Cecilia Cintora-Ahumada
Research Subjects
Research Interests
Cecilia Cintora-Ahumada has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Elena Aréchaga-Ocampo
Departamento de Ciencias Naturales, Universidad Autónoma Metropolitana, Unidad Cuajimalpa, Mexico City 05348, Mexico
1 shared publication - Lizbel León-Solís
Department of Microbiology Escuela Nacional de Ciencias Biológicas Instituto Politécnico Nacional Mexico City Mexico
1 shared publication - Norberto Leyva-García
Laboratorio de Medicina Genómica, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City 14389, Mexico
1 shared publication - Oscar Hernández-Hernández
Laboratory of Genomic Medicine, Department of Genetics, National Rehabilitation Institute (INR-LGII), Mexico City, Mexico
1 shared publication - Osvaldo Arias Pérez
Laboratorio de Medicina Genómica, Departamento de Genética, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra”, Mexico City 14389, Mexico
1 shared publication - Rafael Franco-Cendejas
Affiliation Biomedical Research Subdirection, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City, Mexico
1 shared publication
Latest Publications
- Open Access
Enrichment of H3S28p and H3K9me2 Epigenetic Marks on Inflammatory-Associated Gene Promoters in Response to Severe Burn Injury
Background: Severe burns activate systemic inflammation and lead to an increase in cytokine levels. Epigenetic elements are key regulators of inflammation; however, their involvement in severe burns has not been studied. In this work, we aimed to unveil the histone H3 posttranslational modifications (PTM) profile and their enrichment in promoters of inflammatory genes in response to severe burns. Methods: The levels of H3 PTMs were analyzed by ELISA assays in circulating cells from burn patients. ChIP assays were conducted to evaluate the enrichment of H3K9me2 and H3S28p at the promoter of CXCL8, IL-17, TNFA, IL-6, FOS, and IL-1B genes. Results: We found that eight H3 PTMs decreased at 5 days post-burn. Burn patients showed a decreased enrichment of H3K9me2 in CXCL8, IL-17, and TNFA promoters, whereas IL-6, FOS, and IL-1B promoters displayed an H3S28p enrichment diminution during the first 10 days post-burn. Interestingly, burn-injured septic patients exhibited an increased enrichment of H3K9me2 in TNFA, IL-1B, CXCL8, and IL-17 promoters, whereas H3S28p was increased in promoters of TNFA and IL-1B at 1 dpb. Conclusion: Severe burns trigger epigenetic changes and differential H3 PTM enrichment at inflammation gene promoters. Epigenetic misregulation of H3 may be involved in sepsis occurrence after severe burn injury.
Open AccessEnrichment of H3S28p and H3K9me2 Epigenetic Marks on Inflammatory-Associated Gene Promoters in Response to Severe Burn Injury
Background: Severe burns activate systemic inflammation and lead to an increase in cytokine levels. Epigenetic elements are key regulators of inflammation; however, their involvement in severe burns has not been studied. In this work, we aimed to unveil the histone H3 posttranslational modifications (PTM) profile and their enrichment in promoters of inflammatory genes in response to severe burns. Methods: The levels of H3 PTMs were analyzed by ELISA assays in circulating cells from burn patients. ChIP assays were conducted to evaluate the enrichment of H3K9me2 and H3S28p at the promoter of CXCL8, IL-17, TNFA, IL-6, FOS, and IL-1B genes. Results: We found that eight H3 PTMs decreased at 5 days post-burn. Burn patients showed a decreased enrichment of H3K9me2 in CXCL8, IL-17, and TNFA promoters, whereas IL-6, FOS, and IL-1B promoters displayed an H3S28p enrichment diminution during the first 10 days post-burn. Interestingly, burn-injured septic patients exhibited an increased enrichment of H3K9me2 in TNFA, IL-1B, CXCL8, and IL-17 promoters, whereas H3S28p was increased in promoters of TNFA and IL-1B at 1 dpb. Conclusion: Severe burns trigger epigenetic changes and differential H3 PTM enrichment at inflammation gene promoters. Epigenetic misregulation of H3 may be involved in sepsis occurrence after severe burn injury.