Background: The unique geographical environment at high altitudes may cause a series of diseases, such as acute altitude reaction, cerebral edema, and pulmonary edema. (L.) R. Br. has been reported to have an effect on high-altitude hypoxia. However, the molecular mechanism, especially the expression of long noncoding RNAs (lncRNAs), is not yet clear.
Methods: The expression profiles of lncRNAs in high-altitude hypoxia-induced brain injury mice treated with (L.) R. Br. by using a microarray method.
Results: A total of 226 differentially expressed lncRNAs, 126 significantly dysregulated mRNAs and 23 differentially expressed circRNAs were detected (>2.0-fold, p<0.05). The expression of selected lncRNAs, mRNAs and circRNAs was validated by qRT-PCR. KEGG analysis showed that the mRNAs coexpressed with lncRNAs were involved in inflammation and hypoxia pathways, including the HIF-1, PI3K-Akt, and NF-kappa B signaling pathways. The lncRNA-TF network analysis results indicated that the lncRNAs were regulated mostly by HMGA2, SRY, GATA4, SOX5, and ZBTB16.
Conclusion: This study is the first to report the expression profiles of lncRNAs, mRNAs and circRNAs in mice with high-altitude hypoxia-induced brain injury treated with (L.) R. Br. and may improve the understanding of the molecular mechanism of (L.) R. Br. in treating high altitude hypoxia-induced brain injury.
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| http://dx.doi.org/10.2147/NDT.S246504 | DOI Listing |
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