LncRNA-mRNA integrated networks in the neuroendocrine system of bisphenol a-treated mice induce cellular dysfunctions by disrupting transcriptional homeostasis

• Autores: Oh, Seung-Mi, Lim, Byeonghwi, Park, Yoon-Been, Jang, Min-Jae, Lim, Seok-Won, Lim, Chiwoong, Kim, Do-Young, Park, Yejee, Seo, Young-Jun, Kim, Jun-Mo
• Formato: artículo
• Fecha de Publicación: 2025
• Institución: Instituto Nacional de Enfermedades Neoplásicas
• Repositorio: INEN-Institucional
• Lenguaje: inglés
• OAI Identifier: oai:repositorio.inen.sld.pe:20.500.14703/492
• Enlace del recurso: https://doi.org/10.1080/19768354.2025.2569881; https://hdl.handle.net/20.500.14703/492
• Nivel de acceso: acceso abierto
• Materia: Bisphenol A; hypothalamuspituitary-thyroid (HPT) axis; mRNA-lncRNA interaction network; immuneneuroendocrine network (INEN); transcriptional reprogramming; https://purl.org/pe-repo/ocde/ford#3.02.21

Bisphenol A (BPA) is a widely used xenoestrogen that can disrupt neuroendocrine and immune regulation through multiple hormone receptors. This study investigated BPAinduced long non-coding RNA (lncRNA)-mRNA interactions in the cerebral cortex and hypothalamic-pituitary-thyroid (HPT) axis of adult male mice. Transcriptome sequencing and comprehensive lncRNA annotation identified 14,858 novel lncRNA transcripts. Integrated network analysis using weighted gene co-expression network analysis (WGCNA) revealed four distinct tissue-specific modules: neuronal signaling alterations (Tac1, Htr1b, Npy), RNA splicing modifications (Srsf5), PI3K/Akt-mediated cellular dysfunction (Creb5, Cdkn1a), and immune receptor signaling disruptions (Trbv15, Fcrla). These findings suggest that BPA reprograms transcriptional networks in a tissue-specific manner, potentially disrupting hormone-related neurotransmission, metabolic regulation, and immune signaling via lncRNA-mediated mechanisms. Such systems-level reprogramming of the immune-neuroendocrine network (INEN) provides novel mechanistic insights and biomarker candidates for assessing and mitigating the health impacts of environmental endocrine disruptors.