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Journal articles on the topic 'Renal progenitors'

Author: Grafiati

Published: 10 March 2023

Last updated: 31 July 2025

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1

Hasegawa, Sho, Tetsuhiro Tanaka, and Masaomi Nangaku. "Recent advances in renal regeneration." F1000Research 8 (February 25, 2019): 216. http://dx.doi.org/10.12688/f1000research.17127.1.

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Regeneration of a functional kidney from pluripotent stem cells (PSCs) is challenging because of its complex structure. Kidneys are derived from embryonic metanephros, which are composed of three progenitor cells: nephron progenitors, ureteric bud, and stromal progenitors. Nephron progenitors and ureteric bud have been induced successfully from PSCs as a result of the understanding of their detailed developmental process through cell-lineage tracing analysis. Moreover, these induced progenitors can be used to reconstruct the three-dimensional (3D) structure of kidneys in vitro, including glome

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2

Al-Marsoummi, Sarmad, Aaron A. Mehus, Swojani Shrestha, et al. "Proteasomes Are Critical for Maintenance of CD133+CD24+ Kidney Progenitor Cells." International Journal of Molecular Sciences 24, no. 17 (2023): 13303. http://dx.doi.org/10.3390/ijms241713303.

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Kidney progenitor cells, although rare and dispersed, play a key role in the repair of renal tubules after acute kidney damage. However, understanding these cells has been challenging due to the limited access to primary renal tissues and the absence of immortalized cells to model kidney progenitors. Previously, our laboratory utilized the renal proximal tubular epithelial cell line, RPTEC/TERT1, and the flow cytometry technique to sort and establish a kidney progenitor cell model called Human Renal Tubular Precursor TERT (HRTPT) which expresses CD133 and CD24 and exhibits the characteristics

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3

Sequeira-Lopez, Maria Luisa S., Eugene E. Lin, Minghong Li, Yan Hu, Curt D. Sigmund, and R. Ariel Gomez. "The earliest metanephric arteriolar progenitors and their role in kidney vascular development." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 2 (2015): R138—R149. http://dx.doi.org/10.1152/ajpregu.00428.2014.

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The development of the kidney arterioles is poorly understood. Mature arterioles contain several functionally and morphologically distinct cell types, including smooth muscle, endothelial, and juxtaglomerular cells, and they are surrounded by interconnected pericytes, fibroblasts, and other interstitial cells. We have shown that the embryonic kidney possesses all of the necessary precursors for the development of the renal arterial tree, and those precursors assemble in situ to form the kidney arterioles. However, the identity of those precursors was unclear. Within the embryonic kidney, sever

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4

Peired, Anna Julie, Maria Elena Melica, Alice Molli, Cosimo Nardi, Paola Romagnani, and Laura Lasagni. "Molecular Mechanisms of Renal Progenitor Regulation: How Many Pieces in the Puzzle?" Cells 10, no. 1 (2021): 59. http://dx.doi.org/10.3390/cells10010059.

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Kidneys of mice, rats and humans possess progenitors that maintain daily homeostasis and take part in endogenous regenerative processes following injury, owing to their capacity to proliferate and differentiate. In the glomerular and tubular compartments of the nephron, consistent studies demonstrated that well-characterized, distinct populations of progenitor cells, localized in the parietal epithelium of Bowman capsule and scattered in the proximal and distal tubules, could generate segment-specific cells in physiological conditions and following tissue injury. However, defective or abnormal

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5

Holmes, David. "Budding renal progenitors." Nature Reviews Nephrology 10, no. 1 (2013): 4. http://dx.doi.org/10.1038/nrneph.2013.245.

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6

Phua, Yu Leng, Kevin Hong Chen, Shelby L. Hemker, et al. "Loss of miR-17~92 results in dysregulation of Cftr in nephron progenitors." American Journal of Physiology-Renal Physiology 316, no. 5 (2019): F993—F1005. http://dx.doi.org/10.1152/ajprenal.00450.2018.

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We have previously demonstrated that loss of miR-17~92 in nephron progenitors in a mouse model results in renal hypodysplasia and chronic kidney disease. Clinically, decreased congenital nephron endowment because of renal hypodysplasia is associated with an increased risk of hypertension and chronic kidney disease, and this is at least partly dependent on the self-renewal of nephron progenitors. Here, we present evidence for a novel molecular mechanism regulating the self-renewal of nephron progenitors and congenital nephron endowment by the highly conserved miR-17~92 cluster. Whole transcript

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7

Montenegro, Francesca, Francesca Giannuzzi, Angela Picerno, et al. "How Stem and Progenitor Cells Can Affect Renal Diseases." Cells 13, no. 17 (2024): 1460. http://dx.doi.org/10.3390/cells13171460.

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Stem and progenitor cells have been observed to contribute to regenerative processes in acute renal failure and chronic kidney disease. Recent research has delved into the intricate mechanisms by which stem and progenitor cells exert their influence on kidney diseases. Understanding how these cells integrate with the existing renal architecture and their response to injury could pave the way for innovative treatment strategies aimed at promoting kidney repair and regeneration. Overall, the role of stem and progenitor cells in kidney diseases is multifaceted, with their ability to contribute to

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8

Volovelsky, Oded, Thi Nguyen, Alison E. Jarmas, et al. "Hamartin regulates cessation of mouse nephrogenesis independently of Mtor." Proceedings of the National Academy of Sciences 115, no. 23 (2018): 5998–6003. http://dx.doi.org/10.1073/pnas.1712955115.

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Nephrogenesis concludes by the 36th week of gestation in humans and by the third day of postnatal life in mice. Extending the nephrogenic period may reduce the onset of adult renal and cardiovascular disease associated with low nephron numbers. We conditionally deleted either Mtor or Tsc1 (coding for hamartin, an inhibitor of Mtor) in renal progenitor cells. Loss of one Mtor allele caused a reduction in nephron numbers; complete deletion led to severe paucity of glomeruli in the kidney resulting in early death after birth. By contrast, loss of one Tsc1 allele from renal progenitors resulted in

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9

Peired, Anna Julie, Giulia Antonelli, Maria Lucia Angelotti, et al. "Acute kidney injury promotes development of papillary renal cell adenoma and carcinoma from renal progenitor cells." Science Translational Medicine 12, no. 536 (2020): eaaw6003. http://dx.doi.org/10.1126/scitranslmed.aaw6003.

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Acute tissue injury causes DNA damage and repair processes involving increased cell mitosis and polyploidization, leading to cell function alterations that may potentially drive cancer development. Here, we show that acute kidney injury (AKI) increased the risk for papillary renal cell carcinoma (pRCC) development and tumor relapse in humans as confirmed by data collected from several single-center and multicentric studies. Lineage tracing of tubular epithelial cells (TECs) after AKI induction and long-term follow-up in mice showed time-dependent onset of clonal papillary tumors in an adenoma-

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10

Rymer, Christopher, Jose Paredes, Kimmo Halt, et al. "Renal blood flow and oxygenation drive nephron progenitor differentiation." American Journal of Physiology-Renal Physiology 307, no. 3 (2014): F337—F345. http://dx.doi.org/10.1152/ajprenal.00208.2014.

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During kidney development, the vasculature develops via both angiogenesis (branching from major vessels) and vasculogenesis (de novo vessel formation). The formation and perfusion of renal blood vessels are vastly understudied. In the present study, we investigated the regulatory role of renal blood flow and O2 concentration on nephron progenitor differentiation during ontogeny. To elucidate the presence of blood flow, ultrasound-guided intracardiac microinjection was performed, and FITC-tagged tomato lectin was perfused through the embryo. Kidneys were costained for the vasculature, ureteric

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11

Chu, Jessica Y. S., Sunder Sims-Lucas, Daniel S. Bushnell, Andrew J. Bodnar, Jordan A. Kreidberg, and Jacqueline Ho. "Dicer function is required in the metanephric mesenchyme for early kidney development." American Journal of Physiology-Renal Physiology 306, no. 7 (2014): F764—F772. http://dx.doi.org/10.1152/ajprenal.00426.2013.

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MicroRNAs (miRNAs) are small, noncoding regulatory RNAs that act as posttranscriptional repressors by binding to the 3′-untranslated region (3′-UTR) of target genes. They require processing by Dicer, an RNase III enzyme, to become mature regulatory RNAs. Previous work from our laboratory revealed critical roles for miRNAs in nephron progenitors at midgestation (Ho J, Pandey P, Schatton T, Sims-Lucas S, Khalid M, Frank MH, Hartwig S, Kreidberg JA. J Am Soc Nephrol 22: 1053–1063, 2011). To interrogate roles for miRNAs in the early metanephric mesenchyme, which gives rise to nephron progenitors a

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12

Gupta, Ashwani Kumar, David Z. Ivancic, Bilal A. Naved, Jason A. Wertheim, and Leif Oxburgh. "An efficient method to generate kidney organoids at the air-liquid interface." Journal of Biological Methods 8, no. 2 (2021): e150. http://dx.doi.org/10.14440/jbm.2021.357.

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The prevalence of kidney dysfunction continues to increase worldwide, driving the need to develop transplantable renal tissues. The kidney develops from four major renal progenitor populations: nephron epithelial, ureteric epithelial, interstitial and endothelial progenitors. Methods have been developed to generate kidney organoids but few or dispersed tubular clusters within the organoids hamper its use in regenerative applications. Here, we describe a detailed protocol of asynchronous mixing of kidney progenitors using organotypic culture conditions to generate kidney organoids tightly packe

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13

Meyer-Schwesinger, Catherine. "The Role of Renal Progenitors in Renal Regeneration." Nephron 132, no. 2 (2016): 101–9. http://dx.doi.org/10.1159/000442180.

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14

Bussolati, Benedetta, Aldo Moggio, Federica Collino, et al. "Hypoxia modulates the undifferentiated phenotype of human renal inner medullary CD133+ progenitors through Oct4/miR-145 balance." American Journal of Physiology-Renal Physiology 302, no. 1 (2012): F116—F128. http://dx.doi.org/10.1152/ajprenal.00184.2011.

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Low-oxygen tension is an important component of the stem cell microenvironment. In rodents, renal resident stem cells have been described in the papilla, a relatively hypoxic region of the kidney. In the present study, we found that CD133+ cells, previously described as renal progenitors in the human cortex, were enriched in the renal inner medulla and localized within the Henle's loop and thin limb segments. Once isolated, the CD133+ cell population expressed renal embryonic and stem-related transcription factors and was able to differentiate into mature renal epithelial cells. When injected

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15

Tanigawa, Shunsuke, and Alan O. Perantoni. "Modeling renal progenitors – defining the niche." Differentiation 91, no. 4-5 (2016): 152–58. http://dx.doi.org/10.1016/j.diff.2016.01.007.

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16

Schrankl, Julia, Bjoern Neubauer, Michaela Fuchs, Katharina Gerl, Charlotte Wagner, and Armin Kurtz. "Apparently normal kidney development in mice with conditional disruption of ANG II-AT1 receptor genes in FoxD1-positive stroma cell precursors." American Journal of Physiology-Renal Physiology 316, no. 6 (2019): F1191—F1200. http://dx.doi.org/10.1152/ajprenal.00305.2018.

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An intact renin-angiotensin system involving ANG II type 1 (AT1) receptors is crucial for normal kidney development. It is still unclear in which cell types AT1 receptor signaling is required for normal kidney development, maturation, and function. Because all kidney cells deriving from stroma progenitor cells express AT1 receptors and because stromal cells fundamentally influence nephrogenesis and tubular maturation, we investigated the relevance of AT1 receptors in stromal progenitors and their descendants for renal development and function. For this aim, we generated and analyzed mice with

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17

Rossbach, Bella, Krithika Hariharan, Nancy Mah, et al. "Human iPSC-Derived Renal Cells Change Their Immunogenic Properties during Maturation: Implications for Regenerative Therapies." Cells 11, no. 8 (2022): 1328. http://dx.doi.org/10.3390/cells11081328.

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The success of human induced pluripotent stem cell (hiPSC)-based therapy critically depends on understanding and controlling the immunological effects of the hiPSC-derived transplant. While hiPSC-derived cells used for cell therapy are often immature with post-grafting maturation, immunological properties may change, with adverse effects on graft tolerance and control. In the present study, the allogeneic and autologous cellular immunity of hiPSC-derived progenitor and terminally differentiated cells were investigated in vitro. In contrast to allogeneic primary cells, hiPSC-derived early renal

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18

Takahashi, Takamune, Keiko Takahashi, Sebastian Gerety, Hai Wang, David J. Anderson, and Thomas O. Daniel. "Temporally Compartmentalized Expression of Ephrin-B2 during Renal Glomerular Development." Journal of the American Society of Nephrology 12, no. 12 (2001): 2673–82. http://dx.doi.org/10.1681/asn.v12122673.

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ABSTRACT. Glomerular development proceeds through the spatially ordered and sequential recruitment, proliferation, assembly, and differentiation of endothelial, mesangial, and epithelial progenitors. The molecular determinants of cell-cell recognition and targeting in this process have yet to be defined. The Eph/ephrin family of membrane receptors and counter-receptors are critical participants of developmental vascular assembly in extrarenal sites. Renal expression patterns of ephrin-B2 and EphB4 were investigated using mice expressing β-galactosidase under control of ephrin-B2 or EphB4 promo

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19

Lazzeri, Elena, Clara Crescioli, Elisa Ronconi, et al. "Regenerative Potential of Embryonic Renal Multipotent Progenitors in Acute Renal Failure." Journal of the American Society of Nephrology 18, no. 12 (2007): 3128–38. http://dx.doi.org/10.1681/asn.2007020210.

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20

Tan, Zenglai, Aleksandra Rak-Raszewska, Ilya Skovorodkin, and Seppo J. Vainio. "Mouse Embryonic Stem Cell-Derived Ureteric Bud Progenitors Induce Nephrogenesis." Cells 9, no. 2 (2020): 329. http://dx.doi.org/10.3390/cells9020329.

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Generation of kidney organoids from pluripotent stem cells (PSCs) is regarded as a potentially powerful way to study kidney development, disease, and regeneration. Direct differentiation of PSCs towards renal lineages is well studied; however, most of the studies relate to generation of nephron progenitor population from PSCs. Until now, differentiation of PSCs into ureteric bud (UB) progenitor cells has had limited success. Here, we describe a simple, efficient, and reproducible protocol to direct differentiation of mouse embryonic stem cells (mESCs) into UB progenitor cells. The mESC-derived

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21

Lindström, Nils O., Jinjin Guo, Albert D. Kim, et al. "Conserved and Divergent Features of Mesenchymal Progenitor Cell Types within the Cortical Nephrogenic Niche of the Human and Mouse Kidney." Journal of the American Society of Nephrology 29, no. 3 (2018): 806–24. http://dx.doi.org/10.1681/asn.2017080890.

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Cellular interactions among nephron, interstitial, and collecting duct progenitors drive mammalian kidney development. In mice, Six2+ nephron progenitor cells (NPCs) and Foxd1+ interstitial progenitor cells (IPCs) form largely distinct lineage compartments at the onset of metanephric kidney development. Here, we used the method for analyzing RNA following intracellular sorting (MARIS) approach, single-cell transcriptional profiling, in situ hybridization, and immunolabeling to characterize the presumptive NPC and IPC compartments of the developing human kidney. As in mice, each progenitor popu

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22

Bussolati, Benedetta, Alessia Brossa, and Giovanni Camussi. "Resident Stem Cells and Renal Carcinoma." International Journal of Nephrology 2011 (2011): 1–6. http://dx.doi.org/10.4061/2011/286985.

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According to the cancer stem cell hypothesis tumors are maintained by a cancer stem cell population which is able to initiate and maintain tumors. Tumor-initiating stem cells display stem or progenitor cell properties such as self-renewal and capacity to re-establish tumors that recapitulate the tumor of origin. In this paper, we discuss data relative to the presence of cancer stem cells in human renal carcinoma and their possible origin from normal resident stem cells. The cancer stem cells identified in human renal carcinomas are not derived from the normal CD133+progenitors of the kidney, b

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23

Dessypris, E., SE Graber, SB Krantz, and WJ Stone. "Effects of recombinant erythropoietin on the concentration and cycling status of human marrow hematopoietic progenitor cells in vivo." Blood 72, no. 6 (1988): 2060–62. http://dx.doi.org/10.1182/blood.v72.6.2060.2060.

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Abstract The concentration of human marrow progenitors CFU-E, BFU-E, CFU-GM, and CFU-Mk and the percentage of these progenitor cells in DNA synthesis were studied in nine patients with transfusion-dependent anemia of end- stage renal failure before and 2 weeks after treatment with human recombinant erythropoietin (Epo) at a dose of 150 to 300 U/kg intravenously three times per week. The concentration of CFU-E in the posttreatment marrow increased by a mean of 4.15-fold, BFU-E by 3.37- fold, CFU-GM by 1.86-fold, and CFU-Mk by 1.96-fold as compared with their respective concentrations in the pre

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Dessypris, E., SE Graber, SB Krantz, and WJ Stone. "Effects of recombinant erythropoietin on the concentration and cycling status of human marrow hematopoietic progenitor cells in vivo." Blood 72, no. 6 (1988): 2060–62. http://dx.doi.org/10.1182/blood.v72.6.2060.bloodjournal7262060.

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The concentration of human marrow progenitors CFU-E, BFU-E, CFU-GM, and CFU-Mk and the percentage of these progenitor cells in DNA synthesis were studied in nine patients with transfusion-dependent anemia of end- stage renal failure before and 2 weeks after treatment with human recombinant erythropoietin (Epo) at a dose of 150 to 300 U/kg intravenously three times per week. The concentration of CFU-E in the posttreatment marrow increased by a mean of 4.15-fold, BFU-E by 3.37- fold, CFU-GM by 1.86-fold, and CFU-Mk by 1.96-fold as compared with their respective concentrations in the pretreatment

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Dionne, Lai Kuan, Kyuhwan Shim, Masato Hoshi, et al. "Centrosome amplification disrupts renal development and causes cystogenesis." Journal of Cell Biology 217, no. 7 (2018): 2485–501. http://dx.doi.org/10.1083/jcb.201710019.

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Centrosome number is tightly controlled to ensure proper ciliogenesis, mitotic spindle assembly, and cellular homeostasis. Centrosome amplification (the formation of excess centrosomes) has been noted in renal cells of patients and animal models of various types of cystic kidney disease. Whether this defect plays a causal role in cystogenesis remains unknown. Here, we investigate the consequences of centrosome amplification during kidney development, homeostasis, and after injury. Increasing centrosome number in vivo perturbed proliferation and differentiation of renal progenitors, resulting i

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26

Sheybani-Deloui, Sepideh, Lijun Chi, Marian V. Staite, et al. "Activated Hedgehog-GLI Signaling Causes Congenital Ureteropelvic Junction Obstruction." Journal of the American Society of Nephrology 29, no. 2 (2017): 532–44. http://dx.doi.org/10.1681/asn.2017050482.

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Intrinsic ureteropelvic junction obstruction is the most common cause of congenital hydronephrosis, yet the underlying pathogenesis is undefined. Hedgehog proteins control morphogenesis by promoting GLI-dependent transcriptional activation and inhibiting the formation of the GLI3 transcriptional repressor. Hedgehog regulates differentiation and proliferation of ureteric smooth muscle progenitor cells during murine kidney-ureter development. Histopathologic findings of smooth muscle cell hypertrophy and stroma-like cells, consistently observed in obstructing tissue at the time of surgical corre

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27

Nag, Sparshita, and Ashleigh S. Boyd. "Decellularization of Mouse Kidneys to Generate an Extracellular Matrix Gel for Human Induced Pluripotent Stem Cell Derived Renal Organoids." Organoids 2, no. 1 (2023): 66–78. http://dx.doi.org/10.3390/organoids2010005.

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Chronic Kidney Disease (CKD) is a major cause of morbidity and mortality characterized by progressive renal fibrosis, and in extreme cases, renal failure. Human CKD models that replicate the biological complexity of the kidney and CKD are lacking and will be invaluable in identifying drugs to revert and/or prevent fibrosis. To address this unmet need, we developed 3D renal organoids where human induced pluripotent stem cells (hiPSCs) were differentiated to renal progenitors within a renal extracellular matrix (rECM) gel, based on the premise that an rECM could recreate the renal niche to facil

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Vinsonneau, C., A. Girshovich, M. Ben M'rad, et al. "Intrarenal urothelium proliferation: an unexpected early event following ischemic injury." American Journal of Physiology-Renal Physiology 299, no. 3 (2010): F479—F486. http://dx.doi.org/10.1152/ajprenal.00585.2009.

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Identification of renal cell progenitors and recognition of the events contributing to cell regeneration following ischemia-reperfusion injury (IRI) are a major challenge. In a mouse model of unilateral renal IRI, we demonstrated that the first cells to proliferate within injured kidneys were urothelial cells expressing the progenitor cell marker cytokeratin 14. A systematic cutting of the injured kidney revealed that these urothelial cells were located in the deep cortex at the corticomedullary junction in the vicinity of lobar vessels. Contrary to multilayered bladder urothelium, these intra

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29

Chambers, Brooke E., and Rebecca A. Wingert. "Renal progenitors: Roles in kidney disease and regeneration." World Journal of Stem Cells 8, no. 11 (2016): 367. http://dx.doi.org/10.4252/wjsc.v8.i11.367.

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Ronconi, Elisa, Costanza Sagrinati, Maria Lucia Angelotti, et al. "Regeneration of Glomerular Podocytes by Human Renal Progenitors." Journal of the American Society of Nephrology 20, no. 2 (2008): 322–32. http://dx.doi.org/10.1681/asn.2008070709.

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31

Romagnani, Paola, and Giuseppe Remuzzi. "Renal progenitors in non-diabetic and diabetic nephropathies." Trends in Endocrinology & Metabolism 24, no. 1 (2013): 13–20. http://dx.doi.org/10.1016/j.tem.2012.09.002.

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32

Becherucci, Francesca, Elena Lazzeri, Laura Lasagni, and Paola Romagnani. "Renal progenitors and childhood: from development to disorders." Pediatric Nephrology 29, no. 4 (2014): 711–19. http://dx.doi.org/10.1007/s00467-013-2686-2.

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Drummond, Bridgette E., Brooke E. Chambers, Hannah M. Wesselman, et al. "osr1 Maintains Renal Progenitors and Regulates Podocyte Development by Promoting wnt2ba via the Antagonism of hand2." Biomedicines 10, no. 11 (2022): 2868. http://dx.doi.org/10.3390/biomedicines10112868.

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Knowledge about the genetic pathways that control nephron development is essential for better understanding the basis of congenital malformations of the kidney. The transcription factors Osr1 and Hand2 are known to exert antagonistic influences to balance kidney specification. Here, we performed a forward genetic screen to identify nephrogenesis regulators, where whole genome sequencing identified an osr1 lesion in the novel oceanside (ocn) mutant. The characterization of the mutant revealed that osr1 is needed to specify not renal progenitors but rather their maintenance. Additionally, osr1 p

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Osafune, Kenji. "iPSC technology-based regenerative medicine for kidney diseases." Clinical and Experimental Nephrology 25, no. 6 (2021): 574–84. http://dx.doi.org/10.1007/s10157-021-02030-x.

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AbstractWith few curative treatments for kidney diseases, increasing attention has been paid to regenerative medicine as a new therapeutic option. Recent progress in kidney regeneration using human-induced pluripotent stem cells (hiPSCs) is noteworthy. Based on the knowledge of kidney development, the directed differentiation of hiPSCs into two embryonic kidney progenitors, nephron progenitor cells (NPCs) and ureteric bud (UB), has been established, enabling the generation of nephron and collecting duct organoids. Furthermore, human kidney tissues can be generated from these hiPSC-derived prog

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Urbach, A., A. Yermalovich, J. Zhang, et al. "Lin28 sustains early renal progenitors and induces Wilms tumor." Genes & Development 28, no. 9 (2014): 971–82. http://dx.doi.org/10.1101/gad.237149.113.

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Romagnani, Paola, Laura Lasagni, and Giuseppe Remuzzi. "Renal progenitors: an evolutionary conserved strategy for kidney regeneration." Nature Reviews Nephrology 9, no. 3 (2013): 137–46. http://dx.doi.org/10.1038/nrneph.2012.290.

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Barasch, J., J. Yang, and K. Mori. "INDUCTION OF NEPHRONS FROM RENAL PROGENITORS BY MULTIPLE SIGNALS." ASAIO Journal 49, no. 2 (2003): 198. http://dx.doi.org/10.1097/00002480-200303000-00230.

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38

Barak, Y., L. Sinai-Treiman, Y. Karov, A. Abrahamov, and A. Drukker. "Hematopoietic Progenitors in Children with End-Stage Renal Disease." Pediatric Hematology and Oncology 11, no. 6 (1994): 633–39. http://dx.doi.org/10.3109/08880019409141810.

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Wang, Honghe, Yili Yang, Nirmala Sharma, et al. "STAT1 activation regulates proliferation and differentiation of renal progenitors." Cellular Signalling 22, no. 11 (2010): 1717–26. http://dx.doi.org/10.1016/j.cellsig.2010.06.012.

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40

Závada, Jakub, L. Kideryová, R. Pytlík, and V. Tesař. "Circulating Endothelial Cells and Circulating Endothelial Progenitors in Kidney Disease – Victims, Witnesses, or Accomplices?" Folia Biologica 54, no. 3 (2008): 73–80. http://dx.doi.org/10.14712/fb2008054030073.

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Nephrologists deal with a host of pathologic conditions involving renal and systemic endothelium. Both in native and transplanted kidneys, often the insult to the renal endothelium initiates the pathogenic process ultimately leading to the loss of organ function. Also, systemic atherosclerosis is accelerated in patients with renal dysfunction. In this review we would like to cover the possible role of CECs and their counterparts - circulating EPCs in the pathogenesis of endothelial dysfunction associated with chronic renal failure, ANCA-associated vasculitis, and progression of chronic renal d

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Zhang, Joyce, Felix Kommoss, Branden Lynch, et al. "Abstract 2611: Cellular origin of DICER1 tumor predisposition syndrome informed by lineage-traceable genetically engineered mouse model." Cancer Research 85, no. 8_Supplement_1 (2025): 2611. https://doi.org/10.1158/1538-7445.am2025-2611.

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Abstract Introduction: DICER1 tumor predisposition syndrome is a genetic disorder driven by germline DICER1 pathogenic variants that predisposes pediatric and young adult patients to cancers of various organs. The second, missense mutation in RNase IIIb domain leads to systemic loss of mature 5p-miRNAs. Tumours of various sites are histologically and molecularly similar, suggesting a shared cellular origin and oncogenic mechanisms. To this end, we expanded our first-ever genetically engineered mouse model (GEMM) that recapitulated human Müllerian adenosarcomas, a DICER1 neoplasm, through indu

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Jackson, Ashley R., Monica L. Hoff, Birong Li, Christina B. Ching, Kirk M. McHugh, and Brian Becknell. "Krt5+ urothelial cells are developmental and tissue repair progenitors in the kidney." American Journal of Physiology-Renal Physiology 317, no. 3 (2019): F757—F766. http://dx.doi.org/10.1152/ajprenal.00171.2019.

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Congenital urinary tract obstruction (UTO) is the leading cause of chronic kidney disease in children; however, current management strategies do not safeguard against progression to end-stage renal disease, highlighting the need for interventions to limit or reverse obstructive nephropathy. Experimental UTO triggers renal urothelial remodeling that culminates in the redistribution of basal keratin 5-positive (Krt5+) renal urothelial cells (RUCs) and the generation of uroplakin-positive (Upk)+ RUCs that synthesize a protective apical urothelial plaque. The cellular source of Upk+ RUCs is curren

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Yosypiv, Ihor V., Maria Luisa S. Sequeira-Lopez, Renfang Song, and Alexandre De Goes Martini. "Stromal prorenin receptor is critical for normal kidney development." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 5 (2019): R640—R650. http://dx.doi.org/10.1152/ajpregu.00320.2018.

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Formation of the metanephric kidney requires coordinated interaction among the stroma, ureteric bud, and cap mesenchyme. The transcription factor Foxd1, a specific marker of renal stromal cells, is critical for normal kidney development. The prorenin receptor (PRR), a receptor for renin and prorenin, is also an accessory subunit of the vacuolar proton pump V-ATPase. Global loss of PRR is embryonically lethal in mice, indicating an essential role of the PRR in embryonic development. Here, we report that conditional deletion of the PRR in Foxd1+ stromal progenitors in mice ( cKO) results in neon

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De Filippo, Roger E., Ilenia Zanusso, Stefano Da Sacco, et al. "Amniotic fluid renal progenitors and renal extracellular matrix: a new approach for kidney regeneration." Journal of the American College of Surgeons 219, no. 4 (2014): e55. http://dx.doi.org/10.1016/j.jamcollsurg.2014.07.531.

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Franzin, Rossana, Alessandra Stasi, Giuseppe De Palma, et al. "Human Adult Renal Progenitor Cells Prevent Cisplatin-Nephrotoxicity by Inducing CYP1B1 Overexpression and miR-27b-3p Down-Regulation through Extracellular Vesicles." Cells 12, no. 12 (2023): 1655. http://dx.doi.org/10.3390/cells12121655.

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Cisplatin is one of the most effective chemotherapeutic agents strongly associated with nephrotoxicity. Tubular adult renal progenitor cells (tARPC) can regenerate functional tubules and participate in the repair processes after cisplatin exposition. This study investigated the molecular mechanisms underlying the protective effect of tARPC on renal epithelium during cisplatin nephrotoxicity. By performing a whole-genome transcriptomic analysis, we found that tARPC, in presence of cisplatin, can strongly influence the gene expression of renal proximal tubular cell [RPTEC] by inducing overexpres

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Mukherjee, Elina, Katherine Maringer, Emily Papke, et al. "Endothelial marker-expressing stromal cells are critical for kidney formation." American Journal of Physiology-Renal Physiology 313, no. 3 (2017): F611—F620. http://dx.doi.org/10.1152/ajprenal.00136.2017.

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Kidneys are highly vascularized and contain many distinct vascular beds. However, the origins of renal endothelial cells and roles of the developing endothelia in the formation of the kidney are unclear. We have shown that the Foxd1-positive renal stroma gives rise to endothelial marker-expressing progenitors that are incorporated within a subset of peritubular capillaries; however, the significance of these cells is unclear. The purpose of this study was to determine whether deletion of Flk1 in the Foxd1 stroma was important for renal development. To that end, we conditionally deleted Flk1 (c

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Chan, Charles, Ching-Cheng Chen, Daniel L. Kraft, et al. "Identification and Isolation of the Hematopoietic Stem Cell Niche Initiating Cell Population." Blood 112, no. 11 (2008): 3574. http://dx.doi.org/10.1182/blood.v112.11.3574.3574.

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Abstract Introduction: Identification and understanding of the cells and processes that can generate, sustain and influence the HSC niche and hematopoiesis are critical for the development of a more comprehensive knowledge of normal hematopoiesis, stem cell homing, trafficking, differentiation and hematopoietic pathology. Growth and renewal in many tissues are initiated by stem cells, supported by the microenvironment (niche) in which they reside. While recent work has begun to describe functional interactions between stem cells and their niches, little is known about the formation of stem cel

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Atala, Anthony. "Re: Lin28 Sustains Early Renal Progenitors and Induces Wilms Tumor." Journal of Urology 193, no. 2 (2015): 730–31. http://dx.doi.org/10.1016/j.juro.2014.11.021.

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Bombelli, Silvia, Chiara Meregalli, Chiara Grasselli, et al. "PKHhigh/CD133+/CD24− Renal Stem-Like Cells Isolated from Human Nephrospheres Exhibit In Vitro Multipotency." Cells 9, no. 8 (2020): 1805. http://dx.doi.org/10.3390/cells9081805.

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The mechanism upon which human kidneys undergo regeneration is debated, though different lineage-tracing mouse models have tried to explain the cellular types and the mechanisms involved. Different sources of human renal progenitors have been proposed, but it is difficult to argue whether these populations have the same capacities that have been described in mice. Using the nephrosphere (NS) model, we isolated the quiescent population of adult human renal stem-like PKHhigh/CD133+/CD24− cells (RSC). The aim of this study was to deepen the RSC in vitro multipotency capacity. RSC, not expressing

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Zhang, Jiong, Jeffrey W. Pippin, Ronald D. Krofft, Shokichi Naito, Zhi-Hong Liu, and Stuart J. Shankland. "Podocyte repopulation by renal progenitor cells following glucocorticoids treatment in experimental FSGS." American Journal of Physiology-Renal Physiology 304, no. 11 (2013): F1375—F1389. http://dx.doi.org/10.1152/ajprenal.00020.2013.

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Prednisone is a mainstay of treatment for patients with focal segmental glomerulosclerosis (FSGS), a disease characterized by reduced podocyte number and glomerulosclerosis. Although the systemic immune-modulatory effects of prednisone are well-known, direct tissue effects on glomerular cells are poorly understood. Experimental FSGS was induced in mice with a cytotoxic anti-podocyte antibody, resulting in an abrupt decrease in podocyte number by day 3, proteinuria, and the development of glomerulosclerosis. Administering daily prednisone to mice with FSGS, beginning at day 3, significantly inc

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