scholarly journals Patterning a Complex Organ: Branching Morphogenesis and Nephron Segmentation in Kidney Development

2010 ◽  
Vol 18 (5) ◽  
pp. 698-712 ◽  
Author(s):  
Frank Costantini ◽  
Raphael Kopan
Keyword(s):  
Kidney Development ◽  
Branching Morphogenesis ◽  
Nephron Segmentation ◽  
Complex Organ

scholarly journals MMP9 Limits Apoptosis and Stimulates Branching Morphogenesis During Kidney Development

2009 ◽  
Vol 20 (10) ◽  
pp. 2171-2180 ◽  
Author(s):  
Catherine Arnould ◽  
Martine Lelièvre-Pégorier ◽  
Pierre Ronco ◽  
Brigitte Lelongt
Keyword(s):  
Kidney Development ◽  
Branching Morphogenesis

scholarly journals TROP2 Expressed in the Trunk of the Ureteric Duct Regulates Branching Morphogenesis during Kidney Development

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28607 ◽  
Author(s):  
Yuko Tsukahara ◽  
Minoru Tanaka ◽  
Atsushi Miyajima
Keyword(s):  
Kidney Development ◽  
Branching Morphogenesis

scholarly journals β-catenin regulates the formation of multiple nephron segments in the mouse kidney

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Patrick Deacon ◽  
Charles W. Concodora ◽  
Eunah Chung ◽  
Joo-Seop Park
Keyword(s):  
Kidney Development ◽  
Critical Role ◽  
Mouse Kidney ◽  
Proximal Tubules ◽  
Stable Form ◽  
Loss Of Function ◽  
Nephron Segments ◽  
Mesenchymal To Epithelial Transition ◽  
Nephron Progenitors ◽  
Nephron Segmentation

Abstract The nephron is composed of distinct segments that perform unique physiological functions. Little is known about how multipotent nephron progenitor cells differentiate into different nephron segments. It is well known that β-catenin signaling regulates the maintenance and commitment of mesenchymal nephron progenitors during kidney development. However, it is not fully understood how it regulates nephron segmentation after nephron progenitors undergo mesenchymal-to-epithelial transition. To address this, we performed β-catenin loss-of-function and gain-of-function studies in epithelial nephron progenitors in the mouse kidney. Consistent with a previous report, the formation of the renal corpuscle was defective in the absence of β-catenin. Interestingly, we found that epithelial nephron progenitors lacking β-catenin were able to form presumptive proximal tubules but that they failed to further develop into differentiated proximal tubules, suggesting that β-catenin signaling plays a critical role in proximal tubule development. We also found that epithelial nephron progenitors lacking β-catenin failed to form the distal tubules. Expression of a stable form of β-catenin in epithelial nephron progenitors blocked the proper formation of all nephron segments, suggesting tight regulation of β-catenin signaling during nephron segmentation. This work shows that β-catenin regulates the formation of multiple nephron segments along the proximo-distal axis of the mammalian nephron.

Role of transferrin in branching morphogenesis, growth and differentiation of the embryonic kidney

Development ◽  
1984 ◽  
Vol 82 (1) ◽  
pp. 147-161
Author(s):  
Irma Thesleff ◽  
Peter Ekblom
Keyword(s):  
Cell Proliferation ◽  
Kidney Development ◽  
Culture Media ◽  
Branching Morphogenesis ◽  
Defined Medium ◽  
Target Tissue ◽  
Kidney Tubules ◽  
Tubule Formation ◽  
Serum Factors ◽  
Induction Process

Our previous work has suggested that transferrin is an important serum component for differentiation of the kidney. In this study we have analysed more closely the response of cultured mouse embryonic kidney to exogenous transferrin and the dependence of kidney tubule induction on transferrin. Our results show that transferrin causes a dose-dependent increase in cell proliferation in the differentiating kidney mesenchyme, but no stimulation of cell proliferation in the inductortissue used, the embryonic spinal cord. In cultures of whole kidney rudiments a remarkable increase in the amounts of DNA and protein are caused by transferrin but not by other serum components present in a transferrin-depleted serum. The morphology of the explants was similar when culturedin the presence of human serum and in the transferrin-depleted serum supplemented with transferrin. In transferrincontaining chemically-defined medium the explants flattened and spread out, but the morphology of the kidney tubules was similar as in explants cultured in the presence of serum. Examination of the cultured explants by electron microscopy showed that in all transferrincontaining culture media the mesenchymal cells had differentiated into kidney tubules consisting of epithelial cells lined by a basement membrane. The experiments with the transferrin-depleted serum demonstrate that the main mitogen for kidney development is transferrin, and that other serum factors are mainly required for maintenance of tissue compactness. Our earlier studies have shown that exogenous transferrin is not needed for certain changes preceding overt tubule formation in the kidney mesenchyme, and we suggested that transferrin responsiveness is acquired during the induction of kidney mesenchyme. Our present results do not contradict the postulate, although they demonstrate that the acquisition of the responsiveness is more complicated than previously thought. When the mesenchyme is exposed to inductor tissue for 24 h without transferrin, and then subcultured without the inductor in the presence of transferrin, morphogenesis fails and there is no proliferation of the mesenchyme. The experiment shows that the inductor, the mesenchyme and transferrin must all three be simultaneously present for the acquisition of the transferrin responsiveness. Other experiments show that the induced mesenchyme can be a direct target tissue, since it can proliferate in response to transferrin also in the absence of the inductor. It is evident that the inductor is required for the acquisition of the responsiveness, as suggested. However, there is apparently a large overlap between the transferrin-independent and transferrin-dependent proliferation. The mesenchyme is not a synchronous cell population and cells do not become induced and transferrin-responsive at the same time. Therefore, in the organ culture, it is necessary to have transferrin present also during induction. Although this explanation seems most likely, we cannot exclude that transferrin has two actions, one measurable direct effect on the proliferation of induced mesenchymes, and another yet unidentified effect on the induction process.

scholarly journals Involvement of Laminin Binding Integrins and Laminin-5 in Branching Morphogenesis of the Ureteric Bud during Kidney Development

2001 ◽  
Vol 238 (2) ◽  
pp. 289-302 ◽  
Author(s):  
Roy Zent ◽  
Kevin T. Bush ◽  
Martin L. Pohl ◽  
Vito Quaranta ◽  
Naohiko Koshikawa ◽  
...  
Keyword(s):  
Kidney Development ◽  
Branching Morphogenesis ◽  
Ureteric Bud ◽  
Laminin 5 ◽  
Laminin Binding

Prorenin receptor controls renal branching morphogenesis via Wnt/β-catenin signaling

2017 ◽  
Vol 312 (3) ◽  
pp. F407-F417 ◽  
Author(s):  
Renfang Song ◽  
Adam Janssen ◽  
Yuwen Li ◽  
Samir El-Dahr ◽  
Ihor V. Yosypiv
Keyword(s):  
Kidney Development ◽  
Collecting Duct ◽  
Terminal Differentiation ◽  
Molecular Transport ◽  
Branching Morphogenesis ◽  
Primary Role ◽  
Prorenin Receptor ◽  
Accessory Subunit

The prorenin receptor (PRR) is a receptor for renin and prorenin, and an accessory subunit of the vacuolar proton pump H+-ATPase. Renal branching morphogenesis, defined as growth and branching of the ureteric bud (UB), is essential for mammalian kidney development. Previously, we demonstrated that conditional ablation of the PRR in the UB in PRRUB−/− mice causes severe defects in UB branching, resulting in marked kidney hypoplasia at birth. Here, we investigated the UB transcriptome using whole genome-based analysis of gene expression in UB cells, FACS-isolated from PRRUB−/−, and control kidneys at birth (P0) to determine the primary role of the PRR in terminal differentiation and growth of UB-derived collecting ducts. Three genes with expression in UB cells that previously shown to regulate UB branching morphogenesis, including Wnt9b, β-catenin, and Fgfr2, were upregulated, whereas the expression of Wnt11, Bmp7, Etv4, and Gfrα1 was downregulated. We next demonstrated that infection of immortalized UB cells with shPRR in vitro or deletion of the UB PRR in double-transgenic PRRUB−/−/ BatGal+ mice, a reporter strain for β-catenin transcriptional activity, in vivo increases β-catenin activity in the UB epithelia. In addition to UB morphogenetic genes, the functional groups of differentially expressed genes within the downregulated gene set included genes involved in molecular transport, metabolic disease, amino acid metabolism, and energy production. Together, these data demonstrate that UB PRR performs essential functions during UB branching and collecting duct morphogenesis via control of a hierarchy of genes that control UB branching and terminal differentiation of the collecting duct cells.

scholarly journals β-Catenin in stromal progenitors controls medullary stromal development

2018 ◽  
Vol 314 (6) ◽  
pp. F1177-F1187 ◽  
Author(s):  
Felix J. Boivin ◽  
Darren Bridgewater
Keyword(s):  
Mouse Model ◽  
Stromal Cells ◽  
Marked Reduction ◽  
Kidney Development ◽  
Kidney Tissue ◽  
Branching Morphogenesis ◽  
Cell Populations ◽  
Fibroblast Cells ◽  
Structural Framework ◽  
Distinct Cell

The renal stroma is a population of matrix-producing fibroblast cells that serves as a structural framework for the kidney parenchyma. The stroma also regulates branching morphogenesis and nephrogenesis. In the mature kidney, the stroma forms at least three distinct cell populations: the capsular, cortical, and medullary stroma. These distinct stromal populations have important functions in kidney development, maintenance of kidney function, and disease progression. However, the development, differentiation, and maintenance of the distinct stroma populations are not well defined. Using a mouse model with β-catenin deficiency in the stroma cell population, we demonstrate that β-catenin is not involved in the formation of the stromal progenitors nor in the formation of the cortical stroma population. In contrast, β-catenin does control the differentiation of stromal progenitors to form the medullary stroma. In the absence of stromal β-catenin, there is a marked reduction of medullary stromal markers. As kidney development continues, the maldifferentiated stromal cells locate deeper within the kidney tissue and are eliminated by the activation of an intrinsic apoptotic program. This leads to significant reductions in the medullary stroma population and the lack of medulla formation. Taken together, our results indicate that stromal β-catenin is essential for kidney development by regulating medulla formation through the differentiation of medullary stromal cells.

scholarly journals Histology Atlas of the Developing Mouse Urinary System With Emphasis on Prenatal Days E10.5-E18.5

2019 ◽  
Vol 47 (7) ◽  
pp. 865-886 ◽  
Author(s):  
Susan A. Elmore ◽  
Sanam L. Kavari ◽  
Mark J. Hoenerhoff ◽  
Beth Mahler ◽  
Brittany E. Scott ◽  
...  
Keyword(s):  
Urinary Tract ◽  
Molecular Mechanisms ◽  
Kidney Development ◽  
Initial Point ◽  
Branching Morphogenesis ◽  
Genetically Engineered ◽  
Developmental Abnormalities ◽  
Genetically Engineered Mouse Models ◽  
Stage Of Development ◽  
Hematoxylin And Eosin

Congenital abnormalities of the urinary tract are some of the most common human developmental abnormalities. Several genetically engineered mouse models have been developed to mimic these abnormalities and aim to better understand the molecular mechanisms of disease. This atlas has been developed as an aid to pathologists and other biomedical scientists for identification of abnormalities in the developing murine urinary tract by cataloguing normal structures at each stage of development. Hematoxylin and eosin- and immunohistochemical-stained sections are provided, with a focus on E10.5-E18.5, as well as a brief discussion of postnatal events in urinary tract development. A section on abnormalities in the development of the urinary tract is also provided, and molecular mechanisms are presented as supplementary material. Additionally, overviews of the 2 key processes of kidney development, branching morphogenesis and nephrogenesis, are provided to aid in the understanding of the complex organogenesis of the kidney. One of the key findings of this atlas is the histological identification of the ureteric bud at E10.5, as previous literature has provided conflicting reports on the initial point of budding. Furthermore, attention is paid to points where murine development is significantly distinct from human development, namely, in the cessation of nephrogenesis.

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