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Congenital Anomalies of the Kidney and of the Urinary Tract (CAKUT) cover a broad range of disorders including abnormal kidney development caused by defective nephrogenesis. Here we explored the possible involvement of the low affinity p75 neurotrophin receptor (p75NTR) in CAKUT and nephrogenesis. In mouse, p75NTR was highly expressed in fetal kidney, located within cortical early nephrogenic bodies, and decreased rapidly after birth. In human control fetal kidney, p75NTR was also located within the early nephrogenic bodies as well as in the mature glomeruli, presumably in the mesangium. In CAKUT fetal kidneys, the kidney cortical structure and the localization of p75NTR were often disorganized, and quantification of p75NTR in amniotic fluid revealed a significant reduction in CAKUT compared to control. Finally, invalidation of p75NTR in zebrafish embryo with an antisense morpholino significantly altered pronephros development. Our results indicate that renal p75NTR is altered in CAKUT fetuses, and could participate to early nephrogenesis. Copyright © 2020 Elsevier Inc. All rights reserved.


Camille Fédou, Ophélie Lescat, Guylène Feuillet, Marie Buléon, Eric Neau, Benjamin Breuil, Mélinda Alvès, Julie Batut, Patrick Blader, Stéphane Decramer, Jean Sébastien Saulnier-Blache, Julie Klein, Bénédicte Buffin-Meyer, Joost P Schanstra. The low affinity p75 neurotrophin receptor is down-regulated in congenital anomalies of the kidney and the urinary tract: Possible involvement in early nephrogenesis. Biochemical and biophysical research communications. 2020 Dec 17;533(4):786-791

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PMID: 32988586

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