Autophagy attenuates placental apoptosis, oxidative stress and fetal growth restriction in pregnant ewes

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dc.authoridMa, Yi/0000-0002-3781-314X
dc.contributor.authorZhang, Hao
dc.contributor.authorZheng, Yi
dc.contributor.authorLiu, Xiaoyun
dc.contributor.authorZha, Xia
dc.contributor.authorElsabagh, Mabrouk
dc.contributor.authorMa, Yi
dc.contributor.authorJiang, Honghua
dc.date.accessioned2024-11-07T13:34:44Z
dc.date.available2024-11-07T13:34:44Z
dc.date.issued2023
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractBisphenol A (BPA)-induced oxidative stress (OS) and its potentially associated autophagy and apoptosis have not been studied previously in pregnant ewes. Accordingly, this study investigated the underlying mechanisms of BPA-induced autophagy and apoptosis in the placenta and primary trophoblasts of pregnant ewes exposed to BPA both in vivo and in vitro. In vivo experiment, pregnant Hu ewes (n = 8) were exposed to 5 mg/kg/d of BPA compared to control ewes (n = 8) receiving only corn oil from day 40 through day 110 of gestation. Exposure to BPA during gestation resulted in placental insufficiency, fetal growth restriction (FGR), autophagy, endoplasmic reticulum stress (ERS), mitochondrial dysfunction, OS, and apoptosis in type A placentomes. Regarding in vitro model, primary ovine trophoblasts were exposed to BPA, BPA plus chloroquine (CQ; an autophagy inhibitor) or BPA plus rapamycin (RAP; an autophagy activator) for 12 h. Data illustrated that exposure to BPA enhanced autophagy (ULK1, Beclin-1, LC3, Parkin, and PINK1), ERS (GRP78, CHOP10, ATF4, and ATF6) and apoptosis (Caspase 3, Bcl-2, Bax, P53) but decreased the antioxidant (CAT, Nrf2, HO-1, and NQO1)-related mRNA and protein expressions as well as impaired the mitochondrial function. Moreover, treatment with CQ exacerbated the BPA-mediated OS, mitochondrial dysfunction, apoptosis, and ERS. On the contrary, RAP treatment coun-teracted the BPA-induced trophoblast dysfunctions mentioned above. Overall, the findings illustrated that BPA exposure could contribute to autophagy in the ovine placenta and trophoblasts and that autophagy, in turn, could alleviate BPA-induced apoptosis, mitochondrial dysfunction, ERS, and OS. These results offer new mechanistic insights into the role of autophagy in mitigating BPA-induced placental dysfunctions and FGR.
dc.description.sponsorshipNational Natural Science Foundation of China [31902180]; National 14th Five -Year Plan Key Research and Development Program [2021YFD1600702]; Top Talents Award Plan of Yangzhou University (2020); Cyanine Project of Yangzhou University (2020)
dc.description.sponsorshipThe research was supported by the fund for the National Natural Science Foundation of China (Grant number 31902180), the National 14th Five-Year Plan Key Research and Development Program (2021YFD1600702), the Top Talents Award Plan of Yangzhou University (2020), and the Cyanine Project of Yangzhou University (2020). The authors thank all the members of Hong Rong Wang's laboratory for their contribution to sample determination
dc.identifier.doi10.1016/j.envint.2023.107806
dc.identifier.issn0160-4120
dc.identifier.issn1873-6750
dc.identifier.pmid36841186
dc.identifier.scopus2-s2.0-85148667099
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.envint.2023.107806
dc.identifier.urihttps://hdl.handle.net/11480/16143
dc.identifier.volume173
dc.identifier.wosWOS:000944805400001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofEnvironment International
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_20241106
dc.subjectAutophagy
dc.subjectApoptosis
dc.subjectBisphenol A
dc.subjectFetal growth restriction
dc.subjectSheep
dc.subjectPlacenta
dc.titleAutophagy attenuates placental apoptosis, oxidative stress and fetal growth restriction in pregnant ewes
dc.typeArticle

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