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Dive into the research topics where Mario Bermúdez de León is active.

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Featured researches published by Mario Bermúdez de León.


Toxicological Sciences | 2010

Arsenic induces DNA damage in environmentally exposed Mexican children and adults. Influence of GSTO1 and AS3MT polymorphisms

Adriana Sampayo-Reyes; Alba Hernández; Naouale El-Yamani; Celsa López-Campos; Eduardo Mayet-Machado; Cuauhtémoc B. Rincón-Castañeda; María de Lourdes Limones-Aguilar; Jesús Ernesto López-Campos; Mario Bermúdez de León; Silvia González-Hernández; Diana Hinojosa-Garza; Ricardo Marcos

Inorganic arsenic (i-As) is an environmental carcinogen to which millions of people are chronically exposed mainly via drinking water. In this study, we used the comet assay to evaluate DNA damage in i-As-exposed inhabitants of the north of Mexico. The environmental monitoring and the exposure assessment were done by measuring both drinking water arsenic (As) content and total urinary As. In addition, the studied population was genetically characterized for four different glutathione S-transferase omega1 (GSTO1) polymorphisms (Ala140Asp, Glu155del, Glu208Lys, and Ala236Val) and the As (+3 oxidation state) methyltransferase (AS3MT) Met287Thr polymorphism to determine whether such variants influence As-related genotoxicity. As content in the drinking water of the population was found to range between 1 and 187 microg/l, with a mean concentration value of 16 microg/l. The total urinary As content of the exposed individuals was found to be correlated with the As content in drinking water, and subjects were classified as low (< 30 microg As/g creatinine), medium (31-60 microg As/g creatinine), and highly exposed (> 61 microg As/g creatinine). A positive association was found between the level of exposure and the genetic damage measured as percentage of DNA in tail (p < 0.001), and AS3MT Met287Thr was found to significantly influence the effect (p < 0.034) among children carrying the 287Thr variant allele. Altogether, our results evidenced that people living in As-contaminated areas are at risk and that AS3MT genetic variation may play an important role modulating such risk in northern Mexico, especially among children.


Journal of Neuroscience Research | 2008

Myotonic dystrophy 1 in the nervous system: From the clinic to molecular mechanisms

Mario Bermúdez de León; Bulmaro Cisneros

Myotonic dystrophy type 1 (DM1) is a dominant neuromuscular disorder caused by the expansion of trinucleotide CTG repeats in the 3′‐untranslated region (3′‐UTR) of the DMPK gene. Prominent features of classical DM1 are muscle wasting and myotonia, whereas mental retardation is distinctive for congenital DM1. The main nervous system symptoms of DM1 are cognitive impairment, neuroendocrine dysfunction, and personality and behavior abnormalities. It is thought that expansion of CTG repeats causes DM1 pathology through different molecular mechanisms; however, a growing body of evidence indicates that an RNA gain‐of‐function mechanism plays a major role in the disease development. At the skeletal muscle level, three main molecular events can be distinguished in this model: 1) formation of nuclear foci that are composed at least of mutant DMPK mRNA and recruited RNA‐binding proteins, such as splicing regulators and transcription factors; 2) disturbance of alternative splicing of specific genes; and 3) impairment of cell differentiation. Contrasting with the substantial advances in understanding DM1 muscle pathology, the molecular basis of DM1 in the nervous system has just started to be revealed. This review focuses in the DM1 nervous system pathology and provides an overview of the genetic and molecular studies analyzing the effects of the DMPK gene CUG expanded repeats on cell function in neuronal systems. A comparison between the molecular mechanisms of DM1 in the skeletal muscle and those identified in DM1 nervous system models is provided. Finally, future directions in the study of DM1 in the nervous system are discussed.


Brazilian Journal of Microbiology | 2013

Measuring of Mycobacterium tuberculosis growth: a correlation of the optical measurements with colony forming units

Katia Peñuelas-Urquides; Licet Villarreal-Treviño; Beatriz Silva-Ramírez; Liliana Rivadeneyra-Espinoza; Salvador Said-Fernández; Mario Bermúdez de León

The quantification of colony forming units (cfu), turbidity, and optical density at 600 nm (OD600) measurements were used to evaluate Mycobacterium tuberculosis growth. Turbidity and OD600 measurements displayed similar growth curves, while cfu quantification showed a continuous growth curve. We determined the cfu equivalents to McFarland and OD600 units.


Neuroreport | 2005

Dystrophin Dp71 in PC12 cell adhesion

Jose Arturo Enríquez-Aragón; Joel Cerna-Cortés; Mario Bermúdez de León; Francisco García-Sierra; Everardo González; Dominique Mornet; Bulmaro Cisneros

Previously, we reported that PC12 cells with decreased Dp71 expression (antisense-Dp71 cells) display deficient nerve-growth-factor-induced neurite outgrowth. In this study, we show that disturbed neurite outgrowth of antisense-Dp71 cells is accompanied by decreased adhesion activity on laminin, collagen and fibronectin. In wild-type cells, the immunostaining of Dp71 and &bgr;1-integrin overlaps in the basal area contacting the substrate, but staining of both proteins decrease in the antisense-Dp71 cells. Morphology of antisense-Dp71 cells at the electron microscopic level is characterized by the lack of filopodia, cellular projections involved in adhesion. Our findings suggest that Dp71 is required for the efficient PC12 cell attachment to &bgr;1-integrin-dependent substrata and that decreased adhesion activity of the antisense-Dp71 cells could determine their deficiency to extend neurites.


Drug Metabolism and Disposition | 2006

Pregnane X Receptor-Dependent Induction of the CYP3A4 Gene by o,p′-1,1,1,-Trichloro-2,2-Bis (p-Chlorophenyl)ethane

Irma Martha Medina-Díaz; Georgina Arteaga-Illán; Mario Bermúdez de León; Bulmaro Cisneros; Adolfo Sierra-Santoyo; Libia Vega; Frank J. Gonzalez; Guillermo Elizondo

CYP3A4, the predominant cytochrome P450 (P450) expressed in human liver and intestine, contributes to the metabolism of approximately half the drugs in clinical use today. CYP3A4 catalyzes the 6β-hydroxylation of a number of steroid hormones and is involved in the bioactivation of environmental procarcinogens. The expression of CYP3A4 is affected by several stimuli, including environmental factors such as insecticides and pesticides. The o,p′-1,1,1,-trichloro-2,2-bis (p-chlorophenyl)ethane (DDT) isomer of DDT comprises approximately 20% of technical grade DDT, which is an organochloride pesticide. We have recently shown that o,p′-DDT exposure increases CYP3A4 mRNA levels in HepG2 cells. To determine the mechanism by which o,p′-DDT induces CYP3A4 expression, transactivation and electrophoretic mobility shift assays were carried out, revealing that o,p′-DDT activates the CYP3A4 gene promoter through the pregnane X receptor (PXR). CYP3A4 gene promoter activation resulted in both an increase in CYP3A4 mRNA levels and an increase in the total CYP3A4 activity in HepG2 cells. We also observed induction of CYP3A4 and mouse Cyp3a11 mRNA in the intestine of CYP3A4-transgenic mice after exposure to 1 mg/kg o,p′-DDT. At higher doses, a decrease of CYP3A4 inducibility was observed together with an increase in levels of interleukin 6 mRNA, a proinflammatory cytokine that strongly represses CYP3A4 transcription. The present study indicates that regulation of other genes under PXR control may be altered by o,p′-DDT exposure.


Journal of Cellular Biochemistry | 2010

Characterization of an Importin α/β-recognized nuclear localization signal in β-dystroglycan†

Bárbara Lara-Chacón; Mario Bermúdez de León; Daniel Leocadio; Pablo Gómez; Lizeth Fuentes-Mera; Ivette Martínez-Vieyra; Arturo Ortega; David A. Jans; Bulmaro Cisneros

β‐dystroglycan (β‐DG) is a widely expressed transmembrane protein that plays important roles in connecting the extracellular matrix to the cytoskeleton, and thereby contributing to plasma membrane integrity and signal transduction. We previously observed nuclear localization of β‐DG in cultured cell lines, implying the existence of a nuclear targeting mechanism that directs it to the nucleus instead of the plasma membrane. In this study, we delineate the nuclear import pathway of β‐DG, characterizing a functional nuclear localization signal (NLS) in the β‐DG cytoplasmic domain, within amino acids 776–782. The NLS either alone or in the context of the whole β‐DG protein was able to target the heterologous GFP protein to the nucleus, with site‐directed mutagenesis indicating that amino acids R779 and K780 are critical for NLS functionality. The nuclear transport molecules Importin (Imp)α and Impβ bound with high affinity to the NLS of β‐DG and were found to be essential for NLS‐dependent nuclear import in an in vitro reconstituted nuclear transport assay; cotransfection experiments confirmed the dependence on Ran for nuclear accumulation. Intriguingly, experiments suggested that tyrosine phosphorylation of β‐DG may result in cytoplasmic retention, with Y892 playing a key role. β‐DG thus follows a conventional Impα/β‐dependent nuclear import pathway, with important implications for its potential function in the nucleus. J. Cell. Biochem. 110: 706–717, 2010.


Journal of Neurochemistry | 2010

Induction of dystrophin Dp71 expression during neuronal differentiation: opposite roles of Sp1 and AP2α in Dp71 promoter activity

Sara Luz Morales‐Lázaro; Ricardo González-Ramírez; Pablo Gómez; Victor Tapia-Ramírez; Mario Bermúdez de León; Bulmaro Cisneros

In this study, we delineated the molecular mechanisms that modulate Dp71 expression during neuronal differentiation, using the N1E‐115 cell line. We demonstrated that Dp71 expression is up‐regulated in response to cAMP‐mediated neuronal differentiation of these cells, and that this induction is controlled at promoter level. Functional deletion analysis of the Dp71 promoter revealed that a 5′‐flanking 159‐bp DNA fragment that contains Sp1 and AP2 binding sites is necessary and sufficient for basal expression of this TATA‐less promoter, as well as for its induction during neuronal differentiation. Electrophoretic mobility shift and chromatin immunoprecipitation assays revealed that Sp1 and AP2α bind to their respective DNA elements within the Dp71 basal promoter. Overall, mutagenesis assays on the Sp1 and AP2 binding sites, over‐expression of Sp1 and AP2α, as well as knock‐down experiments on Sp1 and AP2α gene expression established that Dp71 basal expression is controlled by the combined action of Sp1 and AP2α, which act as activator and repressor, respectively. Furthermore, we demonstrated that induction of Dp71 expression in differentiated cells is the result of the maintenance of positive regulation exerted by Sp1, as well as of the loss of AP2α binding, which ultimately releases the promoter from repression.


Molecular Biology Reports | 2012

Myotonic dystrophy type 1-associated CTG repeats disturb the expression and subcellular distribution of microtubule-associated proteins MAP1A, MAP2, and MAP6/STOP in PC12 cells

Prisiliana Velázquez-Bernardino; Francisco García-Sierra; Oscar Hernández-Hernández; Mario Bermúdez de León; Geneviève Gourdon; Mário Gomes-Pereira; Bulmaro Cisneros

To study the effect of DM1-associated CTG repeats on neuronal function, we developed a PC12 cell-based model that constitutively expresses the DMPK gene 3′-untranslated region with 90 CTG repeats (CTG90 cells). As CTG90 cells exhibit impaired neurite outgrowth and as microtubule-associated proteins (MAPs) are crucial for microtubule stability, we analyzed whether MAPs are a target of CTG repeats. NGF induces mRNA expression of Map2, Map1a and Map6 in control cells (PC12 cells transfected with the empty vector), but this induction is abolished for Map2 and Map1a in CTG90 cells. MAP2 and MAP6/STOP proteins decrease in NGF-treated CTG90 cells, whereas MAP1A increases. Data suggest that CTG repeats might alter somehow the expression of MAPs, which appears to be related with CTG90 cell-deficient neurite outgrowth. Decreased MAP2 levels found in the hippocampus of a DM1 mouse model indicates that targeting of MAPs expression by CTG repeats might be relevant to DM1.


Journal of Virological Methods | 2013

In vitro transcribed RNA molecules for the diagnosis of pandemic 2009 influenza A(H1N1) virus by real-time RT-PCR.

Mario Bermúdez de León; Katia Peñuelas-Urquides; Miguel E. Aguado-Barrera; María José Currás-Tuala; Brenda Leticia Escobedo-Guajardo; Rosa Nelly González-Ríos; Viviana Mata-Tijerina; Ofelia Vázquez-Monsiváis

The 2009 influenza A(H1N1) outbreak allowed the implementation of new epidemiologic surveillance tools in several countries around the world. A new molecular protocol with appropriate sensitivity and specificity using real-time RT-PCR was developed by the Centers for Disease Control and Prevention (CDC) to identify the pandemic 2009 influenza A (H1N1) virus in human specimens. In the CDC protocol, positive controls are available only upon request and they are taken from cell cultures infected with 2009 influenza A(H1N1) virus, representing a handling risk for laboratory technicians. The poor availability of positive control materials in diagnostic laboratories may limit the public health response. The aim of the work presented in this paper was to develop positive controls for the diagnostic testing of influenza A(H1N1) virus that could be used in the CDC real-time RT-PCR protocol. A series of plasmid constructs bearing partial sequences of the viral genes were created and each construct was used as a template for in vitro transcription. RNA molecules were obtained successfully at high yield, i.e., 2×10(7) assays per microliter. Thus, the inclusion of these molecules in the influenza panel as positive controls is proposed. The in vitro transcribed RNA could also be used as quality standards in the design of international proficiency studies.


The Indian journal of tuberculosis | 2018

Association between vitamin D receptor gene polymorphisms and pulmonary tuberculosis in a Mexican population

Beatriz Silva-Ramírez; Cyntia A. Saenz-Saenz; Leonardo A. Bracho-Vela; Katia Peñuelas-Urquides; Viviana Mata-Tijerina; Brenda Leticia Escobedo-Guajardo; Nelly R. González-Ríos; Ofelia Vázquez-Monsiváis; Mario Bermúdez de León

BACKGROUND AND AIMS The impact of host genetic variation in susceptibility of tuberculosis is well documented. The vitamin D receptor gene (VDR) is a transacting transcription factor which mediates innate immune response by enhancing the expression of several antimicrobial peptides, including cathelicidin. An association between VDR polymorphisms with tuberculosis (TB) has been investigated in different ethnic groups; however there are contradictions and inconsistencies in the results. The aim of this study was to evaluate the association between polymorphisms of functional VDR with the susceptibility to pulmonary tuberculosis in a Mexican population. METHODS A case-control study was performed in, 257 patients with pulmonary tuberculosis and 457 healthy controls recruited from: family medicine clinics of the Mexican Social Security Institute. The VDR gene polymorphisms Fok I (rs 2228570), BsmI (rs1544410), ApaI (rs7975232) and TaqI (rs731236) were genotyped by TaqMan assays. Statistical analysis was performed using: Epi Info V-7 and SNP Stats software. RESULTS No statistically significant associations were observed in genotype and haplotype distribution between BsmI, ApaI and TaqI polymorphisms and disease susceptibility. The CC genotype for the VDR gene FokI was significantly more frequent in patients than in controls (29.6% versus 17.5%, OR=1.97; 95% CI=1.37-2.8, PC=0.0004). Moreover, TT genotype was decreased in patients as compared to the control group (24.1% versus 34.8%, OR=0.59; 95% CI=0.42-0.84, PC=0.004). CONCLUSION To our best knowledge, this is the first case-control study that finds an association between CC genotype of FokI SNP in the VDR gene with pulmonary tuberculosis in Mexican patients. However more validation studies should be performed to prove our conclusions.

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Katia Peñuelas-Urquides

Mexican Social Security Institute

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Beatriz Silva-Ramírez

Mexican Social Security Institute

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Adriana Sampayo-Reyes

Mexican Social Security Institute

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Fabiola Castorena-Torres

Instituto Politécnico Nacional

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Francisco García-Sierra

Instituto Politécnico Nacional

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Laura González-Escalante

Mexican Social Security Institute

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Alba Hernández

Autonomous University of Barcelona

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