Evidence map›Paper›PMID 40141367›Full record

ArticleInternational journal of molecular sciences2025

Cultured Macrophage Models for the Investigation of Lysosomal Glucocerebrosidase and Gaucher Disease.

Max Louwerse, Kateryna O Bila, Martijn J C van der Lienden, Arnout Jan M de Beaufort, Rolf G Boot, Marta Artola, Marco van Eijk, Johannes M F G Aerts

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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

8 authors.

Max LouwerseDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-8584-9745
Kateryna O BilaDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-2470-1130
Martijn J C van der LiendenDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-6458-1479
Arnout Jan M de BeaufortDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.
Rolf G BootDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-7031-3390
Marta ArtolaDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-3051-3902
Marco van EijkDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0001-7751-4112
Johannes M F G AertsDepartment of Medical Biochemistry, Leiden Institute of Chemistry, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0001-8168-2565

Funding

Institute for Chemical Immunology ICI #I00029Recon4IMD #101080997
6 · The paper itself

Abstract

Macrophages are specialised cells that degrade a range of substrates during their lifetime. In inherited lysosomal storage disorders, particularly the sphingolipidoses, macrophages transform into storage cells and contribute to pathology. An appropriate cultured macrophage model is desired for fundamental research and the assessment of considered therapeutic interventions. We compared commonly used macrophage cell lines, RAW264.7, J774A.1, and THP-1 cells, with human monocyte-derived macrophages (HMDMs) isolated from peripheral blood. Specific lysosomal glucosidases were analysed by enzymatic activity measurements and visualised with fluorescent activity-based probes. Special attention was given to lysosomal glucocerebrosidase (GBA1), the enzyme deficient in Gaucher disease in which lipid-laden macrophages are a hallmark. In macrophage cell lines and HMDMs, various (glyco)sphingolipids relevant to GBA1 activity were determined. Finally, the feasibility of inactivation of GBA1 with a cell-permeable suicide inhibitor was established, as well as the monitoring of uptake of therapeutic recombinant human GBA1. Major differences among various cell lines were noted in terms of morphology, lysosomal enzyme expression, and glycosphingolipid content. HMDMs appear to be the most suitable model for investigations into GBA1 and Gaucher disease. Moreover, they serve as a valuable model for mannose-receptor mediated uptake of therapeutic human GBA1, effectively mimicking enzyme replacement therapy for Gaucher disease.

Indexed as

Gaucher DiseaseGlucosylceramidaseLysosomesMacrophagesAnimalsCell LineGlycosphingolipidsHumansMiceRAW 264.7 CellsTHP-1 CellsGlucosylceramidaseGlycosphingolipidsGaucher diseaseglucocerebrosidaselysosomemacrophagemonocyte

Identifiers

PMID40141367
PMCPMC11943430

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Registered trials

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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.