Rn7SK small nuclear RNA is involved in cellular senescence.
Aging
/ genetics
Cell Differentiation
/ genetics
Cell Proliferation
/ genetics
Cell Survival
/ genetics
Cellular Senescence
/ genetics
Humans
Mesenchymal Stem Cells
/ cytology
Osteogenesis
/ genetics
RNA, Small Nuclear
/ genetics
Regenerative Medicine
Signal Transduction
/ genetics
Stem Cells
/ metabolism
Transfection
beta-Galactosidase
/ genetics
Rn7SK
aging
mesenchymal stem cells
noncoding RNAs
senescence
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
17
06
2018
accepted:
11
12
2018
pubmed:
15
1
2019
medline:
27
5
2020
entrez:
15
1
2019
Statut:
ppublish
Résumé
Rn7SK is a conserved small nuclear noncoding RNA which its function in aging has not been studied. Recently, we have demonstrated that Rn7SK overexpression reduces cell viability and is significantly downregulated in stem cells, human tumor tissues, and cell lines. In this study, we analyzed the role of Rn7SK on senescence in adipose tissue-derived mesenchymal stem cells (AD-MSCs). For this purpose, Rn7SK expression was downregulated and upregulated via transfection and transduction, respectively, in AD-MSCs and subsequently, various distinct characteristics of senescence including cell viability, proliferation, colony formation, senescence-associated β galactosidase activity, and differentiation potency was analyzed. Our results demonstrated the transient knockdown of Rn7SK in MSCs leads to delayed senescence, while its overexpressions shows opposite effects. When osteogenic differentiation was started, however, they exhibited a greater differentiation potential than the original MSCs, suggesting a potential tool for stem cell-based regenerative medicine.
Substances chimiques
RNA, Small Nuclear
0
beta-Galactosidase
EC 3.2.1.23
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
14234-14245Informations de copyright
© 2019 Wiley Periodicals, Inc.