@misc{oai:repo.qst.go.jp:00083431,
 author = {Miho, Noguchi and Tomokazu, Ihara and Keiji, Suzuki and Akinari, Yokoya and Miho, Noguchi and Akinari, Yokoya},
 month = {Sep},
 note = {Recent studies reported that, in oncogene induced senescence, autophagy is activated during senescence initiation period to ensure rapid protein synthesis. However, senescent cells undergo metabolic and epigenetic changes during their long survival period, and autophagic activity might fluctuate with these changes. To elucidate whether autophagy fluctuates through the progress of senescence, we investigated temporal activity of autophagy over 30 days in normal human diploid cells, hTERT BJ-5ta, exposed to 20 Gy X-rays. Based on the expression levels of p21 and p16, we confirmed that the senescence-like growth arrest was surely induced after irradiation, and senescence was completely established by 7 days post-irradiation. We measured autophagic activity using quantification of LC3-II which is localized in autophagosomes. Autophagosomes are degraded by fusing with lysosomes. Autophagic activity consequently needs to be evaluated including the amount of degraded autophagosomes. We used chloroquine (CQ) as an inhibitor of lysosomal degradation and determined net LC3-II levels including those in the degraded autophagosomes. We found that LC3-II level increased to the same level as control under CQ treatment condition at 1 day after irradiation. At 3 and 7 days, the LC3-II levels with CQ were significantly lower compared to that of control with CQ. At 30 days, it turned to elevate. These results indicate that, in X-ray irradiated cells, autophagy is not significantly activated during senescence initiation, but activated after senescence is established. This delayed activation of autophagy is not seen in oncogene induced senescence, thus it might be due to radiation damage to organelles in cytoplasm., 日本放射線影響学会第64回大会},
 title = {Autophagic activity rises only after senescence is established in cells exposed to radiation},
 year = {2021}
}