0000000000289085

AUTHOR

M. Luz Martínez-chantar

showing 4 related works from this author

Identification of a gene-pathway associated with non-alcoholic steatohepatitis.

2007

Background/Aims We have integrated gene expression profiling of liver biopsies of NASH patients with liver samples of a mouse model of steatohepatitis (MAT1A-KO) to identify a gene-pathway associated with NASH. Methods Affymetrix U133 Plus 2.0 microarrays were used to evaluate nine patients with NASH, six patients with steatosis, and six control subjects; Affymetrix MOE430A microarrays were used to evaluate wild-type and MAT1A-KO mice at 15 days, 1, 3, 5 and 8 months after birth. Transcriptional profiles of patients with NASH and MAT1A-KO mice were compared with those of their proficient controls. Results We identified a gene-pathway associated with NASH, that accurately distinguishes betwe…

AdultMalePathologymedicine.medical_specialtySp1 Transcription FactorGene ExpressionHyperphosphorylationBiologyBioinformaticsdigestive systemSp1MiceGene-pathwayGene expressionmedicineAnimalsHumansPhosphorylationPromoter Regions GeneticGeneNon-alcoholic steatohepatitisMice KnockoutS-adenosylmethionineHepatologyMicroarray analysis techniquesGene Expression Profilingnutritional and metabolic diseasesMethionine AdenosyltransferaseMiddle AgedMicroarray Analysismedicine.diseasedigestive system diseasesFatty LiverGene expression profilingLiverFemaleSteatosisSteatohepatitisDNA microarray
researchProduct

The human liver fatty acid binding protein (FABP1) gene is activated by FOXA1 and PPARα; and repressed by C/EBPα: Implications in FABP1 down-regulati…

2013

Liver fatty acid binding protein (FABP1) prevents lipotoxicity of free fatty acids and regulates fatty acid trafficking and partition. Our objective is to investigate the transcription factors controlling the human FABP1 gene and their regulation in nonalcoholic fatty liver disease (NAFLD). Adenovirus-mediated expression of multiple transcription factors in HepG2 cells and cultured human hepatocytes demonstrated that FOXA1 and PPARα are among the most effective activators of human FABP1, whereas C/EBPα is a major dominant repressor. Moreover, FOXA1 and PPARα induced re-distribution of FABP1 protein and increased cytoplasmic expression. Reporter assays demonstrated that the major basal activ…

Hepatocyte Nuclear Factor 3-alphaMaleRepressorBiologyFatty Acid-Binding ProteinsFatty acid-binding proteinMiceTransactivationNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCCAAT-Enhancer-Binding Protein-alphamedicineAnimalsHumansPPAR alphaadipocyte protein 2Molecular BiologyTranscription factorCells Culturedchemistry.chemical_classificationFatty acidHep G2 CellsCell Biologymedicine.diseaseMolecular biologyFatty LiverMice Inbred C57BLLipotoxicitychemistrybiology.proteinProtein BindingBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
researchProduct

Fatty Liver and Fibrosis in Glycine N-Methyltransferase Knockout Mice Is Prevented by Nicotinamide

2010

Deletion of glycine N-methyltransferase (GNMT), the main gene involved in liver S-adenosylmethionine (SAM) catabolism, leads to the hepatic accumulation of this molecule and the development of fatty liver and fibrosis in mice. To demonstrate that the excess of hepatic SAM is the main agent contributing to liver disease in GNMT knockout (KO) mice, we treated 1.5-month-old GNMT-KO mice for 6 weeks with nicotinamide (NAM), a substrate of the enzyme NAM N-methyltransferase. NAM administration markedly reduced hepatic SAM content, prevented DNA hypermethylation, and normalized the expression of critical genes involved in fatty acid metabolism, oxidative stress, inflammation, cell proliferation, …

Liver CirrhosisNiacinamidemedicine.medical_specialtyPathologyS-AdenosylmethionineCirrhosisGene ExpressionGlycine N-MethyltransferaseBiologyArticleLiver diseasechemistry.chemical_compoundMiceFibrosisInternal medicinemedicineAnimalsRas signalingMice KnockoutDNA methylationHepatologyFatty acid metabolismFatty livermedicine.diseaseGlycine N-methyltransferaseFatty LiverEndocrinologyJAK/STAT signalingchemistryGNMThepatocytesHepatic fibrosisGene Deletion
researchProduct

Repression of the nuclear receptor small heterodimer partner by steatotic drugs and in advanced nonalcoholic fatty liver disease.

2015

The small heterodimer partner (SHP) (NR0B2) is an atypical nuclear receptor that lacks a DNA-binding domain. It interacts with and inhibits many transcription factors, affecting key metabolic processes, including bile acid, cholesterol, fatty acid, and drug metabolism. Our aim was to determine the influence of steatotic drugs and nonalcoholic fatty liver disease (NAFLD) on SHP expression and investigate the potential mechanisms. SHP was found to be repressed by steatotic drugs (valproate, doxycycline, tetracycline, and cyclosporin A) in cultured hepatic cells and the livers of different animal models of NAFLD: iatrogenic (tetracycline-treated rats), genetic (glycine N-methyltransferase-defi…

MaleTranscription GeneticThiazepinesResponse elementReceptors Cytoplasmic and NuclearBiologyMiceNon-alcoholic Fatty Liver DiseaseCyclosporin amedicineCCAAT-Enhancer-Binding Protein-alphaAnimalsHumansProtein kinase APromoter Regions GeneticTranscription factorCells CulturedPharmacologyMitogen-Activated Protein Kinase 1KinaseValproic AcidFatty liverTetracyclinemedicine.diseaseFatty LiverDoxycyclineCancer researchSmall heterodimer partnerCyclosporineMolecular MedicineSignal transductionSignal TransductionMolecular pharmacology
researchProduct