Peroxisome proliferator-activated receptor gamma is induced during differentiation of colon epithelium cells

Lefebvre, M. C.; Paulweber, Bernhard; Fajas, Lluís; Woods, John; McCrary, Christine; Colombel, J F; Najïb, Jamila; Fruchart, J.C.; Datz, Christian; Vidal, Hubert; Desreumaux, Pierre; Auwerx, Johan

doi:10.1677/joe.0.1620331

Cited by 149 publications

(113 citation statements)

References 34 publications

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“…4). These results are similar to previous data obtained in vitro (2,3) or in vivo in human and rodent (4,7,23). However, the addition of GLN in the medium lowered PPARγ protein content but had no effect at mRNAs, suggesting that GLN impact may involve the regulation of receptor translation since PPARγ protein achieved similar levels when cells were grown in medium containing GLN (Fig.…”

Section: Discussionsupporting

confidence: 91%

“…6). A cytoplasmic localisation of the receptor is associated with inactive PPARγ in several cancer samples (3,(46)(47)(48)(49). It is expected that GLN inhibits receptor translocation to the nucleus by increasing receptor phosphorylation which reduces PPARγ independent transactivation at the receptor A/B domain (50,51).…”

Section: Discussionmentioning

confidence: 99%

“…In the gastrointestinal tract, PPARγ expression increases concomitantly with cell differentiation either along the intestine crypt villi axis or in colon tubular glands (2)(3)(4). Drori et al demonstrated that PPARγ is implicated in cell lineage in association with coactivator Hic-5 (5).…”

Section: Introductionmentioning

confidence: 99%

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Expression of PPARγ is reduced by medium supplementation with L-glutamine in human colorectal Caco-2 cells

Fiatte¹,

Huin²,

Collet³

et al. 1998

Int J Mol Med

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Abstract. Peroxisome proliferator-activated receptor-γ (PPARγ) belongs to the nuclear hormone receptor family. This receptor is implicated in colon cell differentiation and in colon cancer. Receptor activation by specific agonists has been shown to protect against colon cancer progression. PPARγ protein content within cells is modulated by several mechanisms, including proteasome degradation, activation of Wnt signalling pathways and presence of fermentation products such as butyrate. Herein, we investigated the impact of L-glutamine on PPARγ expression during the differentiation of Caco-2 cells grown in medium containing dialyzed fetal calf serum supplemented or not with L-glutamine. Using RT-PCR and Western blotting, we demonstrated that PPARγ expression was decreased when L-glutamine was added to the medium. Using immunohistochemistry, we demonstrated that PPARγ immunostaining was mainly found in cytoplasm when cells were cultured with L-glutamine while it was found in nuclei and cytoplasm when cells were grown without the addition of L-glutamine. Supershift retardation assays demonstrated a decrease of PPARγ binding onto consensus peroxisome proliferator response element. We concluded that L-glutamine modulated PPARγ expression in Caco-2 cells.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Expression of PPARγ is reduced by medium supplementation with L-glutamine in human colorectal Caco-2 cells

Fiatte¹,

Huin²,

Collet³

et al. 1998

Int J Mol Med

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show abstract

“…13,14 PPAR␥ is a member of the superfamily of nuclear receptors and has important anti-inflammatory activity, 15,16 because it inhibits the activation of nuclear factor B (NF B) and the expression of the proinflammatory cytokines IL-1␤ and tumor necrosis factor-␣ (TNF-␣). [17][18][19] The colon expresses a high density of PPAR␥, 20,21 and much evidence points to the involvement of the PPAR␥ receptor in the regulation of intestinal inflammation. 20,22 Recently, Gertsch et al 23 demonstrated that the sesquiterpene (E)-␤-caryophyllene (BCP) selectively binds to CB2 and acts as a full agonist.…”

mentioning

confidence: 99%

β-Caryophyllene Inhibits Dextran Sulfate Sodium-Induced Colitis in Mice through CB2 Receptor Activation and PPARγ Pathway

Bento

Marcon

Dutra

et al. 2011

The American Journal of Pathology

208

145

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Cannabinoid receptor 2 (CB2) activation is suggested to trigger the peroxisome proliferator-activated receptor-␥ (PPAR␥) pathway, and agonists of both receptors improve colitis. Recently, the plant metabolite (E)-␤-caryophyllene (BCP) was shown to bind to and activate CB2. In this study, we examined the antiinflammatory effect of BCP in dextran sulfate sodium (DSS)-induced colitis and analyzed whether this effect was mediated by CB2 and PPAR␥. Oral treatment with BCP reduced disease activity, colonic macro-and microscopic damage, myeloperoxidase and N-acetylglucosaminidase activities, and levels and mRNA expression of colonic tumor necrosis factor-␣, IL-1␤, interferon-␥, and keratinocyte-derived chemokine. Inflammatory bowel diseases (IBDs) are a group of chronic diseases that affect the gastrointestinal tract and have been mainly subdivided as ulcerative colitis and Crohn's disease. 1 The IBDs are characterized by a strong leukocyte activation and infiltration into the intestinal tissues, the release of proinflammatory cytokines 2 and enzymes, and the formation of reactive oxygen species. All of these events can induce an extensive and unbalanced activation of the mucosal immune system, driven by the commensal flora. 3 Recent evidence suggests a role for the cannabinoid system in IBD regulation. Cannabinoid receptors 1 and 2 (CB1 and CB2) are expressed in normal human colon 4,5 and are up-regulated in IBD colonic tissue. In addition, an enhanced level of endocannabinoids was found in biopsy specimens from patients with ulcerative colitis. 5 It is thought that CB1 activation results in a decrease of intestinal hypermotility and hypersecretion, whereas the activation of CB2 results in the inhibition of proinflammatory mediators. In addition, both CB2 and CB1 knockout mice are more susceptible to the development of experimental colitis, and the activation of these receptors is extremely important for the abrogation of intestinal inflammation. 6 The role of CB2, however, is directly involved with innate immune system, because CB2 is primarily expressed in immune cells, such as macrophages, CD4 ϩ and CD8 ϩ T cells, monocytes, and polymorphonuclear neutro-

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“…3 In addition to adipose tissue, gastrointestinal epithelial cells express significant amounts of PPAR␥. [3][4][5] Other investigations, as well as our own, have shown that ligand activation of PPAR␥ leads to growth inhibition and induces the differentiation of colon cancer cells. 6 -8 It has been suggested that the inhibition of the DNA binding and transcriptional activity of the cell growth-promoting E2F/DP transcription factor represents 1 of the mechanisms by which PPAR␥ promotes adipogenesis.…”

mentioning

confidence: 77%

PPAR? agonists inhibit cell growth and suppress the expression of cyclin D1 and EGF-like growth factors in ras-transformed rat intestinal epithelial cells

et al. 2001

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Peroxisome proliferator-activated receptor gamma is induced during differentiation of colon epithelium cells

Cited by 149 publications

References 34 publications

Expression of PPARγ is reduced by medium supplementation with L-glutamine in human colorectal Caco-2 cells

Expression of PPARγ is reduced by medium supplementation with L-glutamine in human colorectal Caco-2 cells

β-Caryophyllene Inhibits Dextran Sulfate Sodium-Induced Colitis in Mice through CB2 Receptor Activation and PPARγ Pathway

PPAR? agonists inhibit cell growth and suppress the expression of cyclin D1 and EGF-like growth factors in ras-transformed rat intestinal epithelial cells

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