ArticleMolecular psychiatry2021
TCF7L2 lncRNA: a link between bipolar disorder and body mass index through glucocorticoid signaling.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Study of Estrogen Receptor-Mediated PGx-eQTLs Identifies Genetic Determinants of Breast Cancer Endocrine Therapy Response.International journal of molecular sciences · 2026Article
- Written in the Stars: Astrocyte Biology From Evolution to Disease.Acta physiologica (Oxford, England) · 2026Review
- The Regulatory Potential of Long Non-Coding RNAs in Bipolar Disorder.International journal of molecular sciences · 2026Review
- The Habenula's role in major depressive disorder: recent insights from preclinical and human studies.Translational psychiatry · 2026Review
- Inflammatory Factors Derived From Metabolic Dysfunction-Alcoholic Fatty Liver Disease: Inducers of Anxiety and Spatial Memory Impairment.Mediators of inflammation · 2026Article
- Glucocorticoids regulate the human non-coding genome.bioRxiv : the preprint server for biology · 2025Article
- Genetic modulation of lncPSMB1 confers non-syndromic cleft lip with or without cleft palate susceptibility by promoting cell apoptosis.Communications biology · 2025Article
- Neuronal TCF7L2 in Lateral Habenula Is Involved in Stress-Induced Depression.International journal of molecular sciences · 2024Article
- Androgen receptor-mediated pharmacogenomic expression quantitative trait loci: implications for breast cancer response to AR-targeting therapy.Breast cancer research : BCR · 2024Article
- Astrocytic transcriptional and epigenetic mechanisms of drug addiction.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Astrocytic β-catenin signaling via TCF7L2 regulates synapse development and social behavior.Molecular psychiatry · 2024Article
- Myocardial Recovery in Recent Onset Dilated Cardiomyopathy: Role ofCirculation research · 2023Article
- Heightened inflammation in bipolar disorder occurs independent of symptom severity and is explained by body mass index.Brain, behavior, & immunity - health · 2023Article
- Review
- Glucocorticoids unmask silent non-coding genetic risk variants for common diseases.Nucleic acids research · 2022Article
- The genetics of bipolar disorder with obesity and type 2 diabetes.Journal of affective disorders · 2022Review
- Identification of Two Genetic Loci Associated with Leukopenia after Chemotherapy in Patients with Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Bipolar disorder (BD) and obesity are highly comorbid. We previously performed a genome-wide association study (GWAS) for BD risk accounting for the effect of body mass index (BMI), which identified a genome-wide significant single-nucleotide polymorphism (SNP) in the gene encoding the transcription factor 7 like 2 (TCF7L2). However, the molecular function of TCF7L2 in the central nervous system (CNS) and its possible role in the BD and BMI interaction remained unclear. In the present study, we demonstrated by studying human induced pluripotent stem cell (hiPSC)-derived astrocytes, cells that highly express TCF7L2 in the CNS, that the BD-BMI GWAS risk SNP is associated with glucocorticoid-dependent repression of the expression of a previously uncharacterized TCF7L2 transcript variant. That transcript is a long non-coding RNA (lncRNA-TCF7L2) that is highly expressed in the CNS but not in peripheral tissues such as the liver and pancreas that are involved in metabolism. In astrocytes, knockdown of the lncRNA-TCF7L2 resulted in decreased expression of the parent gene, TCF7L2, as well as alterations in the expression of a series of genes involved in insulin signaling and diabetes. We also studied the function of TCF7L2 in hiPSC-derived astrocytes by integrating RNA sequencing data after TCF7L2 knockdown with TCF7L2 chromatin-immunoprecipitation sequencing (ChIP-seq) data. Those studies showed that TCF7L2 directly regulated a series of BD risk genes. In summary, these results support the existence of a CNS-based mechanism underlying BD-BMI genetic risk, a mechanism based on a glucocorticoid-dependent expression quantitative trait locus that regulates the expression of a novel TCF7L2 non-coding transcript.
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