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  • Uteroplacental insufficiency in rats induces renal apoptosis and delays nephrogenesis completion

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    Author(s)
    Cuffe, JSM
    Briffa, JF
    Rosser, S
    Siebel, AL
    Romano, T
    Hryciw, DH
    Wlodek, ME
    Moritz, KM
    Griffith University Author(s)
    Cuffe, James S.
    Skelly, Deanne
    Year published
    2018
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    Abstract
    Aim: Uteroplacental insufficiency in rats reduces nephron endowment, leptin concentrations and programs cardiorenal disease in offspring. Cross-fostering growth restricted (Restricted) offspring onto a mother with normal lactation restores leptin concentrations and nephron endowment. This study aimed to determine if the reduced nephron endowment in Restricted offspring is due to delayed glomerular formation and dysregulation of renal genes regulating branching morphogenesis, apoptosis or leptin signalling. Furthermore, we aimed to investigate if cross-fostering Restricted offspring onto Control mothers could improve glomerular ...
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    Aim: Uteroplacental insufficiency in rats reduces nephron endowment, leptin concentrations and programs cardiorenal disease in offspring. Cross-fostering growth restricted (Restricted) offspring onto a mother with normal lactation restores leptin concentrations and nephron endowment. This study aimed to determine if the reduced nephron endowment in Restricted offspring is due to delayed glomerular formation and dysregulation of renal genes regulating branching morphogenesis, apoptosis or leptin signalling. Furthermore, we aimed to investigate if cross-fostering Restricted offspring onto Control mothers could improve glomerular maturation and restore renal gene abundance. Methods: Uteroplacental insufficiency was induced by bilateral uterine vessel ligation (Restricted) or sham (Control) surgery on gestation day 18 (E18). Kidneys were collected at E20, postnatal day 1 (PN1) and PN7. An additional cohort was cross-fostered onto separate mothers at birth and kidneys collected at PN7. Results: Kidneys were lighter in the Restricted group, but weight was restored with cross-fostering. At E20, Bax, Flt1 and Vegfa abundance were increased in Restricted offspring, while Ret and Bcl2 transcripts were increased only in Restricted females. At PN7, Gdnf and Ret abundance were higher in Restricted offspring, as was Casp3. Restricted offspring had a wider nephrogenic zone with more immature glomeruli suggesting a delayed or extended nephrogenic period. Cross-fostering had subtle effects on gene abundance and glomerular maturity. Conclusion: Uteroplacental insufficiency induced apoptosis in the developing kidney and delayed and extended nephrogenesis. Cross-fostering Restricted offspring onto Control mothers had beneficial effects on kidney growth and renal maturity, which may contribute to the restoration of nephron endowment.
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    Journal Title
    Acta Physiologica
    DOI
    https://doi.org/10.1111/apha.12982
    Copyright Statement
    © 2017 Scandinavian Physiological Society. This is the peer reviewed version of the following article: Uteroplacental insufficiency in rats induces renal apoptosis and delays nephrogenesis completion, Acta Physiologica, page 1-14, 2017, which has been published in final form at 10.1111/apha.12982. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving (http://olabout.wiley.com/WileyCDA/Section/id-828039.html)
    Note
    This publication has been entered into Griffith Research Online as an Advanced Online Version.
    Subject
    Physiology not elsewhere classified
    Human Movement and Sports Sciences
    Medical Physiology
    Publication URI
    http://hdl.handle.net/10072/351673
    Collection
    • Journal articles

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