Apoptosis-associated proteins in oral hairy leukoplakia.
Apoptosis-associated proteins in oral hairy leukoplakia.
复制标题
口腔毛状白斑中的细胞凋亡相关蛋白。
DOI：
10.1111/j.1601-0825.1996.tb00238.x
复制
发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Regezi,JA
中科院分区：
文献类型：
--
作者：
Chrysomali,E;Greenspan,JS;Dekker,N;Greenspan,D;Regezi,JA
目的为了验证Epstein-巴尔病毒（EBV）的抗凋亡能力可能导致口腔毛状白斑（HL）中凋亡相关蛋白表达改变的假设，我们通过免疫组织化学方法对HL组织和正常上皮中的这些蛋白进行了评估。材料和方法从存档的组织标本中选择了20例福尔马林固定、石蜡包埋的HL病变标本和6例正常对照粘膜标本。Bcl-2根据染色强度和模式，在免疫组织化学染色的组织切片中评价Bcl‐x、Bax和p53凋亡相关蛋白。在序贯field.Results中估计p53阳性瘤细胞的百分比：大体上，HL和对照组织上皮中Bcl-2和Bcl-x蛋白的表达仅存在轻微差异。角质形成细胞中Bcl-2的染色弱于假定的黑素细胞和朗格汉斯细胞。还观察到棘细胞的不确定弥漫性细胞质染色。整个上皮的角化细胞对Bcl‐x蛋白染色呈阳性，尽管上层染色较弱。HL中的“气球状”角质形成细胞很少呈Bcl‐x阳性。HL中Bax染色与对照组织不同，其异质性更强。HL中的染色反应在“气球”角质形成细胞所在的上上皮水平为弱至阴性。弱到中度核p53蛋白染色检测到平均25.3%的基础角质形成细胞在所有的HL标本，但一个弱染色只看到两个对照samples.CONCLUSIONS：我们发现只有轻微的化学证据表明，细胞凋亡相关蛋白的表达在HL改变。p53似乎在HL中过表达;我们推测这可能与EBV感染相关的野生型p53蛋白的上调或稳定有关。
OBJECTIVE To test the hypothesis that the anti‐apop totic ability of Epstein‐Barr virus (EBV) may result in altered expression of apoptosis‐associated proteins in oral hairy leukoplakia (HL), we evaluated HL tissue and normal epithelium for these proteins by immunohistochemistry.MATERIALS AND METHODS Twenty formalin‐fixed, paraffin‐embedded specimens of HL lesions and six spedmens of normal control mucosa were selected from archived tissue specimens. Bcl‐2. Bcl‐x, Bax and p53 apoptoris‐associated proteins were evaluated in immu‐nohistochemically stained tissue sections according to staining intensity and pattern. The percentage of p53‐positive burl cells was estimated in sequential fields.RESULTS: Generalty, there were only slight differences in the expression of Bcl‐2 and Bcl‐x proteins in the epithelium of HL and control tissue. The staining for Bcl‐2 was weaker in keratinocytes than in putative melano‐cytes and Langerhans cells. Equivocal diffuse cytoplasmic staining of prickle cells was also noted. Keratinocytes throughout the epithelium stained positively for Bcl‐x protein, although upper layers were more weakly stained. The ‘balloon’ keratinocytes in HL were infrequently positive for Bcl‐x. Bax staining in HL differed from that in control tissue in being more heterogeneous. The staining reaction in HL was weak to negative in upper epithelial levels where ‘balloon’ keratinocytes were located. Weak to moderate nuclear p53 protein staining was detected in a mean of 25.3% of basal keratinocytes in all but one of the HL specimens; weak staining was seen in only two control specimens.CONCLUSIONS: We found only slight immunohistochemid evidence that expression of the apoptosis‐associated proteins is altered in HL. p53 appears to be over‐expressed in HL; we speculate that this may be related to upregulation or stabilization of wild‐type p53 protein related to EBV infedon.