m⁶A RNA Methylation Decreases Atherosclerotic Vulnerable Plaque Through Inducing T Cells

Knockdown of fat mass and obesity-associated gene (FTO) can induce N6-methyladenosine (m⁶A) ribonucleic acid (RNA) methylation. The objective of this study was to explore the effect of m 6A RNA methylation on atherosclerotic vulnerable plaque by FTO knockdown.

A total of 50 New Zealand white rabbits were randomly divided into pure high-fat group, sham operation group, vulnerable plaque group, empty load group, and FTO knockdown group (10 rabbits/group).

Flow cytometry showed that helper T (Th) cells in the FTO knockdown group accounted for a significantly higher proportion of lymphocytes than in the vulnerable plaque group and empty load group (P<0.05). Th cells were screened by cell flow. The level of m⁶A RNA methylation in the FTO knockdown group was significantly higher than in the vulnerable plaque group and empty load group (P<0.05). The levels of total cholesterol, triglyceride, and low-density lipoprotein C were higher at the 12^th week than at the 1^st week, but the high-density lipoprotein C level was lower at the 12^th week than at the 1^st week. At the 12th week, the interleukin-7 level was significantly lower in the adeno-associated virus-9 (AVV9)-FTO short hairpin RNA group than in the control and AVV9-green fluorescent protein groups (P<0.001).

After successfully establishing a vascular parkinsonism rabbit model, m⁶A RNA methylation can decrease Th cells and vulnerable atherosclerotic plaques.