Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndrome
Abstract Background Down syndrome (DS) is the most common chromosomal survival aneuploidy. The increase in DS life expectancy further heightens the risk of dementia, principally early‐onset Alzheimer's disease (AD). AD risk in DS is higher, considering that this population may also develop meta...
Main Authors: | , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Wiley
2022-06-01
|
Series: | Molecular Genetics & Genomic Medicine |
Subjects: | |
Online Access: | https://doi.org/10.1002/mgg3.1938 |
_version_ | 1828810729360195584 |
---|---|
author | Jesús Manuel Pérez‐Villarreal Katia Aviña‐Padilla Evangelina Beltrán‐López Alma Marlene Guadrón‐Llanos Esther López‐Bayghen Javier Magaña‐Gómez Marco Antonio Meraz‐Ríos Alfredo Varela‐Echavarría Carla Angulo‐Rojo |
author_facet | Jesús Manuel Pérez‐Villarreal Katia Aviña‐Padilla Evangelina Beltrán‐López Alma Marlene Guadrón‐Llanos Esther López‐Bayghen Javier Magaña‐Gómez Marco Antonio Meraz‐Ríos Alfredo Varela‐Echavarría Carla Angulo‐Rojo |
author_sort | Jesús Manuel Pérez‐Villarreal |
collection | DOAJ |
description | Abstract Background Down syndrome (DS) is the most common chromosomal survival aneuploidy. The increase in DS life expectancy further heightens the risk of dementia, principally early‐onset Alzheimer's disease (AD). AD risk in DS is higher, considering that this population may also develop metabolic diseases such as obesity, dyslipidemias, and diabetes mellitus. The extra genetic material that characterizes DS causes an imbalance in the genetic dosage, including over‐expression of AD's key pathophysiological molecules and the gene expression regulators, the microRNAs (miRNAs). Two miRNAs, chromosome 21‐encoded, miR‐155, and let‐7c, are associated with cognitive impairment and dementia in adults; but, expression dynamics and relationship with clinical variables during the DS's lifespan had remained hitherto unexplored. Methods The anthropometric, clinical, biochemical, and profile expression of circulating miR‐155 and let‐7c were analyzed in a population of 52 control and 50 DS subjects divided into the young group (Aged ≤20 years) and the adult group (Aged ≥21 years). Results The expression changes for miR‐155 were not significant; nevertheless, a negative correlation with HDL‐Cholesterol concentrations was observed. Notably, let‐7c was over‐expressed in DS from young and old ages. Conclusion Overall, our results suggest that let‐7c plays a role from the early stages of DS's cognitive impairment while overexpression of miR‐155 may be related to lipid metabolism changes. Further studies of both miRNAs will shed light on their potential as therapeutic targets to prevent or delay DS's cognitive impairment. |
first_indexed | 2024-12-12T09:17:19Z |
format | Article |
id | doaj.art-7bbf8839004d4efb9bd2da1daa09cb4a |
institution | Directory Open Access Journal |
issn | 2324-9269 |
language | English |
last_indexed | 2024-12-12T09:17:19Z |
publishDate | 2022-06-01 |
publisher | Wiley |
record_format | Article |
series | Molecular Genetics & Genomic Medicine |
spelling | doaj.art-7bbf8839004d4efb9bd2da1daa09cb4a2022-12-22T00:29:21ZengWileyMolecular Genetics & Genomic Medicine2324-92692022-06-01106n/an/a10.1002/mgg3.1938Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndromeJesús Manuel Pérez‐Villarreal0Katia Aviña‐Padilla1Evangelina Beltrán‐López2Alma Marlene Guadrón‐Llanos3Esther López‐Bayghen4Javier Magaña‐Gómez5Marco Antonio Meraz‐Ríos6Alfredo Varela‐Echavarría7Carla Angulo‐Rojo8Laboratorio de Neurociencias, Centro de Investigación Aplicada a la Salud Pública (CIASaP), Facultad de Medicina Universidad Autónoma de Sinaloa Culiacán MexicoInstituto de Neurobiología Universidad Nacional Autónoma de México Querétaro MexicoLaboratorio Edificio Central, Facultad de Ciencias Químico‐Biológicas Universidad Autónoma de Sinaloa Culiacán MexicoLaboratorio de Diabetes y comorbilidades, Centro de Investigación Aplicada a la Salud Pública (CIASaP), Facultad de Medicina Universidad Autónoma de Sinaloa Culiacán MexicoDepartamento de Toxicología Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV‐IPN) México City MexicoMaestría en Ciencias Biomédicas, Facultad de Ciencias Químico‐Biológicas Universidad Autónoma de Sinaloa Culiacán MexicoDepartamento de Biomedicina Molecular Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV‐IPN) México City MexicoInstituto de Neurobiología Universidad Nacional Autónoma de México Querétaro MexicoLaboratorio de Neurociencias, Centro de Investigación Aplicada a la Salud Pública (CIASaP), Facultad de Medicina Universidad Autónoma de Sinaloa Culiacán MexicoAbstract Background Down syndrome (DS) is the most common chromosomal survival aneuploidy. The increase in DS life expectancy further heightens the risk of dementia, principally early‐onset Alzheimer's disease (AD). AD risk in DS is higher, considering that this population may also develop metabolic diseases such as obesity, dyslipidemias, and diabetes mellitus. The extra genetic material that characterizes DS causes an imbalance in the genetic dosage, including over‐expression of AD's key pathophysiological molecules and the gene expression regulators, the microRNAs (miRNAs). Two miRNAs, chromosome 21‐encoded, miR‐155, and let‐7c, are associated with cognitive impairment and dementia in adults; but, expression dynamics and relationship with clinical variables during the DS's lifespan had remained hitherto unexplored. Methods The anthropometric, clinical, biochemical, and profile expression of circulating miR‐155 and let‐7c were analyzed in a population of 52 control and 50 DS subjects divided into the young group (Aged ≤20 years) and the adult group (Aged ≥21 years). Results The expression changes for miR‐155 were not significant; nevertheless, a negative correlation with HDL‐Cholesterol concentrations was observed. Notably, let‐7c was over‐expressed in DS from young and old ages. Conclusion Overall, our results suggest that let‐7c plays a role from the early stages of DS's cognitive impairment while overexpression of miR‐155 may be related to lipid metabolism changes. Further studies of both miRNAs will shed light on their potential as therapeutic targets to prevent or delay DS's cognitive impairment.https://doi.org/10.1002/mgg3.1938Alzheimer's diseasedown syndromedyslipidemiasmicroRNAsobesity |
spellingShingle | Jesús Manuel Pérez‐Villarreal Katia Aviña‐Padilla Evangelina Beltrán‐López Alma Marlene Guadrón‐Llanos Esther López‐Bayghen Javier Magaña‐Gómez Marco Antonio Meraz‐Ríos Alfredo Varela‐Echavarría Carla Angulo‐Rojo Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndrome Molecular Genetics & Genomic Medicine Alzheimer's disease down syndrome dyslipidemias microRNAs obesity |
title | Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndrome |
title_full | Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndrome |
title_fullStr | Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndrome |
title_full_unstemmed | Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndrome |
title_short | Profiling of circulating chromosome 21‐encoded microRNAs, miR‐155, and let‐7c, in down syndrome |
title_sort | profiling of circulating chromosome 21 encoded micrornas mir 155 and let 7c in down syndrome |
topic | Alzheimer's disease down syndrome dyslipidemias microRNAs obesity |
url | https://doi.org/10.1002/mgg3.1938 |
work_keys_str_mv | AT jesusmanuelperezvillarreal profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT katiaavinapadilla profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT evangelinabeltranlopez profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT almamarleneguadronllanos profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT estherlopezbayghen profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT javiermaganagomez profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT marcoantoniomerazrios profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT alfredovarelaechavarria profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome AT carlaangulorojo profilingofcirculatingchromosome21encodedmicrornasmir155andlet7cindownsyndrome |