2007 JASN IMPACT FACTOR 7.111	HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP
advanced	CURRENT ISSUE	ARCHIVES	JASN Express	ONLINE SUBMISSION

This Article Full Text Full Text (PDF) All Versions of this Article: ASN.2007080864v1 19/5/943    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Tran, S. Articles by Zhang, S.-L. PubMed PubMed Citation Articles by Tran, S. Articles by Zhang, S.-L. Related Collections Related Article

Maternal Diabetes Modulates Renal Morphogenesis in Offspring

Stella Tran^*, Yun-Wen Chen^*, Isabelle Chenier^*, John S.D. Chan^*, Susan Quaggin, Marie-Josée Hébert^*, Julie R. Ingelfinger and Shao-Ling Zhang^*

^* University of Montreal, Centre Hospitalier de l’Université de Montréal–Hôtel-Dieu, Research Centre, Montreal, Quebec, Canada; Samuel Lunenfeld Research Institute, University of Toronto, Toronto, Ontario, Canada; and Pediatric Nephrology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts

Correspondence: Dr. Shao-Ling Zhang University of Montreal, Centre Hospitalier de l’Université de Montréal–Hôtel-Dieu, Research Centre, Pavillon Masson, 3850 Saint Urbain Street, Montreal, Quebec H2W 1T7, Canada. Phone: 514-890-8000, ext. 15633; Fax: 514-412-7204; E-mail: shao.ling.zhang{at}umontreal.ca

Received for publication August 7, 2007. Accepted for publication January 10, 2008.

Maternal diabetes leads to an adverse in utero environment, but whether maternal diabetes impairs nephrogenesis is unknown. Diabetes was induced with streptozotocin in pregnant Hoxb7–green fluorescence protein mice at embryonic day 13, and the offspring were examined at several time points after birth. Compared with offspring of nondiabetic controls, offspring of diabetic mice had lower body weight, body size, kidney weight, and nephron number. The observed renal dysmorphogenesis may be the result of increased apoptosis, because immunohistochemical analysis revealed significantly more apoptotic podocytes as well as increased active caspase-3 immunostaining in the renal tubules compared with control mice. Regarding potential mediators of these differences, offspring of diabetic mice had increased expression of intrarenal angiotensinogen and renin mRNA, upregulation of NF-B isoforms p50 and p65, and activation of the NF-B pathway. In conclusion, maternal diabetes impairs nephrogenesis, possibly via enhanced intrarenal activation of the renin-angiotensin system and NF-B signaling.

Related Article

Perinatal Nephron Programming Is not So Sweet in Maternal Diabetes

Dale R. Abrahamson and Brooke M. Steenhard
J. Am. Soc. Nephrol. 2008 19: 837-839. [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673