Denis G, Humblet C, Verlaet M, Boniver J, Defresne M P
Department of Pathological Anatomy and Cytology, University of Liège, University Hospital, Belgium.
Anticancer Res. 1998 Sep-Oct;18(5A):3315-21.
Neoplasia can results from a lack of cell elimination by apoptosis. In order to determine if mechanisms controlling apoptosis are disturbed during neoplastic transformation in a model of murine radio-induced thymic lymphomas, we have assessed the kinetics of p53, Bax and Bcl-2 in situ expression after induction of thymic apoptosis by irradiation or glucocorticoids at first in normal mice.
TUNEL method was used for in situ detection of apoptosis and protein expression was determined by indirect immunohistochemistry.
After hydrocortisone injection, levels of p53 and Bax, but not Bcl-2, expression were raised. A whole body sublethal irradiation led to an increase of p53 and Bcl-2, but not Bax, expression.
This is the first in vivo report of in situ protein expression in the thymus after apoptogenic treatments of mice. The results suggest that Bax could be involved in glucocorticoid-mediated apoptosis. The increased levels of Bcl-2 expression are discussed.
肿瘤形成可能源于凋亡导致的细胞清除不足。为了确定在小鼠放射性诱导胸腺淋巴瘤模型的肿瘤转化过程中，控制凋亡的机制是否受到干扰，我们首先在正常小鼠中评估了照射或糖皮质激素诱导胸腺凋亡后p53、Bax和Bcl-2的原位表达动力学。
采用TUNEL法原位检测凋亡，通过间接免疫组织化学法测定蛋白表达。
注射氢化可的松后，p53和Bax的表达水平升高，但Bcl-2的表达未升高。全身亚致死剂量照射导致p53和Bcl-2的表达增加，但Bax的表达未增加。
这是小鼠经凋亡诱导处理后胸腺原位蛋白表达的首篇体内报道。结果表明Bax可能参与糖皮质激素介导的凋亡。文中讨论了Bcl-2表达水平升高的情况。
