Journal article

Renal developmental defects resulting from in utero hypoxia are associated with suppression of ureteric beta-catenin signaling

Lorine J Wilkinson, Cailda S Neal, Reetu R Singh, Duncan B Sparrow, Nyoman D Kurniawan, Adler Ju, Stuart M Grieve, Sally L Dunwoodie, Karen M Moritz, Melissa H Little

KIDNEY INTERNATIONAL | ELSEVIER SCIENCE INC | Published : 2015

Abstract

Gestational stressors, including glucocorticoids and protein restriction, can affect kidney development and hence final nephron number. Since hypoxia is a common insult during pregnancy, we studied the influence of oxygen tension on kidney development in models designed to represent a pathological hypoxic insult. In vivo mouse models of moderate, transient, midgestational (12% O₂, 48 h, 12.5 dpc) or severe, acute, early-gestational (5.5-7.5% O₂, 8 h, 9.5-10.5 dpc) hypoxia were developed. The embryo itself is known to mature under hypoxic conditions with embryonic tissue levels of oxygen estimated to be 5%-8% (physiological hypoxia) when the mother is exposed to ambient normoxia. Both in vivo..

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Grants

Awarded by National Health and Medical Research Council of Australia



Funding Acknowledgements

We thank Antje Blumenthal and Randal Moon for the provision of reagents, and Bob Chapman for technical assistance. This work was supported by the National Health and Medical Research Council of Australia (APP1009338). KMM is an NHMRC Senior Research Fellow (APP631361). MHL is an NHMRC Senior Principal Research Fellow (APP1042093). SLD is an NHMRC Senior Research Fellow (APP1042002).