Journal
FRONTIERS IN GENETICS
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fgene.2022.909095
Keywords
osteoclast; lncRNA; mRNA; HIF-1 alpha; condyle
Categories
Funding
- National Natural Science Foundation of China [82100955]
- Shanghai Shenkang Hospital Development Center clinical Science and Technology Innovation Project [SHDC12020113]
- Shanghai Science and Technology Innovation Action Plan Medical Innovation Research Special Project [20Y11904000]
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In this study, RNA sequencing was used to analyze the expression profiles of lncRNAs and mRNAs in conditional HIF-1 alpha-knockout osteoclasts. Differential expression of 1,320 mRNAs and 95 lncRNAs was observed, with lncRNAs MSTRG.7566.12 and MSTRG.31769.2 showing strong negative correlation with the expression of genes such as Mmp9 and Ctsk. These findings provide insights into the regulation of osteoclast differentiation by HIF-1 alpha at the genetic level and suggest potential therapeutic targets for bone diseases related to HIF-1 alpha.
Background: Osteoclasts, which are multinucleated cells formed by monocyte fusion, play a key role in bone resorption. Hypoxia-inducible factor (HIF)-1 alpha is vital for the development of osteoclasts in hypoxic environments and during bone resorption. However, additional research is required to further study the HIF-1 alpha-dependent regulation of osteoclast differentiation at the genetic level. Methods: In our study, RNA sequencing (RNA-seq) was used to identify the expression profiles of long noncoding RNAs (lncRNAs) and mRNAs in conditional HIF-1 alpha-knockout osteoclasts. Results: A total of 1,320 mRNAs and 95 lncRNAs were differentially expressed. The expression of lncRNAs MSTRG.7566.12 and MSTRG.31769.2 were strongly negatively correlated with that of Mmp9, Ctsk, etc. Conclusion: Our research provides a basis for further understanding the role of mRNAs and lncRNAs in conditional HIF-1 alpha-knockout osteoclasts, and many of these molecules may be potential targets for treating bone diseases related to HIF-1 alpha.
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