SUBCELLULAR-LOCALIZATION OF HEPATITIS-B CORE ANTIGEN IN RELATION TO HEPATOCYTE REGENERATION IN CHRONIC HEPATITIS-B
SUBCELLULAR-LOCALIZATION OF HEPATITIS-B CORE ANTIGEN IN RELATION TO HEPATOCYTE REGENERATION IN CHRONIC HEPATITIS-B
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DOI：
10.1016/0016-5085(95)90760-2
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发表时间：
1995-12-01
期刊：
影响因子：
29.4
通讯作者：
LIAW, YF
中科院分区：
文献类型：
--
作者：
CHU, CM;YEH, CT;LIAW, YF
背景与目的：为了检验活动性慢性乙型肝炎中乙型肝炎核心抗原（HBcAg）的显性胞质表达是否继发于肝损伤和再生，研究了慢性乙型肝炎中HBcAg的亚细胞定位、肝脏炎症活动性和肝细胞再生之间的关系。方法：对 30 例患者的临床和实验室数据与 HBcAg 局部分布的相关性进行研究。通过 HBcAg 和增殖细胞核抗原的双重免疫染色研究了 HBcAg 的亚细胞定位与肝细胞细胞周期的关系。结果：细胞质 HBcAg 为主的患者的生化和组织学活性以及增殖细胞核抗原表达水平显着高于核 HBcAg 为主的患者。增殖细胞核抗原表达水平与生化和组织学活性以及细胞质HBcAg表达程度呈正相关，但与核HBcAg表达程度呈负相关。 49% 的细胞质 HBcAg 肝细胞中显示增殖细胞核抗原表达，但只有 2% 的细胞核 HBcAg 肝细胞中显示增殖细胞核抗原表达。结论：这些发现表明，肝损伤后，存活肝细胞的再生可能导致细胞内 HBcAg 从细胞核转移到细胞质。结果，细胞核 HBcAg 表达的程度降低，同时细胞质 HBcAg 表达增加。
Background & Aims: To test whether the dominant cytoplasmic expression of hepatitis B core antigen (HBcAg) in active chronic hepatitis B is secondary to liver damage and regeneration, the relationship between subcellular localization of HBcAg, liver inflammatory activity, and hepatocyte regeneration in chronic hepatitis B was studied. Methods: Correlation of the clinical and laboratory data with the topographical distribution of HBcAg was studied in 30 patients. The subcellular localization of HBcAg in relation to hepatocyte cell cycles was studied by double immunostaining of HBcAg and proliferating cell nuclear antigen. Results: Patients with predominant cytoplasmic HBcAg had significantly higher levels of biochemical and histological activities and proliferating cell nuclear antigen expression than patients with predominant nuclear HBcAg. The levels of proliferating cell nuclear antigen expression correlated positively with biochemical and histological activities and degrees of cytoplasmic HBcAg expression but negatively with degrees of nuclear HBcAg expression. Proliferating cell nuclear antigen expression was shown in 49% of hepatocytes with cytoplasmic HBcAg but in only 2% of hepatocytes with nuclear HBcAg. Conclusions: These findings suggested that, following liver damage, the regeneration of surviving hepatocytes might cause the shift of intracellular HBcAg from nucleus to cytoplasm. As a result, the extent of nuclear HBcAg expression reduces with concomitant increase in cytoplasmic HBcAg expression.