Transforming growth factor β-mediated micromechanics modulates disease progression in primary myelofibrosis.
Animals
Biomechanical Phenomena
Disease Progression
Fibroblasts
/ metabolism
Humans
Hypertension, Pulmonary
/ complications
Mice, Nude
Models, Biological
Primary Myelofibrosis
/ complications
Receptor, Transforming Growth Factor-beta Type I
/ metabolism
Receptor, Transforming Growth Factor-beta Type II
/ metabolism
Stress, Mechanical
Transforming Growth Factor beta
/ metabolism
TGF-β
fibroblast activation
invasion
micromechanics
myelofibrosis
proliferation
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
17
04
2020
accepted:
29
05
2020
pubmed:
6
9
2020
medline:
7
5
2021
entrez:
5
9
2020
Statut:
ppublish
Résumé
Primary myelofibrosis (PMF) is a Ph-negative myeloproliferative neoplasm (MPN), characterized by advanced bone marrow fibrosis and extramedullary haematopoiesis. The bone marrow fibrosis results from excessive proliferation of fibroblasts that are influenced by several cytokines in the microenvironment, of which transforming growth factor-β (TGF-β) is the most important. Micromechanics related to the niche has not yet been elucidated. In this study, we hypothesized that mechanical stress modulates TGF-β signalling leading to further activation and subsequent proliferation and invasion of bone marrow fibroblasts, thus showing the important role of micromechanics in the development and progression of PMF, both in the bone marrow and in extramedullary sites. Using three PMF-derived fibroblast cell lines and transforming growth factor-β receptor (TGFBR) 1 and 2 knock-down PMF-derived fibroblasts, we showed that mechanical stress does stimulate the collagen synthesis by the fibroblasts in patients with myelofibrosis, through the TGFBR1, which however seems to be activated through alternative pathways, other than TGFBR2.
Identifiants
pubmed: 32889753
doi: 10.1111/jcmm.15526
pmc: PMC7576271
doi:
Substances chimiques
Transforming Growth Factor beta
0
Receptor, Transforming Growth Factor-beta Type I
EC 2.7.11.30
Receptor, Transforming Growth Factor-beta Type II
EC 2.7.11.30
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
11100-11110Informations de copyright
© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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