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dc.contributor.authorSalazar-Petres, Esteban
dc.contributor.authorCarvalho, Daniela Pereira
dc.contributor.authorLopez-Tello, Jorge
dc.contributor.authorSferruzzi-Perri, Amanda Nancy
dc.date.accessioned2022-03-31T23:30:11Z
dc.date.available2022-03-31T23:30:11Z
dc.date.issued2022-06
dc.identifier.issn0006-3363
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/335630
dc.description.abstractFetal growth depends on placental function, which requires energy from mitochondria. Here we investigated whether mitochondrial function in the placenta relates to the growth of the lightest and heaviest fetuses of each sex within the litter of mice. Placentas from the lightest and heaviest fetuses were taken to evaluate placenta morphology (stereology), mitochondrial energetics (high-resolution respirometry), mitochondrial regulators, nutrient transporters, hormone handling, and signaling pathways (qPCR and Western blotting). We found that mitochondrial complex I and II oxygen consumption rate was greater for placentas supporting the lightest female fetuses, although placental complex I abundance of the lightest females and complexes III and V of the lightest males were decreased compared to their heaviest counterparts. Expression of mitochondrial biogenesis (Nrf1) and fission (Drp1 and Fis1) genes was lower in the placenta from the lightest females, whilst biogenesis-related gene Tfam was greater in the placenta of the lightest male fetuses. In addition, placental morphology and steroidogenic gene (Cyp17a1 and Cyp11a1) expression were aberrant for the lightest females, but glucose transporter (Slc2a1) expression was lower in only the lightest males versus their heaviest counterparts. Differences in intra-litter placental phenotype were related to changes in the expression of hormone-responsive (androgen receptor) and metabolic signaling (AMPK, AKT, and PPARγ) pathways. Thus, in normal mouse pregnancy, placental structure, function, and mitochondrial phenotype are differentially responsive to the growth of the female and male fetus. This study may inform the design of sex-specific therapies for placental insufficiency and fetal growth abnormalities with life-long benefits for the offspring.
dc.publisherSociety for the Study of Reproduction
dc.rightsAll Rights Reserved
dc.rights.urihttp://www.rioxx.net/licenses/all-rights-reserved
dc.titlePlacental structure, function, and mitochondrial phenotype relate to fetal size in each fetal sex in mice
dc.typeArticle
dc.publisher.departmentDepartment of Physiology, Development And Neuroscience
dc.date.updated2022-03-17T12:13:10Z
prism.publicationNameBiology of Reproduction
dc.identifier.doi10.17863/CAM.83061
dcterms.dateAccepted2022-03-16
rioxxterms.versionofrecord10.1093/biolre/ioac056
rioxxterms.versionAM
dc.contributor.orcidSferruzzi-Perri, Amanda [0000-0002-4931-4233]
rioxxterms.typeJournal Article/Review
pubs.funder-project-idWellcome Trust (220456/Z/20/Z)
cam.issuedOnline2022-03-16
cam.orpheus.successMon Apr 25 18:24:14 BST 2022 - Embargo updated
cam.orpheus.counter1
cam.depositDate2022-03-17
pubs.licence-identifierapollo-deposit-licence-2-1
pubs.licence-display-nameApollo Repository Deposit Licence Agreement
rioxxterms.freetoread.startdate2022-07-23


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