Abstract:
:Prostaglandin E2 (PGE2) is a critical factor in the pathogenesis of dioxin-induced neonatal hydronephrosis. Since the PGE2 receptor has four subtypes, EP1 - EP4, this study was aimed to challenge the hypothesis that at least one of the four subtypes is responsible for the pathogenesis of dioxin-induced hydronephrosis. To this end, we used mouse pups, with a C57BL/6 J background, genetically lacking EP1, EP2, or EP3, and wild-type pups in whom EP4 was suppressed by administering ONO-AE3-208 (ONO), an EP4 antagonist, from postnatal day 1 (PND 1) to PND 13. To expose the pups to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) via lactation, the dams were administered TCDD at an oral dose of 20 μg/kg on PND 1. The pups' urine and kidneys were collected on PND 14 for urinalysis and histological examination, respectively. We found that the incidence of hydronephrosis was 80% in the EP1+/+ group, but was markedly reduced to 28.6% in the EP1-/- group despite the fact that PGE2 concentration in the urine was similarly increased in the both groups. In contrast, the incidence of hydronephrosis was 80% and 100% in the EP2+/+ and EP2-/-groups, respectively, and 88.9% and 100% in the EP3+/+ and EP3-/- groups, respectively. With regard to EP4, the incidence of hydronephrosis in vehicle (saline)-treated groups and ONO-treated was 88.9% and 100%, respectively. Therefore, we concluded that among PGE2 receptor subtypes, EP1 plays a predominant role in the onset of TCDD-induced neonatal hydronephrosis in mouse pups.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Aida-Yasuoka K,Nishimura N,Fujisawa N,Endo N,Narumiya S,Tohyama Cdoi
10.1016/j.tox.2019.01.006subject
Has Abstractpub_date
2019-03-01 00:00:00pages
10-17eissn
0300-483Xissn
1879-3185pii
S0300-483X(18)30354-8journal_volume
415pub_type
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