Fig. 2. Increased m⁶A modification and decreased FTO in AIS patients and PT mice.

a, b Total RNA was extracted from the somatosensory cortex of AIS or nonstroke patients. The m⁶A level was determined as the percentage of all adenosine residues in RNA (a). The level of circSCMH1 was measured by qPCR (b). There were six individuals/group. ^*P = 0.0183 (a), ^*P = 0.0184 (b) versus nonstroke. c Western blotting analysis of FTO in the somatosensory cortex of AIS and nonstroke patients. There were six individuals/group. ^*P = 0.0105 versus nonstroke. d Total RNA was extracted from the peri-infarct cortex of PT mice, m⁶A levels were determined as the percentage of all adenosine residues in RNA. n = 6 mice/group. ^**P = 0.0018 (28d), ^***P = 0.0002 (21d), ^***P < 0.0001 (1d, 3d, 7d, 14d) versus sham. e–g Western blotting analysis of FTO in the peri-infarct cortex of mice after PT (e), dMCAO (f), and tMCAO (g) stroke. Two representative immunoblots were presented from 6 mice/group. ^*P = 0.0186 (21d), ^*P = 0.0408 (28d), ^***P < 0.0001 (1d, 3d, 7d), ^***P = 0.0001 (14d) versus sham in e. ^**P = 0.0012 (21d), ^**P = 0.0057 (28d), ^***P < 0.0001 (1d, 3d, 7d), ^***P = 0.0002 (14d) versus sham in f. ^**P = 0.0064 (21d), ^**P = 0.0070 (28d), ^***P < 0.0001 (1d, 3d, 7d, 14d) versus sham in g. The data in a–c were expressed as mean ± SEM; Student’s t-test (two-sided). The data in d–g were expressed as mean ± SEM; one-way ANOVA followed by Holm–Sidak post hoc multiple comparison test. Source data are provided as a Source Data file. AIS acute ischemic stroke, d day, dMCAO distal middle cerebral artery occlusion, FTO fat mass and obesity-associated protein, m⁶A N⁶-methyladenosine, PT photothrombotic, tMCAO transient middle cerebral artery occlusion.