GLI1 activates pro-fibrotic pathways in myelofibrosis fibrocytes.
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
20 05 2022
20 05 2022
Historique:
received:
17
12
2021
accepted:
09
05
2022
revised:
05
05
2022
entrez:
20
5
2022
pubmed:
21
5
2022
medline:
25
5
2022
Statut:
epublish
Résumé
Bone marrow (BM) fibrosis was thought to be induced exclusively by mesenchymal stromal cells (MSCs). However, we and others found that neoplastic fibrocytes induce BM fibrosis in myelofibrosis (MF). Because glioma-associated oncogene-1 (GLI1), an effector of the Hedgehog pathway, plays a role in the induction of BM fibrosis, we wondered whether GLI1 affects fibrocyte-induced BM fibrosis in MF. Multiplexed fluorescence immunohistochemistry analysis of MF patients' BM detected high levels of GLI1 in MF fibrocytes compared to MSCs or normal fibrocytes. Immunostaining, RNA in situ hybridization, gene expression analysis, and western immunoblotting detected high levels of GLI1 and GLI1-induced matrix metalloproteases (MMP) 2 and 9 in MF patients BM-derived cultured fibrocytes. Similarly, MF patients' BM-derived GLI1
Identifiants
pubmed: 35595725
doi: 10.1038/s41419-022-04932-4
pii: 10.1038/s41419-022-04932-4
pmc: PMC9122946
doi:
Substances chimiques
GLI1 protein, human
0
Hedgehog Proteins
0
STAT3 Transcription Factor
0
Zinc Finger Protein GLI1
0
Matrix Metalloproteinase 2
EC 3.4.24.24
Matrix Metalloproteinase 9
EC 3.4.24.35
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
481Informations de copyright
© 2022. The Author(s).
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