LncRNA H19 promotes the committed differentiation of stem cells from apical papilla via miR-141/SPAG9 pathway.
Adaptor Proteins, Signal Transducing
/ metabolism
Adolescent
Cell Differentiation
Cell Proliferation
/ genetics
Dental Papilla
/ cytology
Healthy Volunteers
Humans
MicroRNAs
/ metabolism
Odontogenesis
/ genetics
Osteogenesis
/ genetics
RNA, Long Noncoding
/ genetics
Stem Cells
/ metabolism
Transfection
Young Adult
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
12 02 2019
12 02 2019
Historique:
received:
23
10
2018
accepted:
02
01
2019
revised:
10
12
2018
entrez:
14
2
2019
pubmed:
14
2
2019
medline:
9
4
2020
Statut:
epublish
Résumé
Long noncoding RNAs (lncRNAs) exert significant roles at transcriptional and post-transcriptional levels. Stem cells from apical papilla (SCAPs) differentiate into dentin/bone-like tissues under certain conditions. So far, whether lncRNA-H19 can affect the proliferative behaviors and osteo/odontogenesis of SCAPs, as well as its specific mechanism remain to be elucidated. Here, SCAPs were isolated and transfected with the lentiviruses or packaging vectors. Our results showed that lncRNA-H19 had no significant effect on the proliferative behaviors of SCAPs, as presented by CCK-8 assay, EdU assay and flow cytometry (FCM). Furthermore, alkaline phosphatase (ALP) activity, alizarin red staining, Western blot assay (WB), quantitative real-time polymerase chain reaction (qRT-PCR) and in vivo bone formation assay were conducted to verify the biological influences of H19 on SCAPs. Overexpression of H19 led to the enhanced osteo/odontogenesis of SCAPs, whereas knockdown of H19 inhibited these effects. Mechanistically, H19 competitively bound to miR-141 and prevented SPAG9 from miRNA-mediated degradation, thus significantly elevating phosphorylated levels of p38 and JNK and facilitating the committed differentiation of SCAPs. Taken together, the osteo/odontogenesis of SCAPs was upregulated by overexpression of H19 via miR-141/SPAG9 pathway.
Identifiants
pubmed: 30755596
doi: 10.1038/s41419-019-1337-3
pii: 10.1038/s41419-019-1337-3
pmc: PMC6372621
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
H19 long non-coding RNA
0
MIRN141 microRNA, human
0
MicroRNAs
0
RNA, Long Noncoding
0
SPAG9 protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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