| Literature DB >> 31568847 |
Sheng Zhao1, Lei Pan1, Min Chen1, Yi-Ping Zhu1, Bang-Min Han1, Shu-Jie Xia2, Jun-Tao Jiang3.
Abstract
Maternal exposure to di-n-butyl phthalate (DBP) induces hypospadias via regulation of autophagy in uroepithelial cells. Here, we use gene express analysis to explore the underlying molecular mechanisms. Pregnant rats received DBP orally at a dose of 750 mg/kg/day during gestational days 14-18. Gene expression analysis showed an increased expression of the hedgehog interacting protein (HhIP) gene. In DBP-induced hypospadiac male offspring, immunohistochemistry (IHC) staining and Western blot analysis confirmed increased expression of the HhIP protein and inhibited hedgehog signaling. in vitro experiments suggest the involvement of the reactive oxygen species (ROS)-HhIP-Gli1-autophagy axis in DBP-treated primary rat urethral epithelial cells. Taken together, our findings show that prenatal exposure to DBP induces abnormal hedgehog signaling and autophagy in uroepithelial cells that may play important roles in the development of hypospadias.Entities:
Keywords: Autophagy; Di-n-butyl phthalate (DBP); Hedgehog signaling; HhIP; Hypospadias
Year: 2019 PMID: 31568847 DOI: 10.1016/j.tox.2019.152300
Source DB: PubMed Journal: Toxicology ISSN: 0300-483X Impact factor: 4.221