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Published on: April 25, 2018
Long noncoding RNA AK039312 and AK079370 inhibits bone formation via miR-199b-5p
Chong Yin1, Ye Tian1, Yang Yu2
1Lab for Bone Metabolism, Xi'an Key Laboratory of Special Medicine and Health Engineering, Key Lab for Space Biosciences and Biotechnology, Research Center for Special Medicine and Health Systems Engineering, NPU-UAB Joint Laboratory for Bone Metabolism, School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi, China.
Abstract:
Osteoporosis caused by aging and menopause had become an emerging threat to human health. The reduction of osteoblast differentiation has been considered to be an essential cause of osteoporosis. Osteoblast differentiation could be regulated by LncRNAs, and increasing evidences have proved that LncRNAs may be adopted as potential therapeutic targets for osteoporosis. However, reports on rescue effects of LncRNAs in vivo are relatively limited. In this study, two LncRNAs (AK039312 and AK079370) were screened as osteogenic related LncRNAs. Both AK039312 and AK079370 could inhibit osteoblast differentiation and bone formation through suppressing osteogenic transcription factors. This inhibitory effect was achieved via binding and sequestering miR-199b-5p, and enhanced GSK-3β which further inhibited wnt/β-catenin pathway. Moreover, the siRNAs of AK039312 and AK079370 significantly alleviated postmenopausal osteoporosis, and the combination of si-AK039312 and si-AK079370 was more efficient than applying one si-LncRNA alone. This study has provided new insights for the therapy of osteoporosis.
Insights
Two long non-coding RNAs (lncRNAs), AK039312 and AK079370, were found to inhibit bone formation. Their inhibition was reversed in vivo, suggesting potential therapeutic strategies for osteoporosis.
Area of Science:
- Molecular Biology
- Cell Biology
- Bone Biology
Background:
- Osteoporosis, a health threat linked to aging and menopause, is characterized by reduced osteoblast differentiation.
- Long non-coding RNAs (lncRNAs) regulate osteoblast differentiation and are potential therapeutic targets for osteoporosis.
- In vivo rescue effects of lncRNAs for osteoporosis remain under-investigated.
Purpose of the Study:
- To investigate the role of osteogenic lncRNAs AK039312 and AK079370 in osteoporosis.
- To elucidate the molecular mechanism by which these lncRNAs affect osteoblast differentiation and bone formation.
- To evaluate the therapeutic potential of targeting these lncRNAs in a postmenopausal osteoporosis model.
Main Methods:
- Screening of osteogenic-related lncRNAs.
- Investigating the inhibitory effects of AK039312 and AK079370 on osteoblast differentiation and bone formation.
- Analyzing the molecular mechanism involving miR-199b-5p, GSK-3β, and the wnt/β-catenin pathway.
- Utilizing small interfering RNAs (siRNAs) to target AK039312 and AK079370 in a postmenopausal osteoporosis model.
Main Results:
- AK039312 and AK079370 were identified as inhibitors of osteoblast differentiation and bone formation.
- These lncRNAs suppress osteogenic transcription factors by binding and sequestering miR-199b-5p, leading to enhanced GSK-3β and inhibition of the wnt/β-catenin pathway.
- Administration of siRNAs targeting AK039312 and AK079370 significantly alleviated postmenopausal osteoporosis.
- Combination therapy with si-AK039312 and si-AK079370 demonstrated greater efficacy than single siRNA treatment.
Conclusions:
- AK039312 and AK079370 play critical roles in inhibiting osteoblast differentiation and bone formation.
- Targeting these lncRNAs offers a promising therapeutic strategy for osteoporosis.
- Combined inhibition of AK039312 and AK079370 provides a more effective approach to treating postmenopausal osteoporosis.
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