دورية أكاديمية
Long non-coding RNA-NONMMMUT004552.2 regulates the unloading-induced bone loss through the miRNA-15b-5p/Syne1 in mice
العنوان: | Long non-coding RNA-NONMMMUT004552.2 regulates the unloading-induced bone loss through the miRNA-15b-5p/Syne1 in mice |
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المؤلفون: | Zheng Zhang, Yu Jing, Ang Zhang, JiShan Liu, Heming Yang, Xiaotong Lou, Liyan Xu, Min Liu, Yikun Zhang, Jianwen Gu |
المصدر: | npj Microgravity, Vol 10, Iss 1, Pp 1-11 (2024) |
بيانات النشر: | Nature Portfolio, 2024. |
سنة النشر: | 2024 |
المجموعة: | LCC:Biotechnology LCC:Physiology |
مصطلحات موضوعية: | Biotechnology, TP248.13-248.65, Physiology, QP1-981 |
الوصف: | Abstract Exercise-induced mechanical loading can increase bone strength whilst mechanical unloading enhances bone-loss. Here, we investigated the role of lncRNA NONMMUT004552.2 in unloading-induced bone-loss. Knockout of lncRNA NONMMUT004552.2 in hindlimb-unloaded mice caused an increase in the bone formation and osteoblast activity. The silencing of lncRNA NONMMUT004552.2 also decreased the osteoblast apoptosis and expression of Bax and cleaved caspase-3, increased Bcl-2 protein expression in MC3T3-E1 cells. Mechanistic investigations demonstrated that NONMMUT004552.2 functions as a competing endogenous RNA (ceRNA) to facilitate the protein expression of spectrin repeat containing, nuclear envelope 1 (Syne1) by competitively binding miR-15b-5p and subsequently inhibits the osteoblast differentiation and bone formation in the microgravity unloading environment. These data highlight the importance of the lncRNA NONMMUT004552.2/miR-15b-5p/Syne1 axis for the treatment of osteoporosis. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2373-8065 |
Relation: | https://doaj.org/toc/2373-8065 |
DOI: | 10.1038/s41526-024-00382-8 |
URL الوصول: | https://doaj.org/article/bf9d9ba07e4643b0b2e2fd8033ac20fe |
رقم الأكسشن: | edsdoj.bf9d9ba07e4643b0b2e2fd8033ac20fe |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 23738065 |
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DOI: | 10.1038/s41526-024-00382-8 |