Stromal protein Ecm1 regulates ureteric bud patterning and branching.

The interactions between the nephrogenic mesenchyme and the ureteric bud during kidney development are well documented. While recent studies have shed some light on the importance of the stroma during renal development, many of the signals generated in the stroma, the genetic pathways and interactio...

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Autores principales: Suneeta S Paroly, Fengwei Wang, Lee Spraggon, Joseph Merregaert, Ekatherina Batourina, Benjamin Tycko, Kai M Schmidt-Ott, Sean Grimmond, Melissa Little, Cathy Mendelsohn
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/a68c4ca108624634a444f21b3100d0dc
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spelling oai:doaj.org-article:a68c4ca108624634a444f21b3100d0dc2021-11-18T08:39:24ZStromal protein Ecm1 regulates ureteric bud patterning and branching.1932-620310.1371/journal.pone.0084155https://doaj.org/article/a68c4ca108624634a444f21b3100d0dc2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24391906/?tool=EBIhttps://doaj.org/toc/1932-6203The interactions between the nephrogenic mesenchyme and the ureteric bud during kidney development are well documented. While recent studies have shed some light on the importance of the stroma during renal development, many of the signals generated in the stroma, the genetic pathways and interaction networks involving the stroma are yet to be identified. Our previous studies demonstrate that retinoids are crucial for branching of the ureteric bud and for patterning of the cortical stroma. In the present study we demonstrate that autocrine retinoic acid (RA) signaling in stromal cells is critical for their survival and patterning, and show that Extracellular matrix 1, Ecm1, a gene that in humans causes irritable bowel syndrome and lipoid proteinosis, is a novel RA-regulated target in the developing kidney, which is secreted from the cortical stromal cells surrounding the cap mesenchyme and ureteric bud. Our studies suggest that Ecm1 is required in the ureteric bud for regulating the distribution of Ret which is normally restricted to the tips, as inhibition of Ecm1 results in an expanded domain of Ret expression and reduced numbers of branches. We propose a model in which retinoid signaling in the stroma activates expression of Ecm1, which in turn down-regulates Ret expression in the ureteric bud cleft, where bifurcation normally occurs and normal branching progresses.Suneeta S ParolyFengwei WangLee SpraggonJoseph MerregaertEkatherina BatourinaBenjamin TyckoKai M Schmidt-OttSean GrimmondMelissa LittleCathy MendelsohnPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 12, p e84155 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Suneeta S Paroly
Fengwei Wang
Lee Spraggon
Joseph Merregaert
Ekatherina Batourina
Benjamin Tycko
Kai M Schmidt-Ott
Sean Grimmond
Melissa Little
Cathy Mendelsohn
Stromal protein Ecm1 regulates ureteric bud patterning and branching.
description The interactions between the nephrogenic mesenchyme and the ureteric bud during kidney development are well documented. While recent studies have shed some light on the importance of the stroma during renal development, many of the signals generated in the stroma, the genetic pathways and interaction networks involving the stroma are yet to be identified. Our previous studies demonstrate that retinoids are crucial for branching of the ureteric bud and for patterning of the cortical stroma. In the present study we demonstrate that autocrine retinoic acid (RA) signaling in stromal cells is critical for their survival and patterning, and show that Extracellular matrix 1, Ecm1, a gene that in humans causes irritable bowel syndrome and lipoid proteinosis, is a novel RA-regulated target in the developing kidney, which is secreted from the cortical stromal cells surrounding the cap mesenchyme and ureteric bud. Our studies suggest that Ecm1 is required in the ureteric bud for regulating the distribution of Ret which is normally restricted to the tips, as inhibition of Ecm1 results in an expanded domain of Ret expression and reduced numbers of branches. We propose a model in which retinoid signaling in the stroma activates expression of Ecm1, which in turn down-regulates Ret expression in the ureteric bud cleft, where bifurcation normally occurs and normal branching progresses.
format article
author Suneeta S Paroly
Fengwei Wang
Lee Spraggon
Joseph Merregaert
Ekatherina Batourina
Benjamin Tycko
Kai M Schmidt-Ott
Sean Grimmond
Melissa Little
Cathy Mendelsohn
author_facet Suneeta S Paroly
Fengwei Wang
Lee Spraggon
Joseph Merregaert
Ekatherina Batourina
Benjamin Tycko
Kai M Schmidt-Ott
Sean Grimmond
Melissa Little
Cathy Mendelsohn
author_sort Suneeta S Paroly
title Stromal protein Ecm1 regulates ureteric bud patterning and branching.
title_short Stromal protein Ecm1 regulates ureteric bud patterning and branching.
title_full Stromal protein Ecm1 regulates ureteric bud patterning and branching.
title_fullStr Stromal protein Ecm1 regulates ureteric bud patterning and branching.
title_full_unstemmed Stromal protein Ecm1 regulates ureteric bud patterning and branching.
title_sort stromal protein ecm1 regulates ureteric bud patterning and branching.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/a68c4ca108624634a444f21b3100d0dc
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