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1 Departments of Internal Medicine and 2 Medical Physiology, 3 Division of Research and Education, Scott & White Hospital and The Texas A&M University System Health Science Center, College of Medicine and 4 Central Texas Veterans Health Care System, Temple, Texas 76504; 5 Third Department of Internal Medicine, Tohoku University School of Medicine, Aobaku, Sendai, Japan 980-8574; and 6 Division of Gastroenterology, University of Rome, La Sapienza, Rome, Italy 00100
Cholangiocyte proliferation and loss through apoptosis
occur in cholestatic liver diseases. Our aim was to determine the
mechanisms of apoptosis in an animal model of ductal
hyperplasia. Rats were fed 
-naphthylisothiocyanate (ANIT) for 2 wk
and subsequently fed normal chow for 1, 2, and 4 wk. Proliferation was
assessed in sections by morphometry and in small and large
cholangiocytes by proliferating cellular nuclear antigen immunoblots
and measurement of cAMP levels. Apoptosis and reactive oxygen
species (ROS) levels were also assessed. ANIT feeding increased small
and large cholangiocyte proliferation and apoptosis. Cessation
of ANIT feeding was associated with decreased proliferation and a
further increase in apoptosis in small and large
cholangiocytes. Cholangiocytes from ANIT-fed rats or exposed to ANIT in
vitro showed increased apoptosis and ROS generation.
ANIT-induced duct injury results in enhanced proliferation and
apoptosis in small and large cholangiocytes. The mechanism of
ANIT-induced apoptosis may be due to ROS generation induced directly by ANIT. Our model has implications for understanding the
pathophysiology of cholangiopathies (characterized by the coexistence
of cholangiocyte apoptosis and proliferation).
cyclic adenosine 3',5'-monophosphate; intrahepatic biliary epithelium; DNA replication; reactive oxygen species
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