E-MTAB-5707
RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks
We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 6 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The whole ileum of the mice were harvested for transcriptomic analysis after completing 6 weeks of smoking.
We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 6 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The whole ileum of the mice were harvested for transcriptomic analysis after completing 6 weeks of smoking.