mmpc-logo mmpc-logo
twitter-logo    bluesky-logo
| Create Account | login
Publication
Regulation of Nephron Progenitor Cell Self-Renewal by Intermediary Metabolism.
Authors Liu J, Edgington-Giordano F, Dugas C, Abrams A, Katakam P, Satou R, Saifudeen Z
Submitted By Submitted Externally on 11/16/2018
Status Published
Journal Journal of the American Society of Nephrology : JASN
Year 2017
Date Published 11/1/2017
Volume : Pages 28 : 3323 - 3335
PubMed Reference 28754792
Abstract Nephron progenitor cells (NPCs) show an age-dependent capacity to balance
self-renewal with differentiation. Older NPCs (postnatal day 0) exit the
progenitor niche at a higher rate than younger (embryonic day 13.5) NPCs do.
This behavior is reflected in the transcript profiles of young and old NPCs.
Bioenergetic pathways have emerged as important regulators of stem cell fate.
Here, we investigated the mechanisms underlying this regulation in murine NPCs.
Upon isolation and culture in NPC renewal medium, younger NPCs displayed a
higher glycolysis rate than older NPCs. Inhibition of glycolysis enhanced
nephrogenesis in cultured embryonic kidneys, without increasing ureteric tree
branching, and promoted mesenchymal-to-epithelial transition in cultured
isolated metanephric mesenchyme. Cotreatment with a canonical Wnt signaling
inhibitor attenuated but did not entirely block the increase in nephrogenesis
observed after glycolysis inhibition. Furthermore, inhibition of the
phosphatidylinositol 3-kinase/Akt self-renewal signaling pathway or stimulation
of differentiation pathways in the NPC decreased glycolytic flux. Our findings
suggest that glycolysis is a pivotal, cell-intrinsic determinant of NPC fate,
with a high glycolytic flux supporting self-renewal and inhibition of glycolysis
stimulating differentiation.




Menu

Home
Contact
About MMPC
Animal Husbandry
Tests Data
Search Data
Analysis
Clients
MMPC Centers

Newsletter

Interested in receiving MMPC News?
twitter-logo Mouse Phenotyping
@NationalMMPC



2017 National MMPC. All Rights Reserved.