Lira-Romero, Esmeralda
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Lira-Romero, Esmeralda
Official Name
Lira Romero, Esmeralda
Alternative Name
elira
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ORCID
Scopus Author ID
54581126300
Researcher ID
DYR-7871-2022

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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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Evaluation of a Proteomics-Guided Protein Signature for Breast Cancer Detection in Breast Tissue

2024 , Aldo Moreno-Ulloa , Vareska L. Zárate-Córdova , Israel Ramírez-Sánchez , Juan Carlos Cruz-López , Andric C Perez-ortiz , Cynthia Villarreal-Garza , José Díaz-Chávez , Benito Estrada-Mena , Bani Antonio-aguirre , Perla Ximena Lopez Almanza , Lira-Romero, Esmeralda , Estrada Mena, Francisco Javier

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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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Assessment of CFH and HTRA1 polymorphisms in age-related macular degeneration using classic and machine-learning approaches

2020 , Martínez Velasco, Antonieta Teodora , Pérez Ortiz, Andric Christopher , Antonio-Aguirre, Bani , Martinez-Villaseñor, Lourdes , Palacio-Pastrana, Claudia , Lira, Esmeralda , Zenteno, Juan Carlos , Ramírez-Sánchez, Israel , Zepeda-Palacio, Claudia , Mendoza Vera, Cristina Azucena , Camacho-Ordóñez, Azyadeh , Ortiz Bibriesca, Daniela , Estrada Mena, Francisco Javier

CFH: and HTRA1 are pivotal genes driving increased risk for age-related macular degeneration (AMD) among several populations. Here, we performed a hospital-based case-control study to evaluate the effects of three single nucleotide polymorphisms (SNPs) among Hispanics from Mexico. Materials and methods: 122 cases and 249 controls were genotyped using Taqman probes. Experienced ophthalmologists diagnosed AMD following the American Association of Ophthalmology guidelines. We studied CFH (rs1329428, rs203687) and HTRA1 (rs11200638) SNPs thoroughly by logistic regression models (assuming different modes of inheritance) and machine learning-based methods (ML). HTRA1: rs11200638 is the most significant polymorphism associated with AMD in our studied population. In a multivariate regression model adjusted for clinically and statistically meaningful covariates, the A/G and A/A genotypes increased the odds of disease by a factor of 2.32 and 7.81, respectively (P < .05) suggesting a multiplicative effect of the polymorphic A allele. Furthermore, this observation remains statistically meaningful in the allelic, dominant, and recessive models, and ML algorithms. When stratifying by phenotype, this polymorphism was significantly associated with increased odds for geographic atrophy (GA) in a recessive mode of inheritance (12.4, p < .05). Conclusions: In sum, this work supports a strong association between HTRA1 genetic variants and AMD in Hispanics from Mexico, especially with GA. Moreover, ML was able to replicate the results of conventional biostatistics methods unbiasedly. © 2020 Taylor & Francis Group, LLC.

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Lack of Delta-Sarcoglycan (Sgcd) Results in Retinal Degeneration

2019 , Pérez Ortiz, Andric Christopher , Peralta-Ildefonso, Martha Janneth , Lira, Esmeralda , Ramírez-Sánchez, Israel , Brieva, Jorge , Moya-Albor, Ernesto , Clapp, Carmen , Luna-Angulo, Alexandra , Rendon, Álvaro , Adan-Castro, Elva , Ramírez-Hernández, Gabriela , Díaz-Lezama, Nundehui , Coral-Vázquez, Ramón , Estrada Mena, Francisco Javier

Age-related macular degeneration (AMD) is the leading cause of central vision loss and severe blindness among the elderly population. Recently, we reported on the association of the SGCD gene (encoding for δ-sarcoglycan) polymorphisms with AMD. However, the functional consequence of Sgcd alterations in retinal degeneration is not known. Herein, we characterized changes in the retina of the Sgcd knocked-out mouse (KO, Sgcd−/−). At baseline, we analyzed the retina structure of three-month-old wild-type (WT, Sgcd+/+) and Sgcd−/− mice by hematoxylin and eosin (H&E) staining, assessed the Sgcd-protein complex (α-, β-, γ-, and ε-sarcoglycan, and sarcospan) by immunofluorescence (IF) and Western blot (WB), and performed electroretinography. Compared to the WT, Sgcd−/− mice are five times more likely to have retinal ruptures. Additionally, all the retinal layers are significantly thinner, more so in the inner plexiform layer (IPL). In addition, the number of nuclei in the KO versus the WT is ever so slightly increased. WT mice express Sgcd-protein partners in specific retinal layers, and as expected, KO mice have decreased or no protein expression, with a significant increase in the α subunit. At three months of age, there were no significant differences in the scotopic electroretinographic responses, regarding both a- and b-waves. According to our data, Sgcd−/− has a phenotype that is compatible with retinal degeneration. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.

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