Major depressive disorder (MDD) is a debilitating and widespread illness that exerts significant personal and socioeconomic consequences. Recent genetic and brain-imaging studies suggest that bicaudal C homolog 1 gene (BICC1), which codes for an RNA-binding protein, may be associated with depression. Here, we show that BICC1 mRNA is upregulated in the dorsolateral prefrontal cortex and dentate gyrus of human postmortem MDD patients. We also show that BICC1 is increased in the prefrontal cortex and hippocampus in the rat chronic unpredictable stress (CUS) model of depression. In addition, we show in vivo that a single acute antidepressant dose of ketamine leads to a rapid decrease of BICC1 mRNA, while in vitro, we show that this is likely due to neuronal activity-induced downregulation of BICC1. Finally, we show that BICC1 knockdown in the hippocampus protects rats from CUS-induced anhedonia. Taken together, these findings identify a role for increased levels of BICC1 in the pathophysiology of depressive behavior.
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http://dx.doi.org/10.1038/npp.2014.227 | DOI Listing |
Kaohsiung J Med Sci
December 2024
Hunan University of Medicine, Huaihua, Hunan Province, People's Republic of China.
Epithelial-mesenchymal transition (EMT) is a critical stage in the metastasis of gastric cancer (GC). Further clarification of the EMT process in GC is still needed. This study examined the effects of the NEDD4L/BICC1 axis on GC proliferation and the EMT process.
View Article and Find Full Text PDFPlast Reconstr Surg Glob Open
November 2024
From the University of Luebeck, Luebeck, Germany.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is primarily of adult-onset and caused by pathogenic variants in or . Yet, disease expression is highly variable and includes very early-onset PKD presentations or infancy. In animal models, the RNA-binding molecule Bicc1 has been shown to play a crucial role in the pathogenesis of PKD.
View Article and Find Full Text PDFClin Cancer Res
November 2024
Université Paris-Saclay, Gustave Roussy, Inserm U981, Villejuif, France.
Purpose: Understanding resistance to selective FGFR inhibitors is crucial to improve the clinical outcomes of patients with FGFR2-driven malignancies.
Experimental Design: We analyzed sequential ctDNA, ± whole-exome sequencing, or targeted next-generation sequencing on tissue biopsies from patients with tumors harboring activating FGFR2 alterations progressing on pan-FGFR-selective inhibitors, collected in the prospective UNLOCK program. FGFR2::BICC1 Ba/F3 and patient-derived xenograft models were used for functional studies.
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