The primary fibroblasts were transfected with empty virus or an AAT knockdown virus, and the cells were divided into the following groups: empty virus group, AAT1 knockdown group, AAT2 knockdown group, AAT1 knockdown + SO[sub]2 group, AAT2 knockdown + SO[sub]2 group, AAT1 knockdown + Pyruvate group, AAT2 knockdown + Pyruvate group, empty virus + PD98059 group, AAT1 knockdown + PD98059 group, and AAT2 knockdown + PD98059 group.
Rat myocardial fibroblasts transfected with AAT1 knockdown virus, AAT2 knockdown virus, or empty virus were seeded into the cell migration chamber.
We detected protein expression of AAT1 and AAT2 in cardiac fibroblasts and also detected the generation of SO[sub]2 in the cell supernatant, suggesting that there was an endogenous SO[sub]2/AAT pathway in cardiac fibroblasts.
In rat primary myocardial fibroblasts, the PCNA expression was significantly increased in the AAT1 knockdown group ( F = 31.70, P < 0.01) and in the AAT2 knockdown group compared with the empty virus group ( F = 18.93, P < 0.01).
The images and data both showed that the width of wound in the cultured cells of AAT1 knockdown group at 24 h ( F = 53.01, P < 0.01) and 48 h ( F = 43.35, P < 0.01) was narrower than that of empty group at the same time point.
Compared with the AAT1 knockdown lentivirus group, the expression of PCNA and the activity of CCK8 were significantly decreased in the AAT1 knockdown + SO[sub]2 group.
Compared with the empty lentivirus group, the phosphorylated ERK in the rat primary myocardial fibroblasts of AAT1 knockdown lentivirus group and AAT2 knockdown lentivirus group was significantly increased, respectively.