title: Ceramide is involved in alcohol-induced neural proliferation.
abstract: Prenatal alcohol exposure, especially during early pregnancy, can lead to fetal alcohol syndrome. The pharmacological and toxicological mechanisms of ethanol are related to the effects of ceramide. In this study, we established an alcohol exposure model in wild-type mice and in knockout mice for the key enzyme involved in ceramide metabolism, sphingomyelin synthase 2. This model received daily intragastric administration of 25% ethanol, and pups were used at postnatal days 0, 7, 14, 30 for experiments. Serology and immunofluorescence staining found that ethanol exposure dose-dependently reduced blood sphingomyelin levels in two genotypes of pups, and increased neural cell proliferation and the number of new neurons in the hippocampal dentate gyrus. Western blot analysis showed that the relative expression level of protein kinase C α increased in two notypes of pups after ethanol exposure. Compared with wild-type pups, the expression level of the important activator protein of the ceramide/ceramide-1-phosphate pathway, protein kinase C α, was reduced in the hippocampus of sphingomyelin synthase 2 knockouts. Our findings illustrate that ceramide is involved in alcohol-induced neural proliferation in the hippocampal dentate gyrus of pups after prenatal ethanol exposure, and the mechanism may be associated with increased pression of protein kinase C α activating the ceramide/ceramide-1-phosphate pathway.
authors.affiliation: Institute of Neurobiology, Henan University, Kaifeng 475004, Henan Province, China ; Department of Anatomy, Basic Medical College, Zhengzhou University, Zhengzhou 450052, Henan Province, China.
authors.forename: Zhixin
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Anatomy, Luohe Medical College, Luohe 462002, Henan Province, China.
authors.forename: Tongxing
authors.initials: T
authors.lastname: Deng
authors.affiliation: Institute of Neurobiology, Henan University, Kaifeng 475004, Henan Province, China.
authors.forename: Jiexin
authors.initials: J
authors.lastname: Deng
authors.affiliation: Institute of Neurobiology, Henan University, Kaifeng 475004, Henan Province, China.
authors.forename: Jinbo
authors.initials: J
authors.lastname: Deng
authors.affiliation: Department of Anatomy, Basic Medical College, Zhengzhou University, Zhengzhou 450052, Henan Province, China.
authors.forename: Xiaoqun
authors.initials: X
authors.lastname: Gao
authors.affiliation: Institute of Neurobiology, Henan University, Kaifeng 475004, Henan Province, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Shi
authors.affiliation: Institute of Neurobiology, Henan University, Kaifeng 475004, Henan Province, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Liu
authors.affiliation: Institute of Neurobiology, Henan University, Kaifeng 475004, Henan Province, China.
authors.forename: Zhanyou
authors.initials: Z
authors.lastname: Ma
authors.affiliation: Institute of Neurobiology, Henan University, Kaifeng 475004, Henan Province, China.
authors.forename: Haixiao
authors.initials: H
authors.lastname: Jin
keywords: brain injury; cera-mide-1-phosphate; ceramide; fetal alcohol syndrome; grants-supported paper; neural cells; neural regeneration; neuroregeneration; prenatal alcohol exposure; proliferation; sphingomyelin; sphingomyelin synthase; sphingomyelin synthase 2 knockout mice