Estrada Mena, Francisco Javier
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Estrada Mena, Francisco Javier
Official Name
Estrada Mena, Francisco Javier
Alternative Name
festrada
Main Affiliation
ORCID
Scopus Author ID
57192982524
Researcher ID
AAI-2437-2020

Research Output
Now showing 1 - 10 of 31
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Influence of GST polymorphisms in the age of onset of cataract: Systematic review and meta-analysis

2020 , Antonio-Aguirre, Bani , Palacio Pastrana, Claudia , Mendoza Velásquez, Cristina , Camacho-Ordóñez, Azyadeh , Zepeda-Palacio, Claudia , Estrada Mena, Francisco Javier , Pérez Ortiz, Andric Christopher

Purpose : Cataracts are a clinically heterogeneous disorder affecting up to 12% of the population aged 40 years and older. Multiple environmental and genetic factors influence disease susceptibility. Glutathione S-transferase (GST) genes deletion might be involved in cataractogenesis, through impaired conjugation of reduced glutathione. Excessive ROS could promote earlier lens opacification. To date, no systematic studies have assessed the effect of GST polymorphisms and age of onset of cataracts. Here, we aim to evaluate the association between GST polymorphisms, found through a systematic review, on cataracts age of presentation by meta-analysis. Methods : We conducted a systematic search in MEDLINE, HuGENET, and LILACS databases. We included observational studies that determined genotype based on validated genotyping instruments and with a stringent quality check (e.g., genotyping call rate ≥ 95%, HWE in controls). We abstracted counts of null alleles of GSTM1 and GSTT1 in cases and controls. We performed a meta-analysis of these measurements using random and fixed effects models, subgrouping by age of diagnosis. ©Investigative Ophthalmology & Visual Science

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Dysregulation of mitochondrial function and biogenesis modulators in adipose tissue of obese children

2017 , Zamora-Mendoza, R. , Rosas-Vargas, H. , Ramos-Cervantes, M. T. , García-Zúñiga, P. , Pérez-Lorenzana, H. , Mendoza-Lorenzo, Patricia , Pérez Ortiz, Andric Christopher , Miliar-García, A. , Lara-Padilla, E. , Estrada Mena, Francisco Javier , Ceballos, Guillermo , Rodríguez, Alonso , Villarreal, Francisco J. , Ramírez-Sánchez, Israel

Background/Objectives: We aimed to evaluate mitochondrial biogenesis (MB), structure, metabolism and dysfunction in abdominal adipose tissue from male pediatric patients with obesity. Subjects/Methods: Samples were collected from five children with obesity (percentile ⩾95) and five eutrophic boys (percentile ⩾5/⩽85) (8–12 years old) following parental informed consent. We analyzed the expression of key genes involved in MB (sirtuin-1 (SIRT1), peroxisome proliferator-activated receptor-γ (PPARγ), PPARγ coactivator-1α (PGC1α), nuclear respiratory factors 1 and 2 (NRF1, NRF2) and mitochondrial transcription factor A (TFAM) and surrogates for mitochondrial function/structure/metabolism (porin, TOMM20, complex I and V, UCP1, UCP2, SIRT3, SOD2) by western blot. Citrate synthase (CS), complex I (CI) activity, adenosine triphosphate (ATP) levels, mitochondrial DNA (mtDNA) content and oxidative stress end points were also determined.

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Molecular demonstration of SLC4A1 gene deletion in two Mexican patients with Southeast Asian ovalocytosis

2005-06 , Ramos Kuri, Manuel , Carrillo Farga, Joaquín , Zúñiga, Joaquín , Amador Guerrero, María Teresa , Granados, Julio , Estrada Mena, Francisco Javier

We describe the finding of two Mexican patients with a specific 27-bp deletion in the solute carrier family 4 gene (SLC4A1delta27) (also known as the band 3 gene found on chromosome 17q21-q22), characteristic of Southeast Asian ovalocytosis (SAO). The patients were asymptomatic, and the initial diagnosis was made by microscopic observation of the presence of typical stomatocytic ovalocytes. The gene deletion was confirmed by PCR and DNA sequencing. Both patients were heterozygous for the deletion. One patient is from Tabasco state, in southeastern Mexico, a malaria-endemic zone. The other patient is from Mexico City, which is not a malaria-endemic area. Their families have no non-Mexican ancestors and their previous generations were born in Mexico. Both patients carry the HLA-B*3501 subtype, characteristic of Amerindians and Asian populations. Familial and HLA data led us to conclude that these two patients are the first report of SLC4A1delta27 in Amerindians. The nucleotide analysis showing a perfect match sequence between Southeast Asian and Mexican patients suggests, but does not prove, that the Mexican gene is not a de novo mutation. Instead, this gene might be the result of migration of individuals with Asian ancestry into the Mexican gene pool. We are looking for other families with the mutation to detect, by HLA analysis, the ancient ethnic origin of these patients. ©Human Biology

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Pharmacogenetics of response to neoadjuvant paclitaxel treatment for locally advanced breast cancer

2017 , Pérez Ortiz, Andric Christopher , Ramírez, Israel , Cruz-López, Juan C. , Villarreal-Garza, Cynthia , Luna-Angulo, Alexandra , Lira, Esmeralda , Díaz-Chávez, José , Jiménez-Chaidez, Salvador , Matus-Santos, Juan A. , Sánchez-Chapul, Laura , Mendoza-Lorenzo, Patricia , Estrada Mena, Francisco Javier

Locally advanced breast cancer (LABC) cases have a varying five-year survival rate, mainly influenced by the tumor response to chemotherapy. Paclitaxel activity (response rate) varies across populations from 21.5% to 84%. There are some reports on genetic traits and paclitaxel; however, there is still considerable residual unexplained variability. In this study, we aimed to test the association between eleven novel markers and tumor response to paclitaxel and to explore if any of them influenced tumor protein expression. We studied a cohort of 140 women with LABC. At baseline, we collected a blood sample (for genotyping), fine needle aspirates (for Western blot), and tumor measurements by imaging. After follow-up, we ascertained the response to paclitaxel monotherapy by comparing the percent change in the pre-, post- tumor measurements after treatment. To allocate exposure, we genotyped eleven SNPs with TaqMan probes on RT-PCR and regressed them to tumor response using linear modeling. In addition, we compared protein expression, between breast tumors and healthy controls, of those genes whose genetic markers were significantly associated with tumor response. After adjusting for multiple clinical covariates, SNPs on the LPHN2, ROBO1, SNTG1, and GRIK1 genes were significant independent predictors of poor tumor response (tumor growth) despite paclitaxel treatment. Moreover, proteins encoded by those genes are significantly downregulated in breast tumor samples.

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Novel genome-wide associations for age-related macular degeneration in the sarcoglycan-sarcospan protein complex

2020 , Asaf Calderon, Andrea Michelle , Dewan, Andrew , Ramírez, Israel , Zepeda-Palacio, Claudia , Palacio, Claudia , Antonio-Aguirre, Bani , Mendoza Velásquez, Cristina , Camacho-Ordóñez, Azyadeh , Estrada Mena, Francisco Javier , Pérez Ortiz, Andric Christopher

Purpose : Since the advent of genomic approaches, many chromosomal regions and polymorphisms have been associated with age-related macular degeneration (AMD). However, most of the disease variability might not be still captured by current researched genetic markers due to power issues. We have evidence that at least one component of the sarcoglycan-sarcospan protein complex (Sg-Sspn) gene is associated with increased odds of geographic atrophy (GA) AMD. Moreover, the retina of the knocked-out mouse model for the Sg-Sspn phenotypically resembles GA. Here, we aimed to explore the genome-wide association of the Sg-Sspn complex gene regions with AMD.

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nef/long terminal repeat quasispecies from HIV type 1-infected Mexican patients with different progression patterns and their pathogenesis in hu-PBL-SCID mice

2000 , Gómez-Román, Víctor Raúl , Vásquez, Joel A. , Basualdo, Maria Del Carmen , Estrada Mena, Francisco Javier , Ramos Kuri, Manuel , Soler, Carmen

To examine the genetic features of the long terminal repeat (LTR) derived from six HIV-1-infected individuals enrolled in the Mexico City Cohort, we cloned and sequenced a 505-bp fragment of the proviral LTR from their peripheral blood mononuclear cells (PBMCs). All patients harbored HIV-1 LTR quasispecies corresponding to the B subtype. Three patients with high CD4+ T cell counts (>500/mm3) presented LTR sequences with point mutations in the TAR bulge. The LTR sequence from a patient classified as a long-term nonprogressor (LTNP) presented the most frequent naturally occurring length polymorphism (MFNLP) and two substitutions in the TAR region that were predicted to result in two alternative secondary RNA structures. A novel 18-bp deletion, which eliminates part of the putative binding site for the nuclear factor of activated T cells (NFAT-1), was identified in the overlapping nef/LTR sequence derived from a patient progressing to AIDS. This deletion coincides with the ability of this virus to consistently replicate at low levels in vivo (viral load <500 RNA copies/ml) and in vitro (unsuccessful virus isolation). On one occasion, when virus isolation was successful, the 18-bp deletion was no longer evident and LTR sequences with intact NFAT-1-binding sites were observed. Inoculation of hu-PBL-SCID mice with viruses from several Mexican patients resulted in differential CD4+ T cell depletion patterns 15 days postinfection, which agree with the in vivo CD4+ T cell count data from each patient. © AIDS Research and Human Retroviruses

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Significant Association Between Variant in SGCD and Age-Related Macular Degeneration

2018 , Pérez Ortiz, Andric Christopher , Luna-Angulo, Alexandra , Zenteno, Juan Carlos , Rendon, Álvaro , Cortes-Ballinas, Liliana Guadalupe , Jiménez-Collado, David , Antonio-Aguirre, Bani , Peralta-Ildefonso, Martha Janneth , Ramírez, Israel , Jacob-Kuttothara, Stefany , Estrada Mena, Francisco Javier

CFH and HTRA1 genes are traditional markers of increased risk of age-related macular degeneration (AMD) across populations. Recent findings suggest that additional genes-for instance, in the dystrophin-associated protein complex-might be promising markers for AMD. Here, we performed a case-control study to assess the effect of SGCD single nucleotide polymorphisms (SNPs), a member of this protein family, on AMD diagnosis and phenotype. We performed a case-control study of an under-studied population from Hispanics in Mexico City, with 134 cases with 134 unpaired controls. Cases were 60 years or older (Clinical Age-Related Maculopathy Staging (CARMS) grade 4⁻5, as assessed by experienced ophthalmologists following the American Association of Ophthalmology (AAO) guidelines), without other retinal disease or history of vitreous-retinal surgery. Controls were outpatients aged 60 years or older, with no drusen or retinal pigment epithelium (RPE) changes on a fundus exam and a negative family history of AMD. We examined SNPs in the SGCD gene (rs931798, rs140617, rs140616, and rs970476) by sequencing and real-time PCR. Genotyping quality checks and univariate analyses were performed with PLINK v1.90b3.42. Furthermore, logistic regression models were done in SAS v.9.4 and haplotype configurations in R v.3.3.1. After adjusting for clinical covariates, the G/A genotype of the SGCD gene (rs931798) significantly increases the odds of being diagnosed with AMD in 81% of cases (1.81; 95% CI 1.06⁻3.14; p = 0.031), especially the geographic atrophy phenotype (1.82; 95% CI 1.03⁻3.21; p = 0.038) compared to the G/G homozygous genotype. Moreover, the GATT haplotype in this gene (rs931798, rs140617, rs140616, and rs970476) is associated with lower odds of AMD (adjusted odds ratio (OR) 0.13; 95% CI 0.02⁻0.91; p = 0.041). SGCD is a promising gene for AMD research. Further corroboration in other populations is warranted, especially among other Hispanic ethnicities.

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Development of muscle atrophy and loss of function in a Gulf-War illness model: underlying mechanisms

2020 , Ramírez-Sánchez, Israel , Navarrete-Yañez, Viridiana , Garate-Carrillo, Alejandra , Loredo Mendoza, María Lilia , Lira, Esmeralda , Campeau, Anaamika , Estrada Mena, Francisco Javier , González, David , Carrillo-Terrazas, Marvic , Moreno-Ulloa, Aldo , Guillermo Ceballos , Villarreal, Francisco J.

Gulf War illness (GWI) afflicts military personnel who served during the Persian Gulf War and is notable for cognitive deficits, depression, muscle pain, weakness, intolerance to exercise, and fatigue. Suspect causal agents include the chemicals pyridostigmine (PB), permetrim (PM) and N,N-diethyl-m-toluamide (DEET) used as protectants against insects and nerve gases. No pre-clinical studies have explored the effects on skeletal muscle (SkM). Young male rats were provided PB, PM and DEET at equivalent human doses and physical restraint (to induce stress) for 3 weeks followed a 3-week recovery. GWI gastrocnemius weight was ~ 35% lower versus controls, which correlated with decreases in myofiber area, limb strength, and treadmill time/distance. In GWI rats, SkM fiber type relative abundance changed towards slow type I. Muscle wasting pathway proteins were upregulated while those that promote growth decreased as did mitochondrial endpoints and muscle ATP levels. Proteomic analysis of SkM also documented unique alterations in mitochondrial and metabolic pathways. Thus, exposure to GWI chemicals/stress adversely impacts key metabolic pathways leading to muscle atrophy and loss of function. These changes may account for GWI Veterans symptoms.

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Nuclear density analysis in microscopic images for the characterization of retinal geographic atrophy

2020 , Peralta Ildefonso, Martha Janneth , Moya-Albor, Ernesto , Brieva, Jorge , Lira, Esmeralda , Pérez Ortiz, Andric Christopher , Coral-Vázquez, Ramón , Estrada Mena, Francisco Javier

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in industrialized countries. It is estimated that AMD affects at least 1 in 10 Hispanics. Previous reports have shown that AMD has multiple risk factors. Recently, we demonstrated that some genetic variants in the SGCD gene are involved in AMD developments, especially in early-stage (geographic atrophy, GA). Therefore, to evaluate the relationship between SGCD's absence and the loss of photoreceptors in GA, we worked with a genetically modified mouse model, SGCD deficient (Sgcd-/-) and a control mouse C57BL/6J (Sgcd+/+). First, we obtained hematoxylin and eosin (H&E) retina staining microscopic images. Then, we coarsely selected the outer and inner nuclear retinal layer (ONL and INL respectively) and finally, we applied an automatic nuclei segmentation to calculate the nuclear density in each region. Our results showed that Sgcd absence does not result in photoreceptor loss, on the contrary, it promotes an increment in nuclear density by 8.7% in ONL and 20.1% in INL compared with control eyes (p = 0.0033 and p < 0.0001 respectively). This could be explained by the fact that SGCD codifies the delta-sarcoglycan protein and there is evidence that showed a relationship between the absence of this protein with the activation of a cell proliferation signaling pathway. Finally, our results show that the delta-sarcoglycan protein could play an important role in the pathogenesis of the geographic atrophy. Moreover, there are promising perspectives for the systematic approach applied for cell image analysis, as an important tool to determine the nuclear density for assessing the progression of AMD. ©COPYRIGHT SPIE. Downloading of the abstract is permitted for personal use only.

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Effects of (−)-epicatechin on frontal cortex DAPC and dysbindin of the mdx mice

2017 , Estrada Mena, Francisco Javier , Rodríguez, Alonso , Mendoza-Lorenzo, Patricia , Neri-Gómez, Teresa , Manjarrez-Gutiérrez, Gabriel , Pérez Ortiz, Andric Christopher , Ordonez-Razo, Rosa , Ceballos, Guillermo , Villarreal, Francisco , Ramírez-Sánchez, Israel

Introduction: Multiple components of the dystrophin-associated protein complex (DAPC) are expressed in numerous tissues including the brain. Members of the DAPC and dysbindin are abnormally expressed in the brain of Duchenne Muscular Dystrophy (DMD) patients, which has been associated with cognitive impairments. However, little is known about the expression pattern of individual members of the DAPC in animal models of DMD and their relationship with dysbindin. Methods: Ten mdx mice were randomly allocated into a control and intervention group [(−)-epicatechin (Epi) 1 mg/kg/day for four weeks] and results compared to a wild-type mice. After sacrifice, brain pre-frontal cortices were collected for Western blotting and immunoprecipitation assays, and sagittal sections processed for immunohistochemistry.

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