With all our data taken together we propose a model in which b1/b2-KO mice exhibit an enhanced inflammatory Compound Library response to injury and enhanced myoblast proliferation during regeneration. We believe that b1/b2-KO mice have delayed early regeneration due to the prolonged and enhanced inflammatory response, but once the inflammation subsides, the enhanced myoblast proliferation allows the b1/b2-KO muscles to regenerate rapidly – thus accounting for the rapid ‘catch up’ of muscles between 7 and 10 days post-injury. Further studies using muscle specific knockdown of b-ARs or virally-mediated ‘knock in’ of b-ARs to inflammatory cells of b1/b2-KO mice, or other injury models with a higher inflammatory component would help test this hypothesis. In summary, our findings indicate that b-ARs play an important role in early muscle regeneration, at least in part via a direct effect on myoblast proliferation and differentiation. Manipulation of bAR signaling during these early stages of regeneration may therefore improve the rate, extent and efficacy of the regenerative process, to enhance functional recovery after injury. The tumor suppressor gene p53 is activated in response to various stresses, including ionizing radiation, and acts as a transcription factor to regulate expression of many other genes. The genes regulated by p53 induce multifarious cellular responses, e.g., cell cycle arrest, DNA repair, and programmed cell death. These responses, which correspond to a sequence of biological events leading from p53 gene expression to apoptosis induction, are known as cell fate decision, and contribute to both growth inhibition of tumor cells and genetic homeostasis. However, the cell fate decision mechanism applies unknown criteria to various stress intensities. Because the fluctuation of criteria affects the efficiency of artificial apoptosis induction methods such as cancer radiotherapy, many researchers have attempted to identify the dominant factors of the cell fate decision mechanism. The p53 oscillation was observed at the single-cell level in human breast cancer epithelial MCF7 cells. In IR-sensitive cell lines such as thymus and spleen, oscillatory behavior of p53 was not observed, and the p53 was translocated into mitochondria during 30 minutes after IR-irradiation and directly induced apoptosis. In this study, we focused on the relationship between p53 oscillation and apoptosis induction. The mean amplitude and width of each p53 pulse was constant regardless of IR dose. On the other hand, individual cells exposed to the same IR dose exhibited difference in the number of p53 pulses, and the number of p53 pulses at the single-cell level tended to increase with the IR dose. In contrast, damped oscillation of the p53 level was observed in cell populations of mouse fibroblasts and MCF7 cells in response to IR irradiation, and the amplitudes of oscillations increased with the IR dose. Such oscillations of the p53 level were also observed in mice in vivo, which indicated that oscillations of the p53 level are a general phenomenon in various cell types in higher organisms. An increase in the IR dose effected a change in the fractions of cells that were classified by the number of p53 pulses.