Exploring the Shared Gene Signatures and Molecular Mechanisms between Bladder Urothelial Carcinoma and Metabolic Syndrome

Background: The aim of this study was to investigate the common gene signatures and potential molecular mechanisms of bladder urothelial carcinoma (BLCA) and metabolic syndrome (MS). Methods: Transcriptome data for BLCA and MS were obtained from the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was utilized to identify co-expression networks associated with BLCA and MS, and five hub genes were further screened and validated using logistic least absolute shrinkage and selection operator (LASSO) regression models and receiver operating characteristic (ROC) curve, and external dataset for validation. The relationship between the hub genes and the clinicopathological characteristics and prognosis of BLCA patients was explored in the GEO and The Cancer Genome Atlas (TCGA)-BLCA cohorts, respectively. Differences in the immune microenvironment of BLCA and MS were analyzed using the database CIBERSORT and the R package “ssGSEA”, and the correlation between hub genes and tumor microenvironment, immune score and targeted drugs was analyzed with the help of the TCGA-BLCA cohort. Finally, BLCA single-cell RNA (scRNA) data were used to analyze the expression levels of the hub genes in various cell types of BLCA and molecular mechanisms. Results: Five hub genes were screened by WGCNA and LASSO regression analysis, namely AP2-associated protein kinase 1 (AAK1), ATP-binding cassette subfamily F member 2 (ABCF2), Mitochondrial ribosomal protein L42 (MRPL42), La-related protein 3 (SSB) and TATA-box binding protein-associated factor 10 (TAF10). Analyzed in the GEO and TCGA-BLCA cohorts, we found that the hub genes (TAF10 and ABCF2) were closely associated with the clinicopathological characteristics and prognosis of BLCA patients (AU)

Identification of key genes and biological regulatory mechanisms in diabetic nephropathy: Meta-analysis of gene expression datasets / Identificación de genes clave y mecanismos reguladores biológicos en la nefropatía diabética: metaanálisis de conjuntos de datos de expresión génica

Background: Diabetic nephropathy (DN) which refers to the cases with biopsy proven kidney lesions, is one of the main complications of diabetes all around the world; however, the underlying biological changes causing DN remain to be understood. Studying the alterations in gene expression profiles could give a holistic view of the molecular pathogenicity of DN and aid to discover key molecules as potential therapeutic targets. Here, we performed a meta-analysis study that included microarray gene expression profiles coming from glomerular samples of DN patients in order to acquire a list of consensus Differentially Expressed Genes (meta-DEGs) correlated with DN. Methods: After quality control and normalization steps, five gene expression datasets (GES1009, GSE30528, GSE47183, GSE104948, and GSE93804) were entered into the meta-analysis. The meta-analysis was performed by random effect size method and the meta-DEGs were put through network analysis and different pathway enrichment analyses steps. MiRTarBase and TRRUST databases were utilized to predict the meta-DEGs related miRNAs and transcription factors. A co-regulatory network including DEGs, transcription factors and miRNAs was constructed by Cytoscape, and top molecules were identified based on centrality scores in the network.(AU)

Antecedentes: La nefropatía diabética (ND), que se refiere a los casos con lesiones renales comprobadas por biopsia, es una de las principales complicaciones de la diabetes en todo el mundo. Sin embargo, los cambios biológicos subyacentes que causan la ND aún no se han entendido. Aquí realizamos un estudio de metaanálisis que incluyó perfiles de expresión génica de micromatrices provenientes de muestras glomerulares de pacientes con ND para adquirir una lista de genes expresados diferencialmente (meta-DEG) de consenso correlacionados con ND. Métodos: Después de los pasos de control de calidad y normalización, se ingresaron en el metaanálisis cinco conjuntos de datos de expresión génica (GES1009, GSE30528, GSE47183, GSE104948 y GSE93804). El metaanálisis se realizó mediante el método de tamaño de efecto aleatorio y los meta-DEG se sometieron a análisis de red y a diferentes pasos de análisis de enriquecimiento de ruta. Se utilizaron las bases de datos MiRTarBase y TRRUST para predecir los factores de transcripción y los miARN relacionados con los meta-DEG. Cytoscape construyó una red de corregulación que incluye DEG, factores de transcripción y miARN, y las moléculas principales se identificaron en función de las puntuaciones de centralidad en la red. (AU)

Asthma Exacerbations: The Genes Behind the Scenes

The clinical and socioeconomic burden of asthma exacerbations (AEs) constitutes a major public health problem. In the last 4 years, there has been an increase in ethnic diversity in candidate-gene and genome-wide association studies of AEs, which in the latter case led to the identification of novel genes and underlying pathobiological processes. Pharmacogenomics, admixture mapping analyses, and the combination of multiple “omics” layers have helped to prioritize genomic regions of interest and/or facilitated our understanding of the functional consequences of genetic variation. Nevertheless, the field still lags behind the genomics of asthma, where a vast compendium of genetic approaches has been used (eg, gene–environment interactions, next-generation sequencing, and polygenic risk scores). Furthermore, the roles of the DNA methylome and histone modifications in AEs have received little attention, and microRNA findings remain to be validated in independent studies. Likewise, the most recent transcriptomic studies highlight the importance of the host–airway microbiome interaction in the modulation of risk of AEs. Leveraging -omics and deep-phenotyping data from subtypes or homogenous subgroups of patients will be crucial if we are to overcome the inherent heterogeneity of AEs, boost the identification of potential therapeutic targets, and implement precision medicine approaches to AEs in clinical practice (AU)

La carga clínica y socioeconómica de las exacerbaciones asmáticas (EA) representa un importante problema de salud pública. En los últimos cuatro años, ha aumentado la diversidad étnica en los estudios de asociación de genes candidatos y del genoma completo (GWAS) de las EA, lo que, en este último caso, ha llevado a la identificación de nuevos genes y procesos fisiopatológicos subyacentes. La farmacogenómica, los análisis de mapeo por mezcla y la combinación de múltiples capas "ómicas" han contribuido a priorizar regiones genómicas de interés y/o comprender las consecuencias funcionales de la variación genética. A pesar de esto, el campo todavía está en desarrollo en comparación con la genómica del asma, donde se ha utilizado un amplio compendio de enfoques genéticos (por ejemplo: interacciones gen-ambiente, secuenciación de nueva generación o puntuaciones de riesgo poligénico). Además, el papel de la metilación del ADN y las modificaciones de las histonas en las EA se ha explorado escasamente, y los hallazgos relacionados con los microARNs aún no se han validado en estudios independientes. Asimismo, los estudios transcriptómicos más recientes destacan la importancia de la interacción entre el microbioma de las vías respiratorias y el huésped en la modulación del riesgo de las EA. La integración de datos ómicos y de fenotipado profundo de subtipos o subgrupos homogéneos de pacientes será crucial para superar la heterogeneidad inherente de las EA e impulsar la identificación de dianas terapéuticas potenciales y la implementación de la medicina de precisión para las EA en la práctica clínica (AU)

Metabolic changes of Issatchenkia orientalis under acetic acid stress by transcriptome profile using RNA-sequencing / Cambios metabólicos de Issatchenkia orientalis bajo estrés con ácido acético por perfil de transcriptoma usando secuenciación de ARN

Issatchenkia orientalis (I. orientalis) is tolerant to various environmental stresses especially acetic acid stress in wine making. However, limited literature is available on the transcriptome profile of I. orientalis under acetic acid stress. RNA-sequence was used to investigate the metabolic changes due to underlying I. orientalis 166 (Io 166) tolerant to acetic acid. Transcriptomic analyses showed that genes involved in ergosterol biosynthesis are differentially expressed under acetic acid stress. Genes associated with ribosome function were downregulated, while energy metabolism-related genes were upregulated. Moreover, Hsp70/Hsp90 and related molecular chaperones were upregulated to recognize and degrade misfolded proteins. Compared to Saccharomyces cerevisiae, transcriptomic changes of Io 166 showed many similarities under acetic acid stress. There were significant upregulation of genes in ergosterol biosynthesis and for the application of wine production.(AU)

The yeast two-component SLN1 branch of the HOG pathway and the scaffolding activity of Pbs2 modulate the response to endoplasmic reticulum stress induced by tunicamycin / La rama SLN1 de dos componentes de levadura de la vía HOG y la actividad de andamiaje de Pbs2 modulan la respuesta al estrés del retículo endoplásmico inducido por tunicamicina

In addition to the UPR pathway, yeast cells require components of the HOG pathway to respond to ER stress. In this work, we found that unphosphorylated Sln1 and Ssk1 are required to mount an appropriate response to Tn. We also found that the MAPKKKs Ssk2 participates in the Tn response, but its osmo-redundant protein Ssk22 does not. We also found that the Pbs2 docking sites for Ssk2 (RDS-I and KD) are partially dispensable when mutated separately; however, the prevention of Ssk2 binding to Pbs2, by the simultaneous mutation of RDS-I and KD, caused strong sensitivity to Tn. In agreement with the lack of Hog1 phosphorylation during Tn treatment, a moderate resistance to Tn is obtained when a Pbs2 version lacking its kinase activity is expressed; however, the presence of mutual Pbs2-Hog1 docking sites is essential for the Tn response. Finally, we detected that Tn induced a transcriptional activation of some components of the SLN1 branch. These results indicate that the Tn response requires a complex formed by the MAPK module and components of the SLN1 branch but not their canonical osmoregulatory activities.(AU)

Transcriptome sequencing and global analysis of blue light-responsive genes provide clues for high carotenoid yields in Blakeslea trispora / La secuenciación del transcriptoma y el análisis global de los genes sensibles a la luz azul proporcionan pistas sobre los altos rendimientos de carotenoides en Blakeslea trispora

Blakeslea trispora has great potential uses in industrial production because of the excellent capability of producing a large quantity of carotenoids. However, the mechanisms of light-induced carotenoid biosynthesis even the structural and regulatory genes in pathways remain unclear. In this paper, we reported the first transcriptome study in B. trispora in which we have carried out global survey of expression changes of genes participated in blue light response. We verified that the yield of β-carotene increased 3-fold when transferred from darkness to blue light for 24 h and the enhancement of transcription levels of carRA and carB presented a positive correlation with the increase in carotenoid production. RNA-seq analysis revealed that 1124 genes were upregulated and 740 genes were downregulated respectively after blue light exposure. Annotation through GO, KEGG, Swissprot, and COG databases showed 11119 unigenes compared well with known gene sequences, 5514 unigenes were classified into Gene Ontology, and 4675 unigenes were involved in distinct pathways. Among the blue light-responsive genes, 4 genes (carG1, carG3, carRA and carB) identified to function in carotenoid metabolic pathways were dominantly upregulated. We also discovered that 142 TF genes belonging to 45 different superfamilies showed significant differential expression (p≤ 0.05), 62 of which were obviously repressed by blue light. The detailed profile of transcription data will not only allow us to conduct further functional genomics study in B. trispora, but also enhance our understanding of potential metabolic pathway and regulatory network involved in light-regulated carotenoid synthesis.(AU)

A novel 12-gene signature as independent prognostic model in stage IA and IB lung squamous cell carcinoma patients

Background There is currently no formal consensus on the administration of adjuvant chemotherapy to stage I lung squamous cell carcinoma (LUSC) patients despite the poor prognosis. The side effects of adjuvant chemotherapy need to be balanced against the risk of tumour recurrence. Prognostic markers are thus needed to identify those at higher risks and recommend individualised treatment regimens. Methods Clinical and sequencing data of stage I patients were retrieved from the Lung Squamous Cell Carcinoma project of the Cancer Genome Atlas (TCGA) and three tissue microarray datasets. In a novel K-resample gene selection algorithm, gene-wise Cox proportional hazard regressions were repeated for 50 iterations with random resamples from the TCGA training dataset. The top 200 genes with the best predictive power for survival were chosen to undergo an L1-penalised Cox regression for further gene selection. Results A total of 602 samples of LUSC were included, of which 42.2% came from female patients, 45.3% were stage IA cancer. From an initial pool of 11,212 genes in the TCGA training dataset, a final set of 12 genes were selected to construct the multivariate Cox prognostic model. Among the 12 selected genes, 5 genes, STAU1, ADGRF1, ATF7IP2, MALL and KRT23, were adverse prognostic factors for patients, while seven genes, NDUFB1, CNPY2, ZNF394, PIN4, FZD8, NBPF26 and EPYC, were positive prognostic factors. An equation for risk score was thus constructed from the final multivariate Cox model. The model performance was tested in the sequestered TCGA testing dataset and validated in external tissue microarray datasets (GSE4573, GSE31210 and GSE50081), demonstrating its efficacy in stratifying patients into high- and low-risk groups with significant survival difference both in the whole set (including stage IA and IB) and in the stage IA only subgroup of each set. The prognostic power remains significant after adjusting for standard clinical factors (AU)

A comprehensive analysis of tumor microenvironment-related genes in colon cancer

Background The development and progression of colon cancer are significantly affected by the tumor microenvironment, which has attracted much attention. The goal of our study was primarily to find out all possible tumor microenvironment-related genes in colon cancer. Method This study quantified the immune and stromal landscape using the ESTIMATION algorithm using the gene expression matrix obtained from the UCSC Xena database. Dysregulated genes were harvested using the limma R package, and relevant pathways and biofunctions were identified using enrichment analysis. A least absolute shrinkage and selection operator (LASSO) regression was used to select the pivotal genes from the DEGs. Then, survival analysis was performed to determine the hub genes and a prognostic model was constructed by these hub genes with (or) TNM stage. Besides, associations between hub gene expressions and immune cell infiltration were assessed. Results A total of 725 DEGs were identified. Most of the results of the enrichment analysis were immune-related items. 13 genes were selected as the hub genes and a moderate-to-strong positive correlation between most hub genes and several immune cells were observed. Besides, the prognostic value of the hub genes were comparable to TNM staging. Conclusions Our study provides a better understanding of how interactions between the 13 immune-prognostic hub genes and immune cells in the tumor microenvironment affect biological processes in colon cancer. These genes exhibit an equivalent ability to TNM staging in prognosis prediction. They are particularly expected to become novel prognostic biomarkers and targets of immunotherapies for colon cancer (AU)

Noncoding RNAs as potential biomarkers for DIPG diagnosis and prognosis: XIST and XIST-210 involvement

Purpose Diffuse intrinsic pontine gliomas (DIPGs) are the most fatal primary brainstem tumors in pediatric patients. The identification of new molecular features, mediating their formation and progression, as non-coding RNAs (ncRNAs), would be of great importance for the development of effective treatments. Methods We analyzed the DIPGs transcriptome with the HTA2.0 array and it was compared with pediatric non-brainstem astrocytoma expression profiles (GSE72269). Results More than 50% of the differentially expressed transcripts were ncRNAs and based on this, we proposed a DIPGs ncRNA signature. LncRNAs XIST and XIST-210, and the HBII-52 and HBII-85 snoRNA clusters were markedly downregulated in DIPGs. qPCR assays demonstrated XIST downregulation in all non-brainstem astrocytomas, in a gender, age, and brain location-independent manner, as well as in DIPGs affecting boys; however, DIPGs affecting girls showed both downregulation and upregulation of XIST. Girls’ with longer survival positively correlated with XIST expression. Conclusions The involvement of ncRNAs in DIPGs is imminent and their expression profile is useful to differentiate them from non-neoplastic tissues and non-brain stem astrocytomas, which suggests their potential use as DIPG biomarkers. In fact, XIST and XIST-210 are potential DIPG prognostic biomarkers (AU)

La genómica en cáncer de mama: nuevas perspectivas / Genomics in breast cancer: new directions

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Deciphering the molecular mechanisms involved in HIV-associated lipoatrophy by transcriptomics: a pilot study

HIV-associated lipoatrophy (LA) has considerable implications for risk of metabolic diseases, quality of life, and adherence to treatments. Although it has decreased in high-income countries, it is still very common in resource-limited countries. Understanding the pathophysiological mechanisms of LA can open the possibility to explore new ways to treat or prevent this condition. To identify new markers for an accurate and quick diagnosis will be also of interest. Thus, we aimed to examine functional classes of genes implicated in LA and to identify potential new markers for an accurate/quick diagnosis of LA and future complications. Eighteen participants were recruited: seven healthy volunteers, five non-LA-HIV patients, and six LA-HIV subjects. Clinical lipoatrophy was considered when changes in fat volume in the cheeks next to the nose, lateral aspect of the face, legs, arms, and buttocks were observed by the physicians. mRNA was isolated from peripheral blood mononuclear cells (PBMCs) to perform a transcriptomic and Gene Ontology analysis. To confirm RNA sequencing results, qPCRs were developed. A total of 55 genes were differentially expressed between LA and non-LA patients. Thirty-seven genes were overexpressed, whereas 18 genes were repressed. Functional analysis showed that overexpressed genes were involved in lymphocyte/neutrophil activation, inflammation, and atherogenesis. Several lymphoma markers and members of the lipocalin and aquaporin families were also found more expressed in LA patients. In contrast, most of the genes found less expressed in LA subjects were involved in angiogenesis and protection against myocardial infarction. Our results demonstrated a distinct transcriptomic signature in PBMCs of LA patients in comparison with non-LA-HIV subjects and, therefore, provided novel insights to the pathogenesis of HIV-associated lipoatrophy. Our study also highlights the potential usage of some of these genes as early markers of future complications

Adherence to Mediterranean diet is associated with methylation changes in inflammation-related genes in peripheral blood cells

Epigenetic processes, including DNA methylation, might be modulated by environmental factors such as the diet, which in turn have been associated with the onset of several diseases such as obesity or cardiovascular events. Meanwhile, Mediterranean diet (MedDiet) has demonstrated favourable effects on cardiovascular risk, blood pressure, inflammation and other complications related to excessive adiposity. Some of these effects could be mediated by epigenetic modifications. Therefore, the objective of this study was to investigate whether the adherence to MedDiet is associated with changes in the methylation status from peripheral blood cells. A subset of 36 individuals was selected within the Prevención con Dieta Mediterránea (PREDIMED)-Navarra study, a randomised, controlled, parallel trial with three groups of intervention in high cardiovascular risk volunteers, two with a MedDiet and one low-fat control group. Changes in methylation between baseline and 5 years were studied. DNA methylation arrays were analysed by several robust statistical tests and functional classifications. Eight genes related to inflammation and immunocompetence (EEF2, COL18A1, IL4I1, LEPR, PLAGL1, IFRD1, MAPKAPK2, PPARGC1B) were finally selected as changes in their methylation levels correlated with adherence to MedDiet and because they presented sensitivity related to a high variability in methylation changes. Additionally, EEF2 methylation levels positively correlated with concentrations of TNF-alfa and CRP. This report is apparently the first showing that adherence to MedDiet is associated with the methylation of the reported genes related to inflammation with a potential regulatory impact

Acute kidney injury transcriptomics unveils a relationship between inflammation and ageing

There are no pathophysiolgical therapeutic approaches to acute kidney injury (AKI) and the mortality remains high. In addition chronic kidney disease (CKD) predisposes to AKI and AKI contributes to progression of CKD. Recently a transcriptomics approach unveiled a relationship between AKI, inflammation and the regulation of ageing. A transcriptomics analysis of experimental AKI revealed increased kidney expression of Fn14 and transmembrane chemokine CXCL16, as well as a decreased expression of the kidney-secreted anti-ageing hormone Klotho. Fn14 is the receptor for tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the TNF superfamily. In AKI kidneys there was a positive correlation between Fn14 and CXCL16 mRNA expression and an inverse correlation between Fn14 and Klotho mRNA. Tubular cells were the site of Fn14, CXCL16 and Klotho expression in vivo. Research on the relationships between these three molecules disclosed that TWEAK activation of Fn14 promoted inflammation through secretion of chemokines such as CXL16 in tubular cells in culture and in vivo. Furthermore, TWEAK activation of Fn14 decreased expression of Klotho mRNA and protein in culture and in vivo. Interestingly, both TWEAK activation of CXCL16 mRNA transcription and suppression of Klotho mRNA transcription were mediated by the NFκB transcription factor. In conclusion, TWEAK engagement of Fn14 is a central event promoting NFκB-mediated activation of inflammation pathways and suppression of anti-inflammatory/anti-ageing pathways. This information may influence future therapeutic approaches to AKI and inflammation/aging (AU)

No existen estrategias terapéuticas y fisiopatológicas para el fracaso renal agudo (FRA), por lo que los niveles de mortalidad continúan siendo elevados. Además, la enfermedad renal crónica (ERC) predispone a sufrir FRA y el FRA, a su vez, contribuye a que la ERC avance. Recientemente, una estrategia transcriptómica reveló una relación entre el FRA, la inflamación y la regulación del envejecimiento. Un análisis transcriptómico de modelos experimentales de FRA reveló un aumento de la expresión renal de Fn14 y la quimiocina transmembrana CXCL16, así como un descenso en la expresión de la hormona Klotho antienvejecimiento secretada por el riñón. Fn14 es el receptor de la citoquina tumor necrosis factor-like weak inducer of apoptosis (TWEAK), miembro de la superfamilia de factor de necrosis tumoral. En los riñones con FRA, existía una correlación positiva entre Fn14 y la expresión de ARNm de CXCL16 y una correlación inversa entre Fn14 y el ARNm de Klotho. El lugar donde se da la expresión in vivo de Fn14, CXCL16 y Klotho es las células tubulares. La investigación en las relaciones entre estas tres moléculas reveló que la activación de Fn14 por TWEAK provocó la inflamación mediante la secreción de quimiocinas como la CXCL16 en células tubulares, tanto en cultivo como in vivo. Además, la activación de Fn14 por TWEAK disminuyó la expresión de ARNm de Klotho y de proteína, en cultivo y in vivo. Curiosamente, tanto la activación TWEAK de la trascripción de ARNm de CXCL16 y la supresión de la trascripción de ARNm de Klotho estuvieron mediadas por el factor de transcripción NF-κB. Como conclusión, la unión de TWEAK y Fn14 es un elemento clave en promover de la activación mediada por NF-kB de las vías de inflamación y en la supresión de las vías antiinflamatorias y antienvejecimiento. Esta información puede influir en las futuras estrategias terapéuticas para el FRA y la inflamación/envejecimiento (AU)

Análisis de la expresión de 4 micro-ARN en espermatozoides y su implicación en la fertilidad masculina / Analysis of the expression of four microRNAs in spermatozoa and their role in male fertility

Introducción: Los micro-ARN (mi-ARN) son moléculas de 22-24 nucleótidos implicadas en la regulación de la expresión génica de numerosos procesos. Recientemente, se han identificado perfiles alterados de expresión de mi-ARN en diferentes casos de infertilidad idiopática, sugiriendo un papel relevante de estas moléculas en la regulación de la fertilidad. Objetivo: Caracterizar los patrones de expresión de 4 mi-ARN en ácido ribonucleico espermático procedente de individuos fértiles e infértiles. Material y métodos: Se obtuvo la fracción espermática de 4 muestras de semen de individuos fértiles y 4 muestras de individuos que consultaban por infertilidad. Se aisló el ácido ribonucleico utilizando el método TRIzol® y seguidamente se efectuó un tratamiento con DNasa. La ausencia de ácido desoxirribonucleico en las muestras extraídas se confirmó mediante una reacción en cadena de la polimerasa para el gen de la protamina 1. Seguidamente, con cebadores específicos para los mi-ARN hsa-miR-23a, hsa-miR-744, hsa-let-7f y hsa-miR-1, y el normalizador Mamm-U6, se realizaron reacciones en cadena de la polimerasa a tiempo real mediante tecnología TaqMan. La cuantificación de las diferencias de expresión se realizó mediante el cálculo del estadístico Fold Change y la utilización de un intervalo de confianza del 95%. Resultados: Para cada individuo, se obtuvo una media de 2,6 × 10-5ng de ácido ribonucleico/espermatozoide con una pureza de 1,72 (± 0,05) y sin trazas de ácido desoxirribonucleico. El análisis TaqMan reveló la presencia de hsa-miR-23a, hsa-miR-744 y hsa-let-7f en los espermatozoides de todos los individuos estudiados. La expresión de hsa-let-7f mostró una reducción significativa en 3 de los 4 individuos problema respecto a los individuos control. Conclusión: Los espermatozoides humanos contienen los mi-ARN hsa-miR-23a, hsamiR-744 y hsa-let-7f. Este último muestra una reducción significativa de expresión en 3 de los 4 individuos infértiles analizados sugiriendo la implicación de alteraciones en la expresión de mi-ARN como causa subyacente de algunos casos de infertilidad masculina (AU)

Introduction: MicroRNAs (miRNAs) are 22-24nt molecules involved in the gene expression regulation of many biological processes. Several authors have recently identified altered miRNA expression profiles in cases of male idiopathic infertility, suggesting its fundamental role in fertility regulation. Objective: To characterize the expression of four miRNAs in sperm ribonucleic acid from fertile and infertile men. Material and methods: Four ejaculated samples from fertile donors and four samples from idiopathic infertile patients were obtained. Total RNA was isolated using the TRIzol method followed by a DNase treatment. To confirm proper ribonucleic acid purification, a polymerase chain reaction for the Protamine-1 gene (PRM-1) was performed. Afterwards, real-time polymerase chain reaction with specific primers for the miRNAs hsa-miR-23a, hsa-miR-744, hsa-let-7f and hsa-miR-1, together with the normalization control Mamm-U6, were performed. Differences in expression were quantified by the Fold-Change statistic and 95% confidence intervals. Results: For each individual, an average of 2.6×10-5ng ribonucleic acid/spermatozoa was obtained, with a purity of 1.72 (±0.05) and no traces of deoxyribonucleic acid. TaqMan analysis confirmed the presence of hsa-miR-23a, hsa-miR-744 y hsa-let-7f in all the samples. The expression of hsa-let-7f was significantly lower in three of the four samples from men with idiopathic infertility. Conclusion: Human spermatozoa contain the miRNAs hsa-miR-23a, hsa-miR-744 and hsalet-7f. Hsa-let-7f expression was significantly reduced in three out of four infertile patients, suggesting the involvement of alterations in miRNA expression as the underlying cause of some cases of male infertility (AU)