Published online Apr 15, 1999. doi: 10.3748/wjg.v5.i2.103
Revised: March 18, 1999
Accepted: March 27, 1999
Published online: April 15, 1999
AIM To determine whether proliferating cell nuclear antigen (PCNA) is present in the peripheral circulation and whether PCNA levels correlate with enhanced regenerative activity.
METHODS In animal studies, adult male Sprague-Dawley rats (n = 3-4/group) were sacrificed at 0, 12, 24, 36, 48, 72 and 96 h following 70% partial hepatectomy. At each interval, sera were analyzed by Western blot for PCNA by two monoclonal antibodies (PC-10 and 19F-4). In human studies, sera from 4 patients with liver cirrhosis and 4 healthy controls were tested in a similar manner.
RESULTS The PC-10 monoclonal antibody identified a protein with a molecular mass of 120 KD which remained stable in rat sera for 24 h fol lowing partial hepatectomy, then increased 1.5-fold at 48 h prior to retur ning to baseline at 96 h after partial hepatectomy. However, it was not dete cted in the sera of patients with or without liver disease. In the 19F-4 monoclonal antibody, a protein with a molecular mass of approximately 46 KD was found. which was present in rat sera prior to partial hepatectomy and for 12 h after surgery. Thereafter, levels fell by approximately 50% at 24 h, 65% at 36 h and 75% at 48 h where they remained until 96 h after partial hepat ectomy. The decrease in levels correlated with the extent of partial hepatectomy. In human sera, the appearance of this inhibitory cell nuclear antigen (ICNA) was higher in the sera of patients with cirrhosis than in healthy controls.
CONCLUSION The PC-10 monoclonal antibody can detect a protein in the circulation when active hepatic regenerative activity is taking place. The 19F-4 monoclonal antibody, however, identifies a protein in both rat and human sera that inversely correlates with hepatic regenerative activity. This prote in which is tentatively referred to as inhibitory cell nuclear antigen (ICNA) may be used in documenting the extent of suppression of hepatic regeneration.