Long non-coding RNA LUCAT1 inhibits myocardial oxidative stress and apoptosis after myocardial infarction via targeting microRNA-181a-5p

Figures & data

Table 1. Subjects’ basic clinical information

Parameter	Healthy individuals (n = 67)	AMI patients (n = 72)	P-value
Sex (male,%)	35, 52.2	34,47.2	0.554
Age (years)	56.96 ± 8.07	58.19 ± 9.87	0.421
Hypertension (No., %)	35, 52.2	44, 61.1	0.291
Smoker (No., %)	26, 38.8	35, 48.6	0.244
Diabetes (No., %)	19, 28.4	28, 38.9	0.190
TC (mmol/L)	4.12 ± 0.57	4.30 ± 0.56	0.068
TG (mmol/L)	1.32 ± 0.36	1.39 ± 0.37	0.239
LDL (mmol/L)	2.65 ± 0.41	2.74 ± 0.42	0.192
HDL (mmol/L)	1.27 ± 0.41	1.19 ± 0.34	0.243

TC, total cholesterol; TG, triglycerides; LDL, low-density lipoprotein; HDL, high-density lipoprotein.

Figure 1. The expression of LUCAT1 was reduced in the AMI patients compared to control individuals. ***P < 0.001

Figure 2. The impacts of LUCAT1 on H₂O₂-treated cells. (a) The transfection of p-LUCAT1 reversed the decreased LUCAT1 expression steered by H₂O₂ and the knockdown of LUCAT1 improved the function of H₂O₂. (b) The overexpression of LUCAT1 reversed the abnormally decreased SOD levels caused by H₂O₂, while the underexpression of LUCAT1 increased SOD levels caused by H2O2. (c) ROS levels were increased in the H₂O₂ group, which was further inhibited in the H₂O₂ + p-LUCAT1 group and improved in the H₂O₂ + si-LUCAT1 group. (d) The upregulation of LUCAT1 repressed the enhancement of MDA levels in the H₂O₂-treated cells and the downregulation of LUCAT1 promoted the enhancement of MDA levels. ***P < 0.001, compared with control group; ##P < 0.01, ###P < 0.001, compared with H₂O₂ group

Figure 3. H₂O₂ led to the increased concentration of (a) TNF-α, (b) IL-6, and (c) IL-1β. Interference of LUCAT1 improved these trends, but LUCAT1 exerted inhibited functions on the secretion. ***P < 0.001, compared with control group; ###P < 0.001, compared with H₂O₂ group

Figure 4. The function of LUCAT1 on cell viability and apoptosis. (a) The cell viability was suppressed in the H₂O₂ group, while overexpression of LUCAT1 reversed this trend and silenced LUCAT1 facilitated this trend. (b) The treatment of H₂O₂ facilitate the cell apoptosis, while increased expression of LUCAT1 meliorated this impact and decreased expression of LUCAT1 improved this impact. ***P < 0.001, compared with control group; ##P < 0.01, ###P < 0.001, compared with H₂O₂ group

Figure 5. (a) The predictive binding sites between LUCAT1 and miR-181a-5p. (b) Overexpression of LUCAT1 inhibited the luciferase activity and underexpression of LUCAT1 elevated the luciferase activity in the LUCAT1-WT group. (c) Overexpression of LUCAT1 abrogated the upregulation of miR-181a-5p in the H₂O₂ group and inhibited expression of LUCAT1 accelerated the upregulation of miR-181a-5p in the H₂O₂ group. ***P < 0.001, compared with control group; ###P < 0.001, compared with H₂O₂ group

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.