@article{oai:cis.repo.nii.ac.jp:00000338,
 author = {松岡, 耕二 and 佐々木, 啓子 and CHEN, Kuang Yu and MATUOKA, Koozi and SASAKI, Keiko and CHEN, Kuang Yu},
 issue = {14},
 journal = {千葉科学大学紀要, The University  Bulletin of Chiba Insitute of Science},
 month = {Mar},
 note = {Normal human diploid cells undergo physiological aging by serial subcult ure in vitro as defined by the loss of doubling potential, the appearance of senescence associated β galactosidase activity, a decrease of cellular motility and a change of cell morphology .
Alternatively, these phenotypes can be induced by exposing young cells to a brief oxidative stress such as hydrogen peroxide treatment.
We have previously reported that nicotinamide (NAM), a vitamin and energy metabolism related molecule, reversibly suppresses the senescent phenotypes associated with physiological aging as well as the stress induced aging. The aim of the present study is to inves tigate whether other small molecules that are known to be involved in modulating key signaling pathways may act like NAM in affecting the senescent phenotypes. Specifically, we found the activators for sirtuin, AMP kinase and autophagy signaling all suppress the senescent phenotypes, whereas their inhibitors induce senescent phenotypes. On the other hand, the inhibitors of phosphoi nositide 3 kinase (PI3K) suppressed senescent phenotypes. To further analyze the role of NAM and PI3K in the senescence modulati ng process, we examined the expression of various PI3K catalytic units and the phosphorylation of Akt, a PI3K downstream target. Our study suggested that the expression of senescent phenotypes in human diploid cells is intimately connected to signaling ne tworks involved in energy metabolism and autophagy.},
 pages = {6--14},
 title = {Suppression of Senescent Phenotypes in Normal Human Diploid Cells by Nicotinamide and phosphoinositide 3-kinase inhibitors},
 year = {2021},
 yomi = {マツオカ, コウジ}
}