PIEZO1 activation delays erythroid differentiation of normal and hereditary xerocytosis-derived human progenitor cells.
Journal
Haematologica
ISSN: 1592-8721
Titre abrégé: Haematologica
Pays: Italy
ID NLM: 0417435
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
11
02
2019
accepted:
09
08
2019
pubmed:
16
8
2019
medline:
28
4
2021
entrez:
16
8
2019
Statut:
ppublish
Résumé
Hereditary xerocytosis is a dominantly inherited red cell membrane disorder caused in most cases by gain-of-function mutations in PIEZO1, encoding a mechanosensitive ion channel that translates a mechanic stimulus into calcium influx. We found that PIEZO1 was expressed early in erythroid progenitor cells, and investigated whether it could be involved in erythropoiesis, besides having a role in the homeostasis of mature red cell hydration. In UT7 cells, chemical PIEZO1 activation using YODA1 repressed glycophorin A expression by 75%. This effect was PIEZO1-dependent since it was reverted using specific short hairpin-RNA knockdown. The effect of PIEZO1 activation was confirmed in human primary progenitor cells, maintaining cells at an immature stage for longer and modifying the transcriptional balance in favor of genes associated with early erythropoiesis, as shown by a high
Identifiants
pubmed: 31413092
pii: haematol.2019.218503
doi: 10.3324/haematol.2019.218503
pmc: PMC7049340
doi:
Substances chimiques
Ion Channels
0
PIEZO1 protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
610-622Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright© 2020 Ferrata Storti Foundation.
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