Williams neural stem cells new model for insight into microRNA dysregulation

Palacios‐Reyes, Carmen; Espinosa, Ana; Contreras, Alejandra; Ordoñez, Rosa M.; Hidalgo‐Miranda, Alfredo; Rubio-Gayosso, Iván; Garcia-Alonso, Patricia; Benítez‐King, Gloria; Ramírez-Rodríguez, Gerardo; Nájera, Nayelli; Ita-Islas, Israel; Araujo, A Isibasi; Romero-Córdoba, Sandra; Palma, Ícela

doi:10.2741/e683

Cited by 2 publications

(1 citation statement)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some miRNAs have been identified in syndromes characterized by presenting intellectual disability or in ID of known etiology. For example, Williams syndrome is associated with miR-let-7f-2, miR-let-7g, miR-206, miR-125b, let-7c, and miR-200c [9], and Fragile X syndrome with miR-132, which was associated with the FMRP protein that affects neuronal morphology and synaptic strength [10]. miR-134, miR-25, and miR-137 have been directly related to the proliferation process of neural stem cells and neural progenitor cells [11][12][13].…”

Section: Of 14mentioning

confidence: 99%

Overexpression of miR-25 Downregulates the Expression of ROBO2 in Idiopathic Intellectual Disability

Ordoñez-Razo,

Gutierrez-López,

Araujo-Solis

et al. 2024

IJMS

View full text Add to dashboard Cite

Idiopathic intellectual disability (IID) encompasses the cases of intellectual disability (ID) without a known cause and represents approximately 50% of all cases. Neural progenitor cells (NPCs) from the olfactory neuroepithelium (NEO) contain the same information as the cells found in the brain, but they are more accessible. Some miRNAs have been identified and associated with ID of known etiology. However, in idiopathic ID, the effect of miRNAs is poorly understood. The aim of this study was to determine the miRNAs regulating the expression of mRNAs that may be involved in development of IID. Expression profiles were obtained using NPC–NEO cells from IID patients and healthy controls by microarray. A total of 796 miRNAs and 28,869 mRNAs were analyzed. Several miRNAs were overexpressed in the IID patients compared to controls. miR-25 had the greatest expression. In silico analysis showed that ROBO2 was the target for miR-25, with the highest specificity and being the most down-regulated. In vitro assay showed an increase of miR-25 expression induced a decrease in ROBO2 expression. In neurodevelopment, ROBO2 plays a crucial role in episodic learning and memory, so its down-regulation, caused by miR-25, could have a fundamental role in the intellectual disability that, until now, has been considered idiopathic.

show abstract

Section: Of 14mentioning

confidence: 99%

Overexpression of miR-25 Downregulates the Expression of ROBO2 in Idiopathic Intellectual Disability

Ordoñez-Razo,

Gutierrez-López,

Araujo-Solis

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

Exome chip analyses in adult attention deficit hyperactivity disorder

et al. 2016

View full text Add to dashboard Cite

Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable childhood-onset neuropsychiatric condition, often persisting into adulthood. The genetic architecture of ADHD, particularly in adults, is largely unknown. We performed an exome-wide scan of adult ADHD using the Illumina Human Exome Bead Chip, which interrogates over 250 000 common and rare variants. Participants were recruited by the International Multicenter persistent ADHD CollaboraTion (IMpACT). Statistical analyses were divided into 3 steps: (1) gene-level analysis of rare variants (minor allele frequency (MAF)<1%); (2) single marker association tests of common variants (MAF⩾1%), with replication of the top signals; and (3) pathway analyses. In total, 9365 individuals (1846 cases and 7519 controls) were examined. Replication of the most associated common variants was attempted in 9847 individuals (2077 cases and 7770 controls) using fixed-effects inverse variance meta-analysis. With a Bonferroni-corrected significance level of 1.82E−06, our analyses of rare coding variants revealed four study-wide significant loci: 6q22.1 locus (P=4.46E−08), where NT5DC1 and COL10A1 reside; the SEC23IP locus (P=6.47E−07); the PSD locus (P=7.58E−08) and ZCCHC4 locus (P=1.79E−06). No genome-wide significant association was observed among the common variants. The strongest signal was noted at rs9325032 in PPP2R2B (odds ratio=0.81, P=1.61E−05). Taken together, our data add to the growing evidence of general signal transduction molecules (NT5DC1, PSD, SEC23IP and ZCCHC4) having an important role in the etiology of ADHD. Although the biological implications of these findings need to be further explored, they highlight the possible role of cellular communication as a potential core component in the development of both adult and childhood forms of ADHD.

show abstract

Williams neural stem cells new model for insight into microRNA dysregulation

Cited by 2 publications

References 87 publications

Overexpression of miR-25 Downregulates the Expression of ROBO2 in Idiopathic Intellectual Disability

Overexpression of miR-25 Downregulates the Expression of ROBO2 in Idiopathic Intellectual Disability

Exome chip analyses in adult attention deficit hyperactivity disorder

Contact Info

Product

Resources

About