Chu C M, Yeh C T, Sheen I S, Liaw Y F
Liver Research Unit, Chang Gung Memorial Hospital, Chang Gung Medical College, Taipei, Taiwan.
Gastroenterology. 1995 Dec;109(6):1926-32. doi: 10.1016/0016-5085(95)90760-2.
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.
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.
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.
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.
为了检测慢性乙型肝炎中乙肝核心抗原(HBcAg)的主要细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、肝脏炎症活动和肝细胞再生之间的关系。
研究了30例患者的临床和实验室数据与HBcAg拓扑分布的相关性。通过HBcAg和增殖细胞核抗原的双重免疫染色研究了HBcAg在亚细胞水平上与肝细胞细胞周期的关系。
与以细胞核HBcAg为主的患者相比,以细胞质HBcAg为主的患者的生化和组织学活性水平以及增殖细胞核抗原表达明显更高。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,但与细胞核HbcAg表达程度呈负相关。49%的细胞质HBcAg阳性肝细胞中有增殖细胞核抗原表达,而细胞核HBcAg阳性肝细胞中只有2%有增殖细胞核抗原表达。
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表达程度降低,同时细胞质HBcAg表达增加。