Fig. 6: CircATXN1 Inhibits Partial EndMT via interaction with ALKBH5.
From: Regulation of partial endothelial-to-mesenchymal transition by circATXN1 in ischemic diseases
a Silver stain showing proteins captured with biotin-labeled sense (S) or antisense (AS) probes targeting circATXN1 junction sites in HCMEC lysates (n = 3 biological replicates). b Western blot (upper panel) and RT-PCR (lower panel) of ALKBH5 and circATXN1 using biotin-labeled S or AS probes in HCMECs (n = 3 biological replicates). c RIP (upper panel) and Western blot (lower panel) showing the interaction between ALKBH5 and circATXN1 in HCMECs transfected with circATXN1 (n = 3 biological replicates). d Representative images of dual RNA-FISH and immunofluorescence (n = 3 biological replicates). e Western blot of Fibronectin, VE-cadherin, CD31, αSMA, FSP1, SLUG, and ALKBH5 in HCMECs infected with various constructs and hypoxia-stimulated for 24 h (n = 3 biological replicates). f FUCCI imaging of HCMECs infected with various constructs and hypoxia-stimulated for 24 h (n = 3 biological replicates, scale bars = 100 µm). g Echocardiography of left ventricular ejection fraction (LVEF) at baseline and days 7, 14, and 28 post-MI (n = 6 mice per group). h Scar size measurement at 4 weeks post-MI (n = 6 mice per group, scale bar = 2 mm) (* compared with AAV Scr-sh / ALKBH5fl/fl group, # compared with AAV circATXN1-sh / ALKBH5fl/fl group, & compared with AAV circATXN1-sh / ALKBH5CKO group). Statistical analysis: two-Way ANOVA with multiple comparisons test for (g); ordinary one-Way ANOVA test for (h).
