Evidence map›Paper›PMID 42782417›Full record

ArticleNeurochemical research2026

Characterization of Cellular Alterations in a Novel NAGLU Enzyme-Deficient Cellular Model Generated from U-87MG Cell Line.

Katherin D Niño-Traslaviña, Diego A Suárez, Oscar F Sánchez, Angela J Espejo-Mojica, Carlos J Alméciga-Díaz

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Katherin D Niño-TraslaviñaInstitute for the Study of Inborn Errors of Metabolism, Faculty of Science, Pontificia Universidad Javeriana, Cra 7 No. 42-46, Félix Restrepo, S.J., building 44, room 10-1.5, Bogotá, 110231, Colombia.
Diego A SuárezInstitute for the Study of Inborn Errors of Metabolism, Faculty of Science, Pontificia Universidad Javeriana, Cra 7 No. 42-46, Félix Restrepo, S.J., building 44, room 10-1.5, Bogotá, 110231, Colombia.ORCID http://orcid.org/0000-0001-9519-4706
Oscar F SánchezDepartment of Industrial Engineering, Faculty of Engineering, Pontificia Universidad Javeriana, Cra. 7 No. 40-62, José Gabriel Maldonado, S.J., 110231, Bogotá, Colombia.ORCID http://orcid.org/0000-0003-2237-0945
Angela J Espejo-MojicaInstitute for the Study of Inborn Errors of Metabolism, Faculty of Science, Pontificia Universidad Javeriana, Cra 7 No. 42-46, Félix Restrepo, S.J., building 44, room 10-1.5, Bogotá, 110231, Colombia.ORCID http://orcid.org/0000-0001-9670-6435
Carlos J Alméciga-DíazInstitute for the Study of Inborn Errors of Metabolism, Faculty of Science, Pontificia Universidad Javeriana, Cra 7 No. 42-46, Félix Restrepo, S.J., building 44, room 10-1.5, Bogotá, 110231, Colombia. cjalmeciga@javeriana.edu.co.ORCID http://orcid.org/0000-0001-6484-1173

Funding

Pontificia Universidad Javeriana Doctoral scholarshipPontificia Universidad Javeriana Investigar PUJ 20646 and 20567Pontificia Universidad Javeriana Master scholarship
6 · The paper itself

Abstract

Mucopolysaccharidosis IIIB (MPS IIIB) is an inherited metabolic disorder caused by mutations in NAGLU gene, resulting in the accumulation of heparan sulphate in lysosomes and cell membranes. This accumulation leads to cellular dysfunction, apoptosis, tissue damage, and organ failure. MPS IIIB is considered a neurodegenerative disease that causes motor impairment, developmental delay, sleep disturbance, and dementia. This is usually diagnosed around 3-4 years of age with an incidence of 1 per 200,000 live births. Current research focuses on cellular defects in the central nervous system, particularly in neurons. Conversely, the effects on glial cell types, such as microglia and astrocytes, which play a key role in brain homeostasis, remain unknown. Currently, there is not any glial cell model that allows us to assess different therapeutic strategies. In this study, we generated a glial cell model deficient in the NAGLU enzyme via CRISPR/Cas9 editing system in the U-87MG cell line. Characterization of this cellular model exhibited typical traits for MPS IIIB, including decreased enzyme activity and mitochondrial mass, as well as increased lysosomal mass, neutral lipids, total glycosaminoglycans, and total reactive oxygen species, along with an altered autophagy flux. Thus, it is expected that this model will contribute to the development and assessment of therapeutic strategies, as well as a better understanding of the molecular and cellular basis of MPS IIIB.

Indexed as

AcetylglucosaminidaseMucopolysaccharidosis IIINeurogliaAutophagyCell LineGlycosaminoglycansHumansLysosomesMitochondriaReactive Oxygen SpeciesAcetylglucosaminidaseGlycosaminoglycansReactive Oxygen SpeciesCell modelsCRISPR/Cas9MPS IIIBNAGLU geneU-87MG

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.