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1. Does regression of skin thickening predict improvement of internal organ involvement and survival in patients with diffuse cutaneous systemic sclerosis? A EUSTAR analysis

Author

Wyss, Anja, Jordan, Suzana, Graf, Nicole, Carreira, Patricia E., Distler, Jörg, Cerinic, Marco Matucci, Siegert, Elise, Henes, Jörg, Zanatta, Elisabetta, Riccieri, Valeria, Truchetet, Marie-Elise, Oksel, Fahrettin, Li, Mengtao, Kucharz, Eugene J., Eyerich, Kilian, Del Galdo, Francesco, Vonk, Madelon C., Vold, Anna-Maria Hoffman, Gabrielli, Armando, and Distler, Oliver

Published
2024
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21. Impact of anxiety and depression on the prognosis of copd exacerbations

Author

Martínez-Gestoso, Sandra, García-Sanz, María-Teresa, Carreira, José-Martín, Salgado, Francisco-Javier, Calvo-Álvarez, Uxío, Doval-Oubiña, Liliana, Camba-Matos, Sandra, Peleteiro-Pedraza, Lorena, González-Pérez, Miguel-Angel, Penela-Penela, Pedro, Vilas-Iglesias, Andrés, and González-Barcala, Francisco-Javier

Published
2022
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41. Genome-wide association study meta-analysis identifies five new loci for systemic lupus erythematosus

Author

Julià, Antonio, López-Longo, Francisco Javier, Pérez Venegas, José J., Bonàs-Guarch, Silvia, Olivé, Àlex, Andreu, José Luís, Aguirre-Zamorano, Mª. Ángeles, Vela, Paloma, Nolla, Joan M., de la Fuente, José Luís Marenco, Zea, Antonio, Pego-Reigosa, José María, Freire, Mercedes, Díez, Elvira, Rodríguez-Almaraz, Esther, Carreira, Patricia, Blanco, Ricardo, Taboada, Víctor Martínez, López-Lasanta, María, Corbeto, Mireia López, Mercader, Josep M., Torrents, David, Absher, Devin, Marsal, Sara, and Fernández-Nebro, Antonio

Published
2018
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44. TBP and SNAP50 transcription factors bind specifically to the Pr77 promoter sequence from trypanosomatid non-LTR retrotransposons

Author

Ministerio de Economía y Competitividad (España), Ministerio de Ciencia e Innovación (España), European Commission, Macías, Francisco, Afonso-Lehmann, R.N., Carreira, P., Thomas, María del Ccarmen, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia e Innovación (España), European Commission, Macías, Francisco, Afonso-Lehmann, R.N., Carreira, P., and Thomas, María del Ccarmen

Abstract

Background: Trypanosomatid genomes are colonized by active and inactive mobile DNA elements, such as LINE, SINE-like, SIDER and DIRE retrotransposons. These elements all share a 77-nucleotide-long sequence at their 5′ ends, known as Pr77, which activates transcription, thereby generating abundant unspliced and translatable transcripts. However, transcription factors that mediates this process have still not been reported. Methods: TATA-binding protein (TBP) and small nuclear RNA-activating protein 50 kDa (SNAP50) recombinant proteins and specific antibodies raised against them were generated. Protein capture assay, electrophoretic mobility-shift assays (EMSA) and EMSA competition assays carried out using these proteins and nuclear proteins of the parasite together to specific DNA sequences used as probes allowed detecting direct interaction of these transcription factors to Pr77 sequence. Results: This study identified TBP and SNAP50 as part of the DNA-protein complex formed by the Pr77 promoter sequence and nuclear proteins of Trypanosoma cruzi. TBP establishes direct and specific contact with the Pr77 sequence, where the DPE and DPE downstream regions are docking sites with preferential binding. TBP binds cooperatively (Hill coefficient = 1.67) to Pr77 and to both strands of the Pr77 sequence, while the conformation of this highly structured sequence is not involved in TBP binding. Direct binding of SNAP50 to the Pr77 sequence is weak and may be mediated by protein–protein interactions through other trypanosomatid nuclear proteins. Conclusions: Identification of the transcription factors that mediate Pr77 transcription may help to elucidate how these retrotransposons are mobilized within the trypanosomatid genomes and their roles in gene regulation processes in this human parasite. Graphic abstract: [Figure not available: see fulltext.].

Published
2021

46. Genome-wide association study meta-analysis identifies five new loci for systemic lupus erythematosus

Author

Julia, A, Lopez-Longo, FJ, Venegas, JJP, Bonas-Guarch, S, Olive, A, Andreu, JL, Aguirre-Zamorano, MA, Vela, P, Nolla, JM, de la Fuente, JLM, Zea, A, Pego-Reigosa, JM, Freire, M, Diez, E, Rodriguez-Almaraz, E, Carreira, P, Blanco, R, Taboada, VM, Lopez-Lasanta, M, Corbeto, ML, Mercader, JM, Torrents, D, Absher, D, Marsal, S, and Fernandez-Nebro, A

Subjects
Genome-wide association study, Meta-analysis, Systemic lupus erythematosus, Biological pathway analysis, Genetic susceptibility
Abstract

Background: Systemic lupus erythematosus (SLE) is a common systemic autoimmune disease with a complex genetic inheritance. Genome-wide association studies (GWAS) have significantly increased the number of significant loci associated with SLE risk. To date, however, established loci account for less than 30% of the disease heritability and additional risk variants have yet to be identified. Here we performed a GWAS followed by a meta-analysis to identify new genome-wide significant loci for SLE. Methods: We genotyped a cohort of 907 patients with SLE (cases) and 1524 healthy controls from Spain and performed imputation using the 1000 Genomes reference data. We tested for association using logistic regression with correction for the principal components of variation. Meta-analysis of the association results was subsequently performed on 7,110,321 variants using genetic data from a large cohort of 4036 patients with SLE and 6959 controls of Northern European ancestry. Genetic association was also tested at the pathway level after removing the effect of known risk loci using PASCAL software. Results: We identified five new loci associated with SLE at the genome-wide level of significance (p < 5 x 10(-8)): GRB2, SMYD3, ST8SIA4, LAT2 and ARHGAP27. Pathway analysis revealed several biological processes significantly associated with SLE risk: B cell receptor signaling (p = 5.28 x 10(-6)), CTLA4 co-stimulation during T cell activation (p = 3.06 x 10(-5)), interleukin-4 signaling (p = 3.97 x 10(-5)) and cell surface interactions at the vascular wall (p = 4.63 x 10(-5)). Conclusions: Our results identify five novel loci for SLE susceptibility, and biologic pathways associated via multiple low-effect-size loci.

Published
2018

47. KCNA5 gene is not confirmed as a systemic sclerosis-related pulmonary arterial hypertension genetic susceptibility factor

Author

Bossini Castillo, L, Simeon, Cp, Beretta, L, Broen, J, Vonk, Mc, Callejas, Jl, Carreira, P, Rodriguez Rodriguez, L, Garcia Portales, R, Gonzalez Gay MA, Castellvi, I, Camps, Mt, Tolosa, C, Vicente Rabaneda, E, Egurbide, Mv, Ssg, Ss, Schuerwegh, Aj, Hesselstrand, R, Lunardi, Claudio, van Laar JM, Shiels, P, Herrick, A, Worthington, J, Denton, C, Radstake, Tr, Fonseca, C, and Martin, J.

Subjects
medicine.medical_specialty, Pathology, Linkage disequilibrium, Genotype, systemic sclerosis, Hypertension, Pulmonary, Immunology, Population, Polymorphism, Single Nucleotide, Gastroenterology, Linkage Disequilibrium, White People, Cohort Studies, Kv1.5 Potassium Channel, Gene Frequency, Rheumatology, pulmonary arterial hypertension, Internal medicine, Odds Ratio, medicine, Humans, Immunology and Allergy, SNP, Genetic Predisposition to Disease, Potassium voltage-gated channel shaker-related subfamily member 5, education, skin and connective tissue diseases, Allele frequency, Netherlands, Rheumatology and Autoimmunity, Sweden, education.field_of_study, Scleroderma, Systemic, integumentary system, business.industry, Autoantibody, Odds ratio, medicine.disease, Pulmonary hypertension, United Kingdom, Italy, Spain, Genetic marker, business, Research Article
Abstract

Introduction Potassium voltage-gated channel shaker-related subfamily member 5 (KCNA5) is implicated in vascular tone regulation, and its inhibition during hypoxia produces pulmonary vasoconstriction. Recently, a protective association of the KCNA5 locus with systemic sclerosis (SSc) patients with pulmonary arterial hypertension (PAH) was reported. Hence, the aim of this study was to replicate these findings in an independent multicenter Caucasian SSc cohort. Methods The 2,343 SSc cases (179 PAH positive, confirmed by right-heart catheterization) and 2,690 matched healthy controls from five European countries were included in this study. Rs10744676 single-nucleotide polymorphism (SNP) was genotyped by using a TaqMan SNP genotyping assay. Results Individual population analyses of the selected KCNA5 genetic variant did not show significant association with SSc or any of the defined subsets (for example, limited cutaneous SSc, diffuse cutaneous SSc, anti-centromere autoantibody positive and anti-topoisomerase autoantibody positive). Furthermore, pooled analyses revealed no significant evidence of association with the disease or any of the subsets, not even the PAH-positive group. The comparison of PAH-positive patients with PAH-negative patients showed no significant differences among patients. Conclusions Our data do not support an important role of KCNA5 as an SSc-susceptibility factor or as a PAH-development genetic marker for SSc patients., This work was supported by the following grants: JM was funded by GEN-FER from the Spanish Society of Rheumatology, SAF2009-11110 from the Spanish Ministry of Science, CTS-4977 from Junta de Andalucía, Spain, in part by Redes Temáticas de Investigación Cooperativa Sanitaria Program, RD08/0075 (RIER) from Instituto de Salud Carlos III (ISCIII), Spain, and by Fondo Europeo de Desarrollo Regional (FEDER). TRDJR was funded by the VIDI laureate from the Dutch Association of Research (NWO) and Dutch Arthritis Foundation (National Reumafonds). JM and TRDJR were sponsored by the Orphan Disease Program grant from the European League Against Rheumatism (EULAR). BPCK is supported by the Dutch Diabetes Research Foundation (grant 2008.40.001) and the Dutch Arthritis Foundation (Reumafonds, grant NR 09-1-408). This study was also funded by PI-0590-2010, Consejería de Salud, Junta de Andalucía, Spain.

Published
2012

48. KCNA5 gene is not confirmed as a systemic sclerosis-related pulmonary arterial hypertension genetic susceptibility factor

Author

Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Broen, Jasper C., Vonk, Madelon C., Callejas-Rubio, J. L., Carreira, P., Rodríguez-Rodríguez, Luis, García-Portales, Rosa, González-Gay, M. A., Castellví, I., Camps, M. T., Tolosa, Carlos, Vicente, Esther, Egurbide, M. V., Spanish Scleroderma Group, Schuerwegh, A. J., Hesselstrand, R., Lunardi, C., Laar, Jacob M. van, Shiels, Paul G., Herrick, A., Worthington, J., Denton, C., Radstake, T. R., Fonseca, C., Martín, J., Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Broen, Jasper C., Vonk, Madelon C., Callejas-Rubio, J. L., Carreira, P., Rodríguez-Rodríguez, Luis, García-Portales, Rosa, González-Gay, M. A., Castellví, I., Camps, M. T., Tolosa, Carlos, Vicente, Esther, Egurbide, M. V., Spanish Scleroderma Group, Schuerwegh, A. J., Hesselstrand, R., Lunardi, C., Laar, Jacob M. van, Shiels, Paul G., Herrick, A., Worthington, J., Denton, C., Radstake, T. R., Fonseca, C., and Martín, J.

Abstract

Introduction Potassium voltage-gated channel shaker-related subfamily member 5 (KCNA5) is implicated in vascular tone regulation, and its inhibition during hypoxia produces pulmonary vasoconstriction. Recently, a protective association of the KCNA5 locus with systemic sclerosis (SSc) patients with pulmonary arterial hypertension (PAH) was reported. Hence, the aim of this study was to replicate these findings in an independent multicenter Caucasian SSc cohort. Methods The 2,343 SSc cases (179 PAH positive, confirmed by right-heart catheterization) and 2,690 matched healthy controls from five European countries were included in this study. Rs10744676 single-nucleotide polymorphism (SNP) was genotyped by using a TaqMan SNP genotyping assay. Results Individual population analyses of the selected KCNA5 genetic variant did not show significant association with SSc or any of the defined subsets (for example, limited cutaneous SSc, diffuse cutaneous SSc, anti-centromere autoantibody positive and anti-topoisomerase autoantibody positive). Furthermore, pooled analyses revealed no significant evidence of association with the disease or any of the subsets, not even the PAH-positive group. The comparison of PAH-positive patients with PAH-negative patients showed no significant differences among patients. Conclusions Our data do not support an important role of KCNA5 as an SSc-susceptibility factor or as a PAH-development genetic marker for SSc patients.

Published
2012

49. Analysis of the association between CD40 and CD40 ligand polymorphisms and systemic sclerosis

Author

Teruel, María, Simeón, Carmen P., Broen, Jasper C., Vonk, Madelon C., Carreira, P., Camps, M. T., García-Portales, Rosa, Delgado-Frías, Esmeralda, Gallego, María, Espinosa, Gerard, Spanish Scleroderma Group, Beretta, L., Airó, Paolo, Lunardi, C., Riemekasten, G., Witte, Torsten, Krieg, Thomas, Kreuter, A., Distler, J. H., Hunzelmann, Nicolas, Koeleman, B. P., Voskuyl, Alexandre E., Schuerwegh, A. J., González-Gay, M. A., Radstake, T. R., Martín, J., Teruel, María, Simeón, Carmen P., Broen, Jasper C., Vonk, Madelon C., Carreira, P., Camps, M. T., García-Portales, Rosa, Delgado-Frías, Esmeralda, Gallego, María, Espinosa, Gerard, Spanish Scleroderma Group, Beretta, L., Airó, Paolo, Lunardi, C., Riemekasten, G., Witte, Torsten, Krieg, Thomas, Kreuter, A., Distler, J. H., Hunzelmann, Nicolas, Koeleman, B. P., Voskuyl, Alexandre E., Schuerwegh, A. J., González-Gay, M. A., Radstake, T. R., and Martín, J.

Abstract

Introduction The aim of the present study was to investigate the possible role of CD40 and CD40 ligand (CD40LG) genes in the susceptibility and phenotype expression of systemic sclerosis (SSc). Methods In total, 2,670 SSc patients and 3,245 healthy individuals from four European populations (Spain, Germany, The Netherlands, and Italy) were included in the study. Five single-nucleotide polymorphisms (SNPs) of CD40 (rs1883832, rs4810485, rs1535045) and CD40LG (rs3092952, rs3092920) were genotyped by using a predesigned TaqMan allele-discrimination assay technology. Meta-analysis was assessed to determine whether an association exists between the genetic variants and SSc or its main clinical subtypes. Results No evidence of association between CD40 and CD40LG genes variants and susceptibility to SSc was observed. Similarly, no significant statistical differences were observed when SSc patients were stratified by the clinical subtypes, the serologic features, and pulmonary fibrosis. Conclusions Our results do not suggest an important role of CD40 and CD40LG gene polymorphisms in the susceptibility to or clinical expression of SSc.

Published
2012

50. A multicentre study confirms CD226 gene association with Systemic Sclerosis-related pulmonary fibrosis

Author

Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Broen, Jasper C., Vonk, Madelon C., Ríos-Fernández, Raquel, Espinosa, Gerard, Carreira, P., Camps, M. T., Castillo, María Jesús, González-Gay, M. A., Beltrán, E., Freire, María del Carmen, Narváez, J., Tolosa, Carlos, Witte, Torsten, Kreuter, A., Schuerwegh, A. J., Hoffmann-Vold, A. M., Hesselstrand, R., Lunardi, C., Laar, Jacob M. van, Chee, M. M., Herrick, A., Koeleman, B. P., Denton, C., Fonseca, C., Radstake, T. R., Martín, J., Spanish Scleroderma Group, Bossini-Castillo, L., Simeón, Carmen P., Beretta, L., Broen, Jasper C., Vonk, Madelon C., Ríos-Fernández, Raquel, Espinosa, Gerard, Carreira, P., Camps, M. T., Castillo, María Jesús, González-Gay, M. A., Beltrán, E., Freire, María del Carmen, Narváez, J., Tolosa, Carlos, Witte, Torsten, Kreuter, A., Schuerwegh, A. J., Hoffmann-Vold, A. M., Hesselstrand, R., Lunardi, C., Laar, Jacob M. van, Chee, M. M., Herrick, A., Koeleman, B. P., Denton, C., Fonseca, C., Radstake, T. R., Martín, J., and Spanish Scleroderma Group

Abstract

Introduction CD226 genetic variants have been associated with a number of autoimmune diseases and recently with systemic sclerosis (SSc). The aim of this study was to test the influence of CD226 loci in SSc susceptibility, clinical phenotypes and autoantibody status in a large multicenter European population. Methods A total of seven European populations of Caucasian ancestry were included, comprising 2,131 patients with SSc and 3,966 healthy controls. Three CD226 single nucleotide polymorphisms (SNPs), rs763361, rs3479968 and rs727088, were genotyped using Taqman 5'allelic discrimination assays. Results Pooled analyses showed no evidence of association of the three SNPs, neither with the global disease nor with the analyzed subphenotypes. However, haplotype block analysis revealed a significant association for the TCG haplotype (SNP order: rs763361, rs34794968, rs727088) with lung fibrosis positive patients (P Bonf = 3.18E-02 OR 1.27 (1.05 to 1.54)). Conclusion Our data suggest that the tested genetic variants do not individually influence SSc susceptibility but a CD226 three-variant haplotype is related with genetic predisposition to SSc-related pulmonary fibrosis.

Published
2012

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