Hepatocytes in the bile duct-ligated rat express Bcl-2

Haruki Kurosawa, Florencia G. Que, Lewis R. Roberts, Patricia J. Fesmier, Gregory J. Gores

Research output: Contribution to journalArticle

84 Scopus citations

Abstract

Hepatocytes do not express Bcl-2, a represser of apoptosis. In contrast, cholangiocytes, which are in direct contact with bile, do express Bcl-2. Because cholestasis results in the retention of bile within hepatocytes, we reasoned cholestasis may induce hepatocellular expression of Bcl-2. Thus our aim was to determine whether hepatocytes express Bcl-2 or alter expression of other Bcl-2 family members in cholestasis using the bile duct-ligated (BDL) rat as a model of cholestasis. De novo Bcl-2 expression was observed in hepatocytes of BDL rats assessed by reverse transcriptase-polymerase chain reaction and immunoblot analysis. Immunohistochemistry demonstrated that Bcl- 2 expression in hepatocytes was greater in periportal hepatocytes than pericentral hepatocytes. Expression of Bcl-x (an antiapoptotic Bcl-2 family protein) was not altered by bile duct ligation, whereas expression of Bax (a proapoptotic Bcl-2 family protein) increased slightly as determined by Northern and Western blot analyses. Bcl-2-positive hepatocytes isolated from BDL rats were resistant to induction of apoptosis by 50 μM glycochenodeoxycholate. Our results demonstrate, for the first time, expression of Bcl-2 by hepatocytes during cholestasis. We suggest that hepatocellular expression of Bcl-2 during cholestasis is an adaptive phenomenon to resist apoptosis by toxic bile salts.

Original languageEnglish (US)
Pages (from-to)G1587-G1593
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume272
Issue number6 35-6
DOIs
StatePublished - Jun 1997

Keywords

  • Apoptosis
  • Bax
  • Bcl-x
  • Bile salts

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

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