The role of pparγ in embryonic development of Xenopus tropicalis under triphenyltin-induced teratogenicity

Evidence has shown that triphenyltin (TPT) triggers severe malformations in Xenopus tropicalis embryos, partly due to activation of PPAR gamma (peroxisome proliferator activated receptor gamma) protein. In the present study, we investigated how abundance of ppar gamma and TPT exposure interact and affect X. tropicalis embryonic development. We observed ppar gamma expression signals appeared in the neural crest and neural fold, as well as in the brain, eyes and spinal cord organs. Both ppar gamma overexpression and its Morpholino (MO) knockdown inhibited pax6 (paired box 6) expression, a marker of eye development, and significantly up-and down-regulated lipid and glucose homeostasis related genes, such as lpl (lipoprotein lipase), slc2a4 (solute carrier family 2 (facilitated glucose transporter), member 4) and pck1 (phosphoenolpyruvate carboxykinase 1, cytosolic), thus inducing eye phenotypes. Overexpression of ppar gamma induced small eye phenotype, while ppar gamma MO induced small eye plus turbid eye lens microencephaly and enlarged trunk. In contrast, 5-20 mu g Sn/L (stannum/L) TPT exposure reversed some impacts induced by ppar gamma overexpression, i.e., no small eye, up-regulation of pax6 and down-regulation of ppar gamma, lpl, slc2a4 and pck1. Meanwhile, microinjection of ppar gamma MO combined with exposure to 20 mu g Sn/L TPT caused 85% mortality. In brief, our work clearly indicates that ppar gamma is essential to eye development and inhibition of its expression combined with TPT exposure can be extremely harmful to X. tropicalis embryo. (C) 2018 Elsevier B.V. All rights reserved.