Publicaciones de Bairon Exe Hernández-Rojas
2026
Hernández-Rojas, Bairon; Murgas, Paola; Riadi, Gonzalo
Changes in transposable elements expression in male and female mice liver throughout aging Artículo de revista
En: 2026.
@article{Hernández-Rojas2026,
title = {Changes in transposable elements expression in male and female mice liver throughout aging},
author = {Bairon Hernández-Rojas and Paola Murgas and Gonzalo Riadi},
doi = {10.1007/s11357-025-02065-y},
year = {2026},
date = {2026-01-06},
urldate = {2026-01-06},
abstract = {Aging has traditionally been studied through the lens of protein-coding genes, with a strong bias toward data derived from male organisms. As a result, the role of non-coding elements and potential sex-specific differences remains largely unexplored. Transposable elements (TEs), mobile sequences capable of altering genome structure and regulating gene expression, have recently gained attention for their roles in development and aging. However, despite this growing interest, key aspects of TE expression dynamics are still poorly characterized, particularly in female tissues. To address this gap, we analyzed TE expression in RNA-Seq liver tissue from male (8, 26, 60, 78, and 104 weeks) and female (3, 24, 48, and 72 weeks) mice. Our results reveal distinct TE expression trends between sexes. While previous studies report increased TE expression with aging, we identified a subset of TEs with decreasing expression over time, differing between males and females. We also observed inverse expression trends between a few TEs and their nearby genes, supporting a potential regulatory relationship. We identified TEs with changing expression (CE TEs) through age associated with nearby genes showing strong expression correlations (|ρ|≥ 0.6). In males, correlated genes such as Txnrd2, Mthfd1, and Dkk3 are involved in redox regulation, one-carbon metabolism, and Wnt signaling, respectively, while in females, Thrb and Cd55 are linked to metabolic regulation and immune protection. These associations suggest that TE activity may be functionally coupled to transcriptional programs relevant to liver physiology and aging. These findings highlight the importance of examining TE expression in both sexes and suggest their potential regulatory roles in age-related liver physiology.
},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
2025
Riquelme, Ian; Carrillanca, Daniela; Sánchez-Pérez, Camila; Monterroza, Andrea; Hernández-Rojas, Bairon; Riadi, Gonzalo; Cancino, Gonzalo I; Murgas, Paola
Loss of stimulator of interferon genes (STING) promotes accumulation of cholesterol and triglycerides throughout life in mice Artículo de revista
En: 2025.
@article{nokey,
title = {Loss of stimulator of interferon genes (STING) promotes accumulation of cholesterol and triglycerides throughout life in mice},
author = {Ian Riquelme and Daniela Carrillanca and Camila Sánchez-Pérez and Andrea Monterroza and Bairon Hernández-Rojas and Gonzalo Riadi and Gonzalo I Cancino and Paola Murgas},
doi = {10.1186/s40659-025-00624-3},
year = {2025},
date = {2025-07-02},
urldate = {2025-07-02},
abstract = {The Stimulator of Interferon Genes (STING) pathway is pivotal in innate immunity, facilitating the detection of cytosolic DNA and initiating type I interferon-dependent responses. In addition to its immunological roles, STING has been increasingly associated with metabolic regulation, since research indicates that its inhibition can diminish inflammation, lipid accumulation, and tissue damage in obesity and other metabolic disorders. The findings have prompted the suggestion of STING inhibition as a viable treatment approach for metabolic illness. Nonetheless, the physiological function of STING in lipid homeostasis under normal settings remains largely unexplored, as does the impact of its absence on metabolism throughout various life stages in the absence of disease. This information deficit is crucial, particularly in light of the increasing interest in the long-term pharmacological suppression of STING.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
2022
Herrada, Andrés A.; Olate-Briones, Alexandra; Lazo-Amador, Rodrigo; Liu, Chaohong; Hernández-Rojas, Bairon; Riadi, Gonzalo; Escobedo, Noelia
Lymph Leakage Promotes Immunosuppression by Enhancing Anti-Inflammatory Macrophage Polarization Artículo de revista
En: Frontiers in Immunology, vol. 13, pp. 841641, 2022, ISSN: 1664-3224.
@article{herrada_lymph_2022,
title = {Lymph Leakage Promotes Immunosuppression by Enhancing Anti-Inflammatory Macrophage Polarization},
author = {Andrés A. Herrada and Alexandra Olate-Briones and Rodrigo Lazo-Amador and Chaohong Liu and Bairon Hernández-Rojas and Gonzalo Riadi and Noelia Escobedo},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2022.841641/full},
doi = {10.3389/fimmu.2022.841641},
issn = {1664-3224},
year = {2022},
date = {2022-05-01},
urldate = {2024-12-14},
journal = {Frontiers in Immunology},
volume = {13},
pages = {841641},
abstract = {Lymphatic vasculature is a network of capillaries and vessels capable of draining extracellular fluid back to blood circulation and to facilitate immune cell migration. Although the role of the lymphatic vasculature as coordinator of fluid homeostasis has been extensively studied, the consequences of abnormal lymphatic vasculature function and impaired lymph drainage have been mostly unexplored. Here, by using the
Prox1
+/–
mice with defective lymphatic vasculature and lymphatic leakage, we provide evidence showing that lymph leakage induces an immunosuppressive environment by promoting anti-inflammatory M2 macrophage polarization in different inflammatory conditions. In fact, by using a mouse model of tail lymphedema where lymphatic vessels are thermal ablated leading to lymph accumulation, an increasing number of anti-inflammatory M2 macrophages are found in the lymphedematous tissue. Moreover, RNA-seq analysis from different human tumors shows that reduced lymphatic signature, a hallmark of lymphatic dysfunction, is associated with increased M2 and reduced M1 macrophage signatures, impacting the survival of the patients. In summary, we show that lymphatic vascular leakage promotes an immunosuppressive environment by enhancing anti-inflammatory macrophage differentiation, with relevance in clinical conditions such as inflammatory bowel diseases or cancer.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Prox1
+/–
mice with defective lymphatic vasculature and lymphatic leakage, we provide evidence showing that lymph leakage induces an immunosuppressive environment by promoting anti-inflammatory M2 macrophage polarization in different inflammatory conditions. In fact, by using a mouse model of tail lymphedema where lymphatic vessels are thermal ablated leading to lymph accumulation, an increasing number of anti-inflammatory M2 macrophages are found in the lymphedematous tissue. Moreover, RNA-seq analysis from different human tumors shows that reduced lymphatic signature, a hallmark of lymphatic dysfunction, is associated with increased M2 and reduced M1 macrophage signatures, impacting the survival of the patients. In summary, we show that lymphatic vascular leakage promotes an immunosuppressive environment by enhancing anti-inflammatory macrophage differentiation, with relevance in clinical conditions such as inflammatory bowel diseases or cancer.
2021
Arrey-Salas, Oscar; Caris-Maldonado, José Carlos; Hernández-Rojas, Bairon; Gonzalez, Enrique
Comprehensive Genome-Wide Exploration of C2H2 Zinc Finger Family in Grapevine (Vitis vinifera L.): Insights into the Roles in the Pollen Development Regulation Artículo de revista
En: Genes, vol. 12, no 2, pp. 302, 2021, ISSN: 2073-4425.
@article{arrey-salas_comprehensive_2021,
title = {Comprehensive Genome-Wide Exploration of C2H2 Zinc Finger Family in Grapevine (Vitis vinifera L.): Insights into the Roles in the Pollen Development Regulation},
author = {Oscar Arrey-Salas and José Carlos Caris-Maldonado and Bairon Hernández-Rojas and Enrique Gonzalez},
url = {https://www.mdpi.com/2073-4425/12/2/302},
doi = {10.3390/genes12020302},
issn = {2073-4425},
year = {2021},
date = {2021-02-01},
urldate = {2024-12-14},
journal = {Genes},
volume = {12},
number = {2},
pages = {302},
abstract = {Some C2H2 zinc-finger proteins (ZFP) transcription factors are involved in the development of pollen in plants. In grapevine (Vitis vinifera L.), it has been suggested that abnormalities in pollen development lead to the phenomenon called parthenocarpy that occurs in some varieties of this cultivar. At present, a network involving several transcription factors types has been revealed and key roles have been assigned to members of the C2H2 zinc-finger proteins (ZFP) family in model plants. However, particularities of the regulatory mechanisms controlling pollen formation in grapevine remain unknown. In order to gain insight into the participation of ZFPs in grapevine gametophyte development, we performed a genome-wide identification and characterization of genes encoding ZFP (VviZFP family). A total of 98 genes were identified and renamed based on the gene distribution into grapevine genome. The analysis performed indicate significant changes throughout VviZFP genes evolution explained by high heterogeneity in sequence, length, number of ZF and presence of another conserved domains. Moreover, segmental duplication participated in the gene family expansion in grapevine. The VviZFPs were classified based on domain and phylogenetic analysis into three sets and different groups. Heat-map demonstrated differential and tissue-specific expression patterns of these genes and k-means clustering allowed to identify a group of putative orthologs to some ZFPs related to pollen development. In transgenic plants carrying the promVviZFP13::GUS and promVviZFP68::GUS constructs, GUS signals were detectable in the anther and mature pollen grains. Expression profiling of selected VviZFP genes showed differential expression pattern during flower development and provides a basis for deepening in the understanding of VviZFPs role on grapevine reproductive development.},
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pubstate = {published},
tppubtype = {article}
}


