ABC | Volume 111, Nº4, Octuber 2018

Original Article Yang et al ApoJ in neointimal hyperplasia Arq Bras Cardiol. 2018; 111(4):562-568 Level of Apo J in carotid arteries The mRNA levels of Apo J were measured by real-time PCR. Our results showed that the Apo J mRNA level was strikingly increased 2 weeks after operation, reached to a peak at the 3 rd week, and decreased at the 4 th week post-surgery in the model group. In intervention group, the Apo J mRNA level was strikingly increased and reached to a peak at the 2 nd week, and decreased at the 3 rd and 4 th week post-surgery in the intervention group. In addition, the mRNA level of Apo J was higher in the intervention group than in the model group at Figure 3 – Hematoxylin-eosin (HE) staining in the model group and in intervention group 1 week (w), 2 weeks, 3 weeks and 4 weeks after balloon injury of rat carotid arteries; magnification 400×. Table 2 – Intimal/medial (I/M) area ratio in the study groups Time points Control group Model group Statin intervention group t * p # n I/M n I/M n I/M 1 5 0.04 ± 0.07 5 0.63 ± 0.40 γ 5 0.42 ± 0.04 γ 10.066 < 0.001 2 5 0.01 ± 0.02 4 1.08 ± 0.29 ▲ 4 1.29 ± 0.31 ∆▲ 39.639 < 0.001 3 5 0.03 ± 0.03 4 1.81 ± 0.11 aβ 4 1.47 ± 0.54 ∆β 37.142 < 0.001 4 5 0.05 ± 0.04 4 2.61 ± 1.12 abθ 4 1.50 ± 0.26 ∆θc 20.287 < 0.001 F $ 0.741 9.432 21.393 P # 0.543 < 0.001 < 0.001 * t test used to compare the differences between the two groups. $ F one-way ANOVA (analysis of variance) to compare the difference between all four groups. # p value < 0.05 was considered statistically significant the 1 st week after operation. At the 2 nd week post-surgery, the mRNA level of Apo J was strikingly increased in both groups and was significantly higher in the stain-intervention group than the model group (Table 3). Similar results have been observed in the protein levels of Apo J as shown in Figure 4. Our results showed that rosuvastatin could significantly increase the expression level of Apo J in balloon-injured rat carotid arteries. Discussion In the present study, we found that I/M increased after balloon-injury and reached the maximum at 4w in the model group; also, I/M was slightly increased at 2w and stopped increasing after rosuvastatin administration. Our results suggest that rosuvastatin could significantly reduce the degree of intimal hyperplasia in balloon-injured carotid arteries in rats. The levels of Apo J mRNA and protein in carotid arteries were significantly upregulated after rosuvastatin administration as compared with the model group, and reached to maximum at 2 weeks, which was earlier than the in the model group. Our results suggest that rosuvastatinmay inhibit intimal hyperplasia through upregulation of Apo J after balloon-injury in rats. Apo J has been reported to be closely related to cardiovascular diseases, such as atherosclerosis and restenosis after angioplasty. 14,15 Ishikawa et al. 7 revealed the distribution of Apo J in the extracellular matrix of endarterium in human atherosclerotic aorta, and its potential protective role against human atherosclerosis by cholesterol transport from the aortic wall to the liver. It has been reported that ApoJ is increased in tissue injury and cell stress, and plays vital role in protection against oxidative stress, cell lysis and apoptotic cell death. 16-21 Additionally, ApoJ could be observed in active tissue remodeling. These findings indicate that ApoJ may act as an acute phase reactant. In the present study, we observed a marked neointimal thickening 2 weeks post-surgery, with proliferation and migration VSMCs observed by HE staining in the model group. The proliferation and migration of VSMC were the most active at week 3, and decrease at week 4. In the meantime, the mRNA and protein levels of Apo J were significantly increased at week 2, reached a peak at 3weeks after operation, and then decreased at 4weeks. The results showed high expression of Apo J in the phase of active proliferation and migration of VSMCs. Consistent with other studies, our results suggest that Apo J may be an acute phase reactant after balloon‑injury in rat carotid arteries. 565