in similarly treated wild-type mice. Exacerbated carbon tetrachloride (CCl 4 ) hepatoxicity was also observed in PPAR␤/␦-null as compared with wild-type mice. No differences in messenger RNAs (mRNAs) encoding cytochrome2E1 required for the metabolic activation of AOM and CCl 4 were observed between wild-type or PPAR␤/␦-null mice in response to CCl 4 . Significant differences in the expression of genes reflecting enhanced nuclear factor kappa B (NF-B) activity were noted in PPAR␤/␦-null mice. Conclusion:Results from these studies show that PPAR␤/␦ is protective against liver toxicity induced by AOM and CCl 4 , suggesting that this receptor is hepatoprotective against environmental chemicals that are metabolized in this tissue. (HEPATOLOGY 2008;47:225-235.)

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“…As cardiac transcription factors under control of hypoxia, it is therefore likely that PPARs are important in controlling postnatal cardiac metabolic remodeling, although explicit confirmation of this is awaited. Certainly pharmacological manipulation of PPARβ signaling alters neonatal cardiomyocyte metabolism and hypertrophy in vitro [31,32], and expression of PPARs α, β and  increase in the heart in the days after birth [33], albeit that the physiological stimulus underlying this is unknown.…”

Section: Ppar Signalingmentioning

confidence: 99%

Molecular Control of Cardiac Fetal/Neonatal Remodeling

Breckenridge

2014

JCDD

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Abstract:Immediately following birth, the mammalian heart switches from generating ATP via glycolysis to β-oxidation of lipid. Coincident with this metabolic remodeling, cardiomyocyte mitosis ceases and regenerative capacity is lost. Recently, our understanding of the molecular pathways linking physiological stimuli with gene expression and phenotype changes around birth has increased, although fundamental gaps remain. This review discusses recent work that sheds light on this important area of mammalian cardiovascular development.

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Peroxisome proliferator-activated receptor ?/? activation inhibits hypertrophy in neonatal rat cardiomyocytes

Abstract: These results suggest that PPARbeta/delta activation inhibits PE-induced cardiac hypertrophy and LPS-induced NF-kappaB activation.

Cited by 166 publications

References 40 publications

Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) ligands inhibit growth of UACC903 and MCF7 human cancer cell lines

Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) ligands inhibit growth of UACC903 and MCF7 human cancer cell lines

Peroxisome proliferator-activated receptor-β/δ protects against chemically induced liver toxicity in mice

Molecular Control of Cardiac Fetal/Neonatal Remodeling

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