Sign-up for our newsletter
MAIN
Event Calendar
Awardee Reports
ABOUT DIACOMP
Citing DiaComp
Contact
Committees
Institutions
Awardee Reports
Publications
Bioinformatics
RESOURCES
Protocols & Methods
Reagents & Resources
Mouse Diet
Breeding Schemes
Validation Criteria
IMPC / KOMP Data
Publications
Bioinformatics
CONTACT
PARTICIPANT AREA
Login
▹
Publications
▹
Home
Publication
Nephron progenitor cell death elicits a limited compensatory response associated
with interstitial expansion in the neonatal kidney.
Authors
Muthukrishnan SD, Ryzhov S, Karolak M, Oxburgh L
Submitted By
Leif Oxburgh on 2/20/2018
Status
Published
Journal
Disease models & mechanisms
Year
2018
Date Published
1/1/2018
Volume : Pages
11 :
Not Specified
PubMed Reference
29196442
Abstract
The final nephron number in an adult kidney is regulated by nephron progenitor
cell availability and collecting duct branching in the fetal period. Fetal
environmental perturbations that cause reductions in cell numbers in these two
compartments result in low nephron endowment. Previous work has shown that
maternal dietary factors influence nephron progenitor cell availability, with
both caloric restriction and protein deprivation leading to reduced cell numbers
through apoptosis. In this study, we evaluate the consequences of inducing
nephron progenitor cell death on progenitor niche dynamics and on nephron
endowment. Depletion of approximately 40% of nephron progenitor cells by
expression of diphtheria toxin A at embryonic day 15 in the mouse results in
10-20% nephron reduction in the neonatal period. Analysis of cell numbers within
the progenitor cell pool following induction of apoptosis reveals a compensatory
response in which surviving progenitor cells increase their proliferation and
replenish the niche. The proliferative response is temporally associated with
infiltration of macrophages into the nephrogenic zone. Colony stimulating factor
1 (CSF1) has a mitogenic effect on nephron progenitor cells, providing a
potential explanation for the compensatory proliferation. However, CSF1 also
promotes interstitial cell proliferation, and the compensatory response is
associated with interstitial expansion in recovering kidneys which can be
pharmacologically inhibited by treatment with clodronate liposomes. Our findings
suggest that the fetal kidney employs a macrophage-dependent compensatory
regenerative mechanism to respond to acute injury caused by death of nephron
progenitor cells, but that this regenerative response is associated with
neonatal interstitial expansion.
Complications
All Complications
Bioinformatics
Bone
Cardiomyopathy
Cardiovascular
Gastro-Intestinal (GI)
Nephropathy
Neuropathy & Neurocognition
Pediatric Endocrinology
Retinopathy
Uropathy
Wound Healing
Welcome to the DiaComp Login / Account Request Page.
Email Address:
Password:
Note: Passwords are case-sensitive.
Please save my Email Address on this machine.
Not a member?
If you are a funded DiaComp investigator, a member of an investigator's lab,
or an External Scientific Panel member to the consortium, please
request an account.
Forgot your password?
Enter your Email Address and
click here.
ERROR!
There was a problem with the page:
User Info
User Confirm
Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
Citation text and image have been copied to your clipboard. You may now paste them into your document. Thank you!