Figure 3
The co-overexpression of SOD1 and SOD3 significantly improved the poor functions of elderly AT-MSCs by the activation of the pERK/ERK pathway. (A) The protein expression of wild-type elderly AT-MSCs or with the co-overexpression of SOD1 and SOD3 (n = 3). (B) The ROS expression in wild-type elderly AT-MSCs or with the co-overexpression of SOD1 and SOD3 (n = 3). (C) The cellular senescence of wild-type elderly AT-MSCs or with the co-overexpression of SOD1 and SOD3 (n = 3). (D) Transplantation of wild-type elderly AT-MSCs or with the co-overexpression of SOD1 and SOD3 to an in vivo streptozotocin-induced diabetic ischemic flap mouse model (n = 3). (E) The protein expression of pERK/ERK in infant AT-MSC, wildtype elderly AT-MSCs, elderly AT-MSCs with the individual overexpression of SOD1 or SOD3 or elderly AT-MSCs with the co-overexpression of SOD1 and SOD3 (n = 3). (F) The protein expression of pERK/ERK under the presence of a MEK inhibitor (n = 3). (G) The mRNA expression of wound healing-related growth factors in elderly AT-MSCs with the co-overexpression of SOD1 and SOD3 under the presence of a MEK inhibitor (n = 3). (H) Transplantation of elderly AT-MSCs with the co-overexpression of SOD1 and SOD3 under the presence of a MEK inhibitor to an in vivo streptozotocin-induced diabetic ischemic flap mouse model (n = 3). In all above experiments, elderly AT-MSCs were derived from 3 different donors (n = 3). SOD1 + 3: elderly AT-MSCs with co-overexpression of SOD1 and SOD3. PD098059 (PD) was used as a MEK inhibitor. The data represent the mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05, ns no significance. The experiments were performed in triplicate. Full-length Western blots are presented in Supplementary Figure S4.
