PUBLICATION
Evidences for a New Role of miR-214 in Chondrogenesis
- Authors
- Roberto, V.P., Gavaia, P., Nunes, M.J., Rodrigues, E., Cancela, M.L., Tiago, D.M.
- ID
- ZDB-PUB-180301-3
- Date
- 2018
- Source
- Scientific Reports 8: 3704 (Journal)
- Registered Authors
- Cancela, Leonor
- Keywords
- none
- MeSH Terms
-
- Animals
- Cartilage/metabolism
- Cell Differentiation/genetics
- Cell Differentiation/physiology
- Chondrocytes/cytology
- Chondrocytes/metabolism
- Chondrogenesis/genetics
- Chondrogenesis/physiology*
- Gene Expression Regulation/genetics
- Gene Expression Regulation/physiology
- Mice
- MicroRNAs/genetics
- MicroRNAs/metabolism*
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 29487295 Full text @ Sci. Rep.
Citation
Roberto, V.P., Gavaia, P., Nunes, M.J., Rodrigues, E., Cancela, M.L., Tiago, D.M. (2018) Evidences for a New Role of miR-214 in Chondrogenesis. Scientific Reports. 8:3704.
Abstract
miR-214 is known to play a role in mammalian skeletal development through inhibition of osteogenesis and stimulation of osteoclastogenesis, but data regarding other vertebrates, as well as a possible role in chondrogenesis, remain unknown. Here, we show that miR-214 expression is detected in bone and cartilage of zebrafish skeleton, and is downregulated during murine ATDC5 chondrocyte differentiation. Additionally, we observed a conservation of the transcriptional regulation of miR-214 primary transcript Dnm3os in vertebrates, being regulated by Ets1 in ATDC5 chondrogenic cells. Moreover, overexpression of miR-214 in vitro and in vivo mitigated chondrocyte differentiation probably by targeting activating transcription factor 4 (Atf4). Indeed, miR-214 overexpression in vivo hampered cranial cartilage formation of zebrafish and coincided with downregulation of atf4 and of the key chondrogenic players sox9 and col2a1. We show that miR-214 overexpression exerts a negative role in chondrogenesis by impacting on chondrocyte differentiation possibly through conserved mechanisms.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping