Cytoskeleton stiffness regulates cellular senescence and innate immune response in Hutchinson-Gilford Progeria Syndrome.
accelerated aging
cell nucleus
cellular senescence
skeletal muscle
stem cells
Journal
Aging cell
ISSN: 1474-9726
Titre abrégé: Aging Cell
Pays: England
ID NLM: 101130839
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
18
11
2019
revised:
10
03
2020
accepted:
27
03
2020
pubmed:
28
7
2020
medline:
25
8
2021
entrez:
26
7
2020
Statut:
ppublish
Résumé
Hutchinson-Gilford progeria syndrome (HGPS) is caused by the accumulation of mutant prelamin A (progerin) in the nuclear lamina, resulting in increased nuclear stiffness and abnormal nuclear architecture. Nuclear mechanics are tightly coupled to cytoskeletal mechanics via lamin A/C. However, the role of cytoskeletal/nuclear mechanical properties in mediating cellular senescence and the relationship between cytoskeletal stiffness, nuclear abnormalities, and senescent phenotypes remain largely unknown. Here, using muscle-derived mesenchymal stromal/stem cells (MSCs) from the Zmpste24
Identifiants
pubmed: 32710480
doi: 10.1111/acel.13152
pmc: PMC7431831
doi:
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
e13152Subventions
Organisme : NIH HHS
ID : P01AG062412
Pays : United States
Organisme : NIH HHS
ID : R01HL133254
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG062413
Pays : United States
Organisme : NIA NIH HHS
ID : U19 AG056278
Pays : United States
Organisme : NIH HHS
ID : U19AG056278
Pays : United States
Organisme : NIH HHS
ID : RO1AR065445
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG043376
Pays : United States
Informations de copyright
© 2020 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
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