An inflammation-associated lncRNA induces neuronal damage via mitochondrial dysfunction

Immune disease-associated non-coding SNPs, which often locate in tissue-specific regulatory elements, are emerging as key factors in gene regulation. Among these elements, long non-coding RNAs (lncRNAs) participate in many cellular processes, and their characteristics make these molecules appealing therapeutic targets. In this study, we have studied lncRNA <i>LOC339803</i> in the context of neuronal cells, which is located in autoimmunity-associated region 2p15 and recently described to have a proinflammatory role in intestinal disorders. Using human brain samples and a wide variety of <i>in vitro</i> techniques, we have showed a differential function of this lncRNA in neuronal cells. We have further demonstrated the role of <i>LOC339803</i> in maintaining hexokinase 2 (HK2) levels and thus mitochondrial integrity, partially explaining the implication of the lncRNA in multiple sclerosis (MS) pathogenesis. Our results show the importance of cell-type-specific studies in the case of regulatory lncRNAs. We present <i>LOC339803</i> as a candidate for further studies as a mitochondrial dysfunction marker or possible therapeutic target in neurodegeneration.

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Journal
Molecular Therapy — Nucleic Acids
Published
2025-04-02
DOI
https://doi.org/10.1016/j.omtn.2025.102533
Citations
1
Primary Topic
Cancer-related molecular mechanisms research
Type
article
Field-Weighted Citation Impact
0.94
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article

An inflammation-associated lncRNA induces neuronal damage via mitochondrial dysfunction

J. Javier Meana, Ainara Castellanos‐Rubio, Bibo Yang, Henar Rojas‐Márquez et al.
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Molecular Therapy — Nucleic Acids
Cancer-related molecular mechanisms research
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article

An inflammation-associated lncRNA induces neuronal damage via mitochondrial dysfunction

J. Javier Meana, Ainara Castellanos‐Rubio, Bibo Yang, Henar Rojas‐Márquez, Izortze Santín, Ajai K. Tripathi, Ane Olazagoitia‐Garmendia, Ranjan Dutta, Itziar Martín Ruíz, Lucas Schirmer, Mariana Igoillo‐Esteve, Jon Mentxaka, Yiliang Ding, Juan Anguíta, Cristina Moreno‐Castro, Tim Trobisch, Ariadne Rodriguez Etxebarria
article en
1 citations

Abstract

Immune disease-associated non-coding SNPs, which often locate in tissue-specific regulatory elements, are emerging as key factors in gene regulation. Among these elements, long non-coding RNAs (lncRNAs) participate in many cellular processes, and their characteristics make these molecules appealing therapeutic targets. In this study, we have studied lncRNA <i>LOC339803</i> in the context of neuronal cells, which is located in autoimmunity-associated region 2p15 and recently described to have a proinflammatory role in intestinal disorders. Using human brain samples and a wide variety of <i>in vitro</i> techniques, we have showed a differential function of this lncRNA in neuronal cells. We have further demonstrated the role of <i>LOC339803</i> in maintaining hexokinase 2 (HK2) levels and thus mitochondrial integrity, partially explaining the implication of the lncRNA in multiple sclerosis (MS) pathogenesis. Our results show the importance of cell-type-specific studies in the case of regulatory lncRNAs. We present <i>LOC339803</i> as a candidate for further studies as a mitochondrial dysfunction marker or possible therapeutic target in neurodegeneration.

Molecular Therapy — Nucleic AcidsVol. 36(2)
John Innes Centre (GB), Ikerbasque (ES), Université Libre de Bruxelles (BE), University of the Basque Country (ES), University of Mannheim (DE), Heidelberg University (DE), Norwich Research Park (GB), University Hospital Heidelberg (DE), Cleveland Clinic Lerner College of Medicine (US), BioCruces Health research Institute (ES), Centro de Investigación Biomédica en Red de Salud Mental (ES), Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas (ES), Bernstein Center for Computational Neuroscience Heidelberg-Mannheim (DE), CIC bioGUNE (ES), University Medical Centre Mannheim (DE), Heidelberg University (US)
Good health and well-being
Openalex Percentile: Top 27%
Cancer-related molecular mechanisms research
0.94
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