Abstract
s / Pancreatology 14 (2014) S1eS129 S19 clinically relevant concentrations of ethanol 10mM (E10) ±cigarette smoke extract (CSE, 4 and 40ng/mL) or nicotine (0.1, 0.5 and 1mM) or nicotinederived nitrosamine ketone (NNK, 100mM and 1mM) and proliferation as well as migration assessed. Results: 1. hPSCs express the nAChR isoforms (a3, a7, b and e). Data below are expressed as % of relevant control. 2. Proliferation was increased by: i) E10 + CSE 40ng/mL (125±5.8%, p<0.05); ii) NNK 100nM (118±2.7%, p<0.02), iii) E10 + NNK 100nM or 1mM (131±10.8%, p<0.05; 130±11.5%, p<0.05). 3. Migration was increased by: i) CSE 4 or 40ng/mL (174±17.4%, p<0.05; 210±29.5%, p<0.05) ii) E10 + CSE 4 or 40ng/mL (204±14.5%, p<0.01; 211±17.5%, p<0.01); iii) NNK 100nM or 1mM alone (150±13%, p<0.05; 170±14.3%, p<0.03); iv) E10 + NNK 100nM or 1mM (206±15.7%, p<0.01; 185±15.5%, p<0.02). Conclusion: PSCs are activated by clinically relevant concentrations of CSE and NNK, alone or in combination with ethanol, providing a possible mechanism for smoking induced progression of alcoholic pancreatic fibrosis.
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