ALKBH5 Exacerbates Aortic Dissection by Promoting Inflammatory Response and Apoptosis of Aortic Smooth Muscle Cells via Regulating lnc-TMPO-AS1/EZH2/IRAK4 Signals in an m6A Modification Manner

Figure 3

lncRNA TMPO-AS1 is a downstream target of ALKBH5. (a) 40 candidate lncRNAs that may be involved in AD progression were selected for hierarchical clustering analysis. (b) Only the expression of lnc-TMPO-AS1 was altered when ALKBH5 was either overexpressed or silenced. (c, d) The low expression of lnc-TMPO-AS1 in clinical samples and the significantly negative correlation between it and ALKBH5 were confirmed by qRT-PCR and Pearson’s correlation coefficient analysis, respectively (, ). (e–h) lnc-TMPO-AS1 upregulation could partly weaken the promoting effect of ALKBH5 overexpression on AngII-induced inflammatory response and apoptosis of HASMCs. (i, j) Downregulation of lnc-TMPO-AS1 could partly reverse the impact of ALKBH5 knockdown on the apoptosis of HASMCs induced by AngII. (k) lnc-TMPO-AS1 upregulation could partly reduce the stimulating effect of ALKBH5 overexpression on the incidence of AD in AngII-infused mice, while its knockdown could partly counteract the impact of ALKBH5 knockdown on this index. (l) lnc-TMPO-AS1 could prolong the survival time of mice and partly counteract the effect of ALKBH5. Data represented the from three independent experiments, ; ns represents no statistical difference between groups.

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