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Chronic exposure to nicotine induces biliary growth and fibrosis
Author(s) -
Munshi Md Kamruzzaman,
Priester Sally,
Guerrier Micheleine,
Glaser Shan
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1117.2
Subject(s) - nicotine , ctgf , endocrinology , medicine , chemistry , fosb , masson's trichrome stain , hepatic stellate cell , gene expression , fibrosis , growth factor , gene , biochemistry , receptor
Nicotine stimulates fibrogeneis that is mediated through α7nAChR. Our Aim was to determine the effects of nicotine on cholangiocyte (BEC) growth and profibrogenic gene expression. Methods α7nAChR expression was assessed in liver sections from normal and BDL rats and NRIC (cell line). Normal and BDL rats were treated with nicotine (24 mg/kg/BW per day) or vehicle for 2 wks by osmotic minipumps. In vivo, proliferation was determined by intrahepatic bile duct mass (IBDM) in liver sections. Collagen deposition was evaluated by Masson's trichrome staining. The effect of nicotine (1 μM, 24–48 hrs) on NRIC growth was determined by MTS assay with/without α‐bungarotoxin (ABT, α7nAChR inhibitor). Nicotine‐induced CTGF, TGFβ1, and Col1A1 gene expression was evaluated by qPCR. Results BEC expressed α7nAChR. Nicotine induced an increase in IBDM in normal and BDL rats, and increased collagen deposition surrounding bile ducts in normal and BDL rats. Nicotine‐stimulated proliferation was blocked by ABT. Nicotine stimulated CTGF, TGFβ1, and Col1A1 gene expression. Conclusion Nicotine stimulates the growth of BEC and induces profibrogenic gene expression.