Wang J, Walsh K
Division of Cardiovascular Research, St. Elizabeth's Medical Center and Tufts University School of Medicine, Boston, MA 02135, USA.
Science. 1996 Jul 19;273(5273):359-61. doi: 10.1126/science.273.5273.359.
Proliferating murine C2C12 myoblasts can undergo either terminal differentiation or programmed cell death under conditions of mitogen deprivation. Unlike myoblasts, differentiated myotubes were resistant to apoptosis. During myogenesis the appearance of the apoptosis-resistant phenotype was correlated with the induction of the cyclin-dependent kinase (Cdk) inhibitor p21(CIP1) but not with the appearance of myogenin, a marker expressed earlier in differentiation. Forced expression of the Cdk inhibitors p21(CIP1) or p16(INK4A) blocked apoptosis during myocyte differentiation. These data indicate that induction of Cdk inhibitors may serve to protect differentiating myocytes from programmed cell death as well as play a role in establishing the postmitotic state.
在有丝分裂原剥夺的条件下，增殖的小鼠C2C12成肌细胞可经历终末分化或程序性细胞死亡。与成肌细胞不同，分化的肌管对凋亡具有抗性。在肌生成过程中，抗凋亡表型的出现与细胞周期蛋白依赖性激酶（Cdk）抑制剂p21（CIP1）的诱导相关，而与肌细胞生成素的出现无关，肌细胞生成素是在分化早期表达的一种标志物。Cdk抑制剂p21（CIP1）或p16（INK4A）的强制表达可阻断肌细胞分化过程中的凋亡。这些数据表明，Cdk抑制剂的诱导可能有助于保护分化中的肌细胞免受程序性细胞死亡，以及在建立有丝分裂后状态中发挥作用。
