Nucleus pulposus cell network modelling in the intervertebral disc

Intervertebral disc degeneration (IDD) results from an imbalance between anabolic and catabolic processes in the extracellular matrix (ECM). Due to complex biochemical interactions, a comprehensive understanding is needed. This study presents a regulatory network model (RNM) for nucleus pulposus cel...

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Detalhes bibliográficos
Autores: Tseranidou, Sofia, Segarra-Queralt, Maria, Chemorion, Francis Kiptengwer, Le Maitre, Christine L., Piñero González, Janet, 1977-, Noailly, Jérôme
Tipo de documento: artigo
Estado:Versão publicada
Data de publicação:2025
País:España
Recursos:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositório:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:10230/72089
Acesso em linha:http://hdl.handle.net/10230/72089
http://dx.doi.org/10.1038/s41540-024-00479-6
Access Level:Acceso aberto
Palavra-chave:Disc intervertebral
Bioquímica
Vertebrats -- Anatomia
Descrição
Resumo:Intervertebral disc degeneration (IDD) results from an imbalance between anabolic and catabolic processes in the extracellular matrix (ECM). Due to complex biochemical interactions, a comprehensive understanding is needed. This study presents a regulatory network model (RNM) for nucleus pulposus cells (NPC), representing normal intervertebral disc (IVD) conditions. The RNM includes 33 proteins, and 153 interactions based on literature, incorporating key NPC regulatory mechanisms. A semi-quantitative approach calculates the basal steady state, accurately reflecting normal NPC activity. Model validation through published studies replicated pro-catabolic and pro-anabolic shifts, emphasizing the roles of transforming growth factor beta (TGF-β) and interleukin-1 receptor antagonist (IL-1Ra) in ECM regulation. This IVD RNM is a valuable tool for predicting IDD progression, offering insights into ECM degradation mechanisms and guiding experimental research on IVD health and degeneration.