Induction of Bystander Response in Human Glioma Cells using High-Energy Electrons: A Role for TGF-β1

被引：46

作者：

Gow, M. D.

Seymour, C. B.

Ryan, L. A.

Mothersill, C. E. ^{[1
]}

机构：

[1] McMaster Univ, Med Phys & Appl Radiat Sci Dept, Hamilton, ON L8S 4K1, Canada

来源：

RADIATION RESEARCH | 2010年 / 173卷 / 06期

基金：

加拿大自然科学与工程研究理事会;

关键词：

GROWTH-FACTOR-ALPHA; INDUCED GENOMIC INSTABILITY; PLASMINOGEN-ACTIVATOR; IONIZING-RADIATION; IRRADIATED-CELLS; FACTOR-BETA; HUMAN KERATINOCYTES; HUMAN FIBROBLASTS; NITRIC-OXIDE; CLONOGENIC SURVIVAL;

D O I：

10.1667/RR1895.1

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

We examined bystander cell death produced in T98G cells by exposure to irradiated cell conditioned medium (ICCM) produced by high-energy 20 MeV electrons at a dose rate of 10 Gy min(-1) and doses up to 20 Gy. ICCM induced a bystander response in T98G glioma cells, reducing recipient cell survival by more than 25% below controls at 5 and 10 Gy. Higher doses increased survival to near control levels. ICCM was analyzed for the presence of transforming growth factor a (TGF-alpha) and transforming growth factor 131 (TGF-beta 1). Monoclonal antibodies for TGF-a (mAb TGF-a) and TGF-beta 1 (mAb TGF-beta 1) were added to the ICCM to neutralize any potential effect of the cytokines. The results indicate that TGF-a was not present in the ICCM and addition of mAb TGF-a to the ICCM had no effect on bystander cell survival. No active TGF-beta 1 was present in the ICCM; however, addition of mAb TGF-beta 1 completely abolished bystander death of reporter cells at all doses. These results indicate that bystander cell death can be induced in T98G glioma if a large enough radiation stress is applied and that TGF-beta 1 plays a downstream role in this response. (C) 2010 by Radiation Research Society

引用

页码：769 / 778

页数：10

共 77 条

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