This study was to determine the Semaphorin3B(SEMA3B) role in glioma cells responding to irradiation. Two glioma cell lines,which were used here was wild-type p53(U-87MG),and the other was harboring mutated p53 (U-251).The SEMA3B mRNA could be detected in the two cell lines.The expression level of SEMA3B mRNA was higher in U-87MG cells than in U-251 cells,and increased with time in U-87MG cells after irradiation.Knockdown of SEMA3B expression by shRNA decreased the radiosensitivity of U-87MG cells,this may be associated with the increased G2 accumulation after irradiation.In addition,G2 accumulation after irradiation was enhanced in SEMA3B low-expressing U-87MG cells.These results showed that the SEMA3B was implicated in glioma cells responding to irradiation.
LIU HaiyanXU YuanvuanCHEN YunJIANG XinYU JiahuaYANG LeiGU ChengLIU Fenju
Radiation-induced lung injury is one of the main dose limiting factors for thoracic radiation therapy.Gelsolin(GSN) is a widespread,multifunctional regulator of cellular structure and metabolism.In this work,the roles of GSN in radiation-induced lung injury in Balb/c mice were studied.The GSN levels in plasma reduced progressively in 72 hours after irradiation,and then increased gradually.GSN contents in the bronchoalveolar lavage(BAL) fluid increased after thoracic irradiation,whereas mRNA levels of GSN in the lung tissue decreased significantly within 24 hours after irradiation and then increased again.Mice were intravenously injected with 50 ug GSN antibody 0.5 hour before 20 Gy of thoracic irradiation.GSN antibody pretreatment increased lung inflammation,protein concentration in the BAL fluid and leukocytes infiltration in the irradiated mice.The activities of superoxidase dismutase(SOD) in the plasma and the BAL fluid in irradiated mice injected with GSN antibody were less than that of control groups,whereas the levels of malondialdehyde(MDA)increased.These results suggest that pretreatment of GSN antibody may aggravate radiation-induced pneumonitis.
