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  • 1
    Keywords: EXPRESSION ; IN-VIVO ; GENE ; transcription ; METABOLISM ; MICE ; NUCLEAR RECEPTORS ; LIVER RECEPTOR HOMOLOG-1 ; LRH-1 ; LIVER-RECEPTOR-HOMOLOG-1
    Abstract: Reverse cholesterol transport (RCT) is an antiatherogenic process in which excessive cholesterol from peripheral tissues is transported to the liver and finally excreted from the body via the bile. The nuclear receptor liver receptor homolog 1 (LRH-1) drives expression of genes regulating RCT, and its activity can be modified by different posttranslational modifications. Here, we show that atherosclerosis-prone mice carrying a mutation that abolishes SUMOylation of LRH-1 on K289R develop less aortic plaques than control littermates when exposed to a high-cholesterol diet. The mechanism underlying this atheroprotection involves an increase in RCT and its associated hepatic genes and is secondary to a compromised interaction of LRH-1 K289R with the corepressor prospero homeobox protein 1 (PROX1). Our study reveals that the SUMOylation status of a single nuclear receptor lysine residue can impact the development of a complex metabolic disease such as atherosclerosis.
    Type of Publication: Journal article published
    PubMed ID: 25176150
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  • 2
    ISSN: 1432-0428
    Keywords: Keywords Type II diabetes ; peroxisome proliferator-activated receptor γ ; human pancreas ; islets ; beta cell ; thiazolidinediones ; troglitazone ; rosiglitazone.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Thiazolidinediones are reported to improve pancreatic islet morphology and beta-cell function in rodents, supporting the hypothesis of a direct action of thiazolidinediones on endocrine islet cells. In this study we examined the expression of the peroxisome proliferator-activated receptor γ, a nuclear receptor that is activated by naturally occurring fatty acids and synthetic thiazolidinediones, in normal human endocrine pancreatic cells. Methods. Human islets were isolated from pancreata harvested in ten brain-dead lean non-diabetic adult donors. We analysed the gene and protein expression of the human peroxisome proliferator-activated receptor γ and evaluated the effects of peroxisome proliferator-activated receptor γ agonist on insulin secretion in human islet preparations. Results. The RT-PCR carried out on total RNA from four distinct human islet preparations demonstrated the presence of peroxisome proliferator-activated receptor γ mRNA. Western blot analysis showed the consistent expression of peroxisome proliferator-activated receptor γ protein. Peroxisome proliferator-activated receptor γ was shown to be present in all three endocrine cell types studied (alpha, beta and delta cells) by immunohistochemistry. Conclusion/interpretation. We found that peroxisome proliferator-activated receptor γ is highly expressed in human islet endocrine cells, both at the mRNA and protein levels. These results support the hypothesis of a direct influence of peroxisome proliferator-activated receptor γ agonist on human pancreatic endocrine cells. [Diabetologia (2000) 43: 1165–1169]
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0014-5793
    Keywords: Atherosclerosis ; Extinction ; Gene expression ; Lipoprotein lipase ; NF-1/CTF ; Transcription
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 2016-04-30
    Description: Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its impact on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response (UPRmt) and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the Mdx mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs (NSCs) and melanocyte SCs (McSCs), and increased mouse lifespan. Strategies that conserve cellular NAD+ may reprogram dysfunctional SCs and improve lifespan in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Hongbo -- Ryu, Dongryeol -- Wu, Yibo -- Gariani, Karim -- Wang, Xu -- Luan, Peiling -- D'Amico, Davide -- Ropelle, Eduardo R -- Lutolf, Matthias P -- Aebersold, Ruedi -- Schoonjans, Kristina -- Menzies, Keir J -- Auwerx, Johan -- New York, N.Y. -- Science. 2016 Apr 28. pii: aaf2693.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Integrative and Systems Physiology, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. ; Department of Biology, Institute of Molecular Systems Biology, Eidgenossische Technische Hochschule Zurich (ETHZ), Zurich 8093, Switzerland. ; Laboratory of Integrative and Systems Physiology, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. Laboratory of Molecular Biology of Exercise, School of Applied Science, University of Campinas, CEP 13484-350 Limeira, Sao Paulo, Brazil. ; Laboratory of Stem Cell Bioengineering, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. ; Department of Biology, Institute of Molecular Systems Biology, Eidgenossische Technische Hochschule Zurich (ETHZ), Zurich 8093, Switzerland. Faculty of Science, University of Zurich, Zurich, Switzerland. ; Metabolic Signaling, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. ; Laboratory of Integrative and Systems Physiology, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. Interdisciplinary School of Health Sciences, University of Ottawa Brain and Mind Research Institute, 451 Smyth Rd, K1H 8M5, Ottawa, Canada. kmenzies@uottawa.ca admin.auwerx@epfl.ch. ; Laboratory of Integrative and Systems Physiology, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland. kmenzies@uottawa.ca admin.auwerx@epfl.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27127236" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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