GAS5 protects against osteoporosis by targeting UPF1/SMAD7 axis in osteoblast differentiation
Male
0301 basic medicine
bone marrow
QH301-705.5
Science
Blotting, Western
Smad7 Protein
Mice
03 medical and health sciences
GAS5
Animals
Humans
Biology (General)
In Situ Hybridization, Fluorescence
stromal cells
Electrophoresis, Agar Gel
0303 health sciences
Osteoblasts
Q
R
Cell Differentiation
Cell Biology
osteoporosis
Mice, Inbred C57BL
13. Climate action
osteoblast differentiation
Trans-Activators
Medicine
Osteoporosis
Female
RNA, Long Noncoding
RNA Helicases
DOI:
10.7554/elife.59079
Publication Date:
2020-10-02T12:00:17Z
AUTHORS (14)
ABSTRACT
Osteoporosis is a common systemic skeletal disorder resulting in bone fragility and increased fracture risk. It is still necessary to explore its detailed mechanisms and identify novel targets for the treatment of osteoporosis. Previously, we found that a lncRNA named GAS5 in human could negatively regulate the lipoblast/adipocyte differentiation. However, it is still unclear whether GAS5 affects osteoblast differentiation and whether GAS5 is associated with osteoporosis. Our current research found that GAS5 was decreased in the bones and BMSCs, a major origin of osteoblast, of osteoporosis patients. Mechanistically, GAS5 promotes the osteoblast differentiation by interacting with UPF1 to degrade SMAD7 mRNA. Moreover, a decreased bone mass and impaired bone repair ability were observed in Gas5 heterozygous mice, manifesting in osteoporosis. The systemic supplement of Gas5-overexpressing adenoviruses significantly ameliorated bone loss in an osteoporosis mouse model. In conclusion, GAS5 promotes osteoblast differentiation by targeting the UPF1/SMAD7 axis and protects against osteoporosis.
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CITATIONS (32)
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