Key result
Atorvastatin partly improves ox-LDL-induced endothelial dysfunction but leaves residual mitotic effects.
Why the study?
Few long noncoding RNAs associated with endothelial dysfunction after atorvastatin administration have been reported.
p-value: p=< .05
Atorvastatin partially improves ox-LDL-induced endothelial dysfunction by regulating lncRNAs and mRNAs involved in chronic inflammation, NO biosynthesis, and cytoskeletal processes, though cell cycle and metabolic pathways remain altered.
Does not support changing statin regimens; leaves open lncRNA modulation of residual mitotic effects as hypothesis-generating.
BACKGROUND: Long noncoding RNAs (lncRNAs) play a key role in the development of endothelial dysfunction. However, few lncRNAs associated with endothelial dysfunction after atorvastatin administration have been reported. METHODS: In the present study, differentially expressed (DE) genes in ox-LDL versus control and ox-LDL + atorvastatin versus control were detected. Bioinformatics analysis and integrated analysis of mRNAs and lncRNAs were conducted to study the mechanisms of endothelial dysfunction after atorvastatin administration and to explore the regulation functions of lncRNAs. RESULTS: Here, 532 DE mRNAs and 532 DE lncRNAs were identified (among them, 195 mRNAs and 298 lncRNAs were upregulated, 337 mRNAs and 234 lncRNAs were downregulated) after ox-LDL treatment for 24 hours (fold change ≥2.0, P < .05). After ox-LDL treatment following atorvastatin administration, 750 DE mRNAs and 502 DE lncRNAs were identified (among them, 149 mRNAs and 218 lncRNAs were upregulated and 601 mRNAs and 284 lncRNAs were downregulated). After atorvastatin administration, 167 lncRNAs and 262 mRNAs were still DE. Q-PCR validated the results of microarrays. CONCLUSION: Chronic inflammatory response, nitric oxide biosynthetic process, microtubule cytoskeleton, cell proliferation and cell migration are regulated by lncRNAs, which also participated in the mainly molecular function and biological processes underlying endothelial dysfunction. Atorvastatin partly improved endothelial dysfunction, but the aspects beyond recovery were mainly concentrated in cell cycle, mitosis, and metabolism. Further exploration is required to explicit the mechanism by which lncRNAs participate in endothelial dysfunction.
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Jiang et al. (2018) studied endothelial dysfunction. atorvastatin vs. control was evaluated on differentially expressed mRNAs and lncRNAs (p=< .05). Atorvastatin administration in ox-LDL-induced endothelial dysfunction resulted in 750 differentially expressed mRNAs and 502 lncRNAs, partly improving dysfunction but leaving residual mitotic effects.
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