Upregulation of Sortilin, a Lysosomal Sorting Receptor, Corresponds with Reduced Bioavailability of Latent TGFβ in Mucolipidosis II Cells.
Adaptor Proteins, Vesicular Transport
/ genetics
Cathepsin D
/ metabolism
Cell Line
Cells, Cultured
Fibroblasts
/ metabolism
HeLa Cells
Humans
Lysosomes
/ metabolism
Mucolipidoses
/ metabolism
Protein Transport
Signal Transduction
Transferases (Other Substituted Phosphate Groups)
/ genetics
Transforming Growth Factor beta
/ metabolism
Up-Regulation
TGF-beta
cathepsin D
lysosomes
mucolipidosis II
sortilin
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
26 04 2020
26 04 2020
Historique:
received:
17
02
2020
revised:
14
04
2020
accepted:
20
04
2020
entrez:
3
5
2020
pubmed:
3
5
2020
medline:
7
4
2021
Statut:
epublish
Résumé
Mucolipidosis II (ML-II) is a lysosomal disease caused by defects in the carbohydrate-dependent sorting of soluble hydrolases to lysosomes. Altered growth factor signaling has been identified as a contributor to the phenotypes associated with ML-II and other lysosomal disorders but an understanding of how these signaling pathways are affected is still emerging. Here, we investigated transforming growth factor beta 1 (TGFβ1) signaling in the context of ML-II patient fibroblasts, observing decreased TGFβ1 signaling that was accompanied by impaired TGFβ1-dependent wound closure. We found increased intracellular latent TGFβ1 complexes, caused by reduced secretion and stable localization in detergent-resistant lysosomes. Sortilin, a sorting receptor for hydrolases and TGFβ-related cytokines, was upregulated in ML-II fibroblasts as well as
Identifiants
pubmed: 32357547
pii: biom10050670
doi: 10.3390/biom10050670
pmc: PMC7277838
pii:
doi:
Substances chimiques
Adaptor Proteins, Vesicular Transport
0
Transforming Growth Factor beta
0
Transferases (Other Substituted Phosphate Groups)
EC 2.7.8.-
GNPTAB protein, human
EC 2.7.8.15
Cathepsin D
EC 3.4.23.5
sortilin
Z020Y8WIJ4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NHLBI NIH HHS
ID : R00 HL131866
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM086524
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS128907
Pays : United States
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