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Journal articles on the topic 'Tubular Progenitor'

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Author: Grafiati
Published: 10 March 2023

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1

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 (January 2, 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 regenerative responses of these progenitors can contribute to pathologic conditions. The molecular characteristics of renal progenitors have been extensively studied, revealing that numerous classical and evolutionarily conserved pathways, such as Notch or Wnt/β-catenin, play a major role in cell regulation. Others, such as retinoic acid, renin-angiotensin-aldosterone system, TLR2 (Toll-like receptor 2) and leptin, are also important in this process. In this review, we summarize the plethora of molecular mechanisms directing renal progenitor responses during homeostasis and following kidney injury. Finally, we will explore how single-cell RNA sequencing could bring the characterization of renal progenitors to the next level, while knowing their molecular signature is gaining relevance in the clinic.
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2

Chen, Dong, Zhiyong Chen, Yuning Zhang, Chanyoung Park, Ahmed Al-Omari, and Gilbert W. Moeckel. "Role of medullary progenitor cells in epithelial cell migration and proliferation." American Journal of Physiology-Renal Physiology 307, no. 1 (July 1, 2014): F64—F74. http://dx.doi.org/10.1152/ajprenal.00547.2013.

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This study is aimed at characterizing medullary interstitial progenitor cells and to examine their capacity to induce tubular epithelial cell migration and proliferation. We have isolated a progenitor cell side population from a primary medullary interstitial cell line. We show that the medullary progenitor cells (MPCs) express CD24, CD44, CXCR7, CXCR4, nestin, and PAX7. MPCs are CD34 negative, which indicates that they are not bone marrow-derived stem cells. MPCs survive >50 passages, and when grown in epithelial differentiation medium develop phenotypic characteristics of epithelial cells. Inner medulla collecting duct (IMCD3) cells treated with conditioned medium from MPCs show significantly accelerated cell proliferation and migration. Conditioned medium from PGE2-treated MPCs induce tubule formation in IMCD3 cells grown in 3D Matrigel. Moreover, most of the MPCs express the pericyte marker PDGFR-b. Our study shows that the medullary interstitium harbors a side population of progenitor cells that can differentiate to epithelial cells and can stimulate tubular epithelial cell migration and proliferation. The findings of this study suggest that medullary pericyte/progenitor cells may play a critical role in collecting duct cell injury repair.
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3

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 (June 29, 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 packed with tubular clusters and major renal structures including endothelial network and functional proximal tubules. This protocol provides guidance in the culture of human embryonic stem cells from a National Institute of Health-approved line and their directed differentiation into kidney organoids. Our 18-day protocol provides a rapid method to generate kidney organoids that facilitate the study of different nephrological events including in vitro tissue development, disease modeling and chemical screening. However, further studies are required to optimize the protocol to generate additional renal-specific cell types, interconnected nephron segments and physiologically functional renal tissues.
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4

Gerges, Daniela, Zsofia Hevesi, Sophie H. Schmidt, Sebastian Kapps, Sahra Pajenda, Barbara Geist, Alice Schmidt, Ludwig Wagner, and Wolfgang Winnicki. "Tubular epithelial progenitors are excreted in urine during recovery from severe acute kidney injury and are able to expand and differentiate in vitro." PeerJ 10 (October 20, 2022): e14110. http://dx.doi.org/10.7717/peerj.14110.

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Background Acute kidney injury (AKI) is a serious condition associated with chronic kidney disease, dialysis requirement and a high risk of death. However, there are specialized repair mechanisms for the nephron, and migrated committed progenitor cells are the key players. Previous work has described a positive association between renal recovery and the excretion of tubular progenitor cells in the urine of kidney transplant recipients. The aim of this work was to describe such structures in non-transplanted AKI patients and to focus on their differentiation. Methods Morning urine was obtained from four patients with AKI stage 3 and need for RRT on a consecutive basis. Urine sediment gene expression was performed to assess which part of the tubular or glomerular segment was affected by injury, along with measurement of neprilysin. Urine output and sediment morphology were monitored, viable hyperplastic tubular epithelial clusters were isolated and characterized by antibody or cultured in vitro. These cells were monitored by phase contrast microscopy, gene, and protein expression over 9 days by qPCR and confocal immunofluorescence. Furthermore, UMOD secretion into the supernatant was quantitatively measured. Results Urinary neprilysin decreased rapidly with increasing urinary volume in ischemic, toxic, nephritic, and infection-associated AKI, whereas the decrease in sCr required at least 2 weeks. While urine output increased, dead cells were present in the sediment along with debris followed by hyperplastic agglomerates. Monitoring of urine sediment for tubular cell-specific gene transcript levels NPHS2 (podocyte), AQP1 and AQP6 (proximal tubule), and SLC12A1 (distal tubule) by qPCR revealed different components depending on the cause of AKI. Confocal immunofluorescence staining confirmed the presence of intact nephron-specific epithelial cells, some of which appeared in clusters expressing AQP1 and PAX8 and were 53% positive for the stem cell marker PROM1. Isolated tubule epithelial progenitor cells were grown in vitro, expanded, and reached confluence within 5–7 days, while the expression of AQP1 and UMOD increased, whereas PROM1 and Ki67 decreased. This was accompanied by a change in cell morphology from a disproportionately high nuclear/cytoplasmic ratio at day 2–7 with mitotic figures. In contrast, an apoptotic morphology of approximately 30% was found at day 9 with the appearance of multinucleated cells that were associable with different regions of the nephron tubule by marker proteins. At the same time, UMOD was detected in the culture supernatant. Conclusion During renal recovery, a high replicatory potential of tubular epithelial progenitor cells is found in urine. In vitro expansion and gene expression show differentiation into tubular cells with marker proteins specific for different nephron regions.
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5

Maeshima, Akito, Shunsuke Takahashi, Masao Nakasatomi, and Yoshihisa Nojima. "Diverse Cell Populations Involved in Regeneration of Renal Tubular Epithelium following Acute Kidney Injury." Stem Cells International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/964849.

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Renal tubular epithelium has the capacity to regenerate, repair, and reepithelialize in response to a variety of insults. Previous studies with several kidney injury models demonstrated that various growth factors, transcription factors, and extracellular matrices are involved in this process. Surviving tubular cells actively proliferate, migrate, and differentiate in the kidney regeneration process after injury, and some cells express putative stem cell markers or possess stem cell properties. Using fate mapping techniques, bone marrow-derived cells and endothelial progenitor cells have been shown to transdifferentiate into tubular components in vivo or ex vivo. Similarly, it has been demonstrated that, during tubular cell regeneration, several inflammatory cell populations migrate, assemble around tubular cells, and interact with tubular cells during the repair of tubular epithelium. In this review, we describe recent advances in understanding the regeneration mechanisms of renal tubules, particularly the characteristics of various cell populations contributing to tubular regeneration, and highlight the targets for the development of regenerative medicine for treating kidney diseases in humans.
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6

Li, Ling, Rachel Black, Zhendong Ma, Qiwen Yang, Andrew Wang, and Fangming Lin. "Use of mouse hematopoietic stem and progenitor cells to treat acute kidney injury." American Journal of Physiology-Renal Physiology 302, no. 1 (January 1, 2012): F9—F19. http://dx.doi.org/10.1152/ajprenal.00377.2011.

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New and effective treatment for acute kidney injury remains a challenge. Here, we induced mouse hematopoietic stem and progenitor cells (HSPC) to differentiate into cells that partially resemble a renal cell phenotype and tested their therapeutic potential. We sequentially treated HSPC with a combination of protein factors for 1 wk to generate a large number of cells that expressed renal developmentally regulated genes and protein. Cell fate conversion was associated with increased histone acetylation on promoters of renal-related genes. Further treatment of the cells with a histone deacetylase inhibitor improved the efficiency of cell conversion by sixfold. Treated cells formed tubular structures in three-dimensional cultures and were integrated into tubules of embryonic kidney organ cultures. When injected under the renal capsule, they integrated into renal tubules of postischemic kidneys and expressed the epithelial marker E-cadherin. No teratoma formation was detected 2 and 6 mo after cell injection, supporting the safety of using these cells. Furthermore, intravenous injection of the cells into mice with renal ischemic injury improved kidney function and morphology by increasing endogenous renal repair and decreasing tubular cell death. The cells produced biologically effective concentrations of renotrophic factors including VEGF, IGF-1, and HGF to stimulate epithelial proliferation and tubular repair. Our study indicates that hematopoietic stem and progenitor cells can be converted to a large number of renal-like cells within a short period for potential treatment of acute kidney injury.
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7

Wen, Donghai, Li Ni, Li You, Liying Zhang, Yong Gu, Chuan-Ming Hao, and Jing Chen. "Upregulation of nestin in proximal tubules may participate in cell migration during renal repair." American Journal of Physiology-Renal Physiology 303, no. 11 (December 1, 2012): F1534—F1544. http://dx.doi.org/10.1152/ajprenal.00083.2012.

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The characteristics of renal tubular progenitor/precursor cells and the role of renal tubule regeneration in the repair of remnant kidneys (RKs) after nephrectomy are not well known. In the present study of a murine model of subtotal nephrectomy, we used immunofluorescence (IF), immunoblot analysis, and in situ hybridization methods to demonstrate that nestin expression was transiently upregulated in tubule cells near the incision edges of RKs. The nestin-positive tubules were immature proximal tubules that colabeled with lotus tetragonolobus agglutinin but not with markers of mature tubules (aquaporin-1, Tamm-Horsfall protein, and aquaporin-2). In addition, many of the nestin-expressing tubule cells were actively proliferative cells, as indicated by colabeling with bromodeoxyuridine. Double-label IF and immunoblot analysis also showed that the upregulation of tubular nestin was associated with enhanced transforming growth factor-β1 (TGF-β1) expression in the incision edge of RKs but not α-smooth muscle actin, which is a marker of fibrosis. In cultured human kidney proximal tubule cells (HKC), immunoblot analysis indicated that TGF-β1 induced nestin expression and loss of E-cadherin expression, suggesting an association of nestin expression and cellular dedifferentiation. Knockdown of nestin expression by a short hairpin RNA-containing plasmid led to decreased migration of HKC cells that were induced by TGF-β1. Taken together, our results suggest that the tubule repair that occurs during the recovery process following nephrectomy may involve TGF-β1-induced nestin expression in immature renal proximal tubule cells and the promotion of renal cell migration.
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8

Zhang, Zhao, Diana M. Iglesias, Rachel Corsini, LeeLee Chu, and Paul Goodyer. "WNT/β-Catenin Signaling Is Required for Integration of CD24+Renal Progenitor Cells into Glycerol-Damaged Adult Renal Tubules." Stem Cells International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/391043.

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During development, nephron progenitor cells (NPC) are induced to differentiate by WNT9b signals from the ureteric bud. Although nephrogenesis ends in the perinatal period, acute kidney injury (AKI) elicits repopulation of damaged nephrons. Interestingly, embryonic NPC infused into adult mice with AKI are incorporated into regenerating tubules. Since WNT/β-catenin signaling is crucial for primary nephrogenesis, we reasoned that it might also be needed for the endogenous repair mechanism and for integration of exogenous NPC. When we examined glycerol-induced AKI in adult mice bearing aβ-catenin/TCF reporter transgene, endogenous tubular cells reexpressed the NPC marker, CD24, and showed widespreadβ-catenin/TCF signaling. We isolated CD24+cells from E15 kidneys of mice with the canonical WNT signaling reporter. 40% of cells responded to WNT3ain vitroand when infused into glycerol-injured adult, the cells exhibitedβ-catenin/TCF reporter activity when integrated into damaged tubules. When embryonic CD24+cells were treated with aβ-catenin/TCF pathway inhibitor (IWR-1) prior to infusion into glycerol-injured mice, tubular integration of cells was sharply reduced. Thus, the endogenous canonicalβ-catenin/TCF pathway is reactivated during recovery from AKI and is required for integration of exogenous embryonic renal progenitor cells into damaged tubules. These events appear to recapitulate the WNT-dependent inductive process which drives primary nephrogenesis.
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9

Salikhova, D. I., L. R. Khaerdinova, O. V. Makhnach, and D. V. Goldshtein. "Angiogenic properties of glial progenitor cells derived from human induced pluripotent stem cells." Genes & Cells 17, no. 2 (September 25, 2022): 32–39. http://dx.doi.org/10.23868/202209005.

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Diseases associated with impaired blood supply to the brain ranks second term of mortality in the world, losing the place only to coronary heart disease. The incidence of this disease in the world remains high and increasing significantly with the age. The recent years special attention has been paid to the search for new methods of therapy for ischemic diseases, such as study of angiogenic properties of stem cells and their conditioned medium. The aim of this work is studying the angiogenic properties of glial progenitor cells derived from human induced pluripotent stem cells. The study was carried out by testing the proliferative activity, mobility, migration of endothelial cells line EA.hy926 under the influence of glial progenitor cells and their conditioned medium. Also the research was conducted by ability to formation of the tubular and capillary-like structure by cells line EA.hy926 by modeling angiogenesis in the basement membrane matrix in vitro. The conditioned medium obtained by glial progenitor cells at concentrations of total protein 1 and 5 g/ml has a positive influence on the proliferative activity and mobility of the endothelial cells line EA.hy926. At the same time it does not accelerate the formation of the primary tubular and capillary-like structure by the modeling angiogenesis in the basement membrane matrix in vitro. But glial progenitor cells contribute to the formation of tubular and capillary-like structure due to contact-dependent signaling between the two cell types. The primary formed tubular structure had a long processes and large branch points under co cultivation with glial progenitor cells. Sprouting centers also had long and more convoluted processes and large cell clusters during the formation of a capillary-like structure. The glial progenitor cells and their conditioned medium had a positive effect on endothelial cell migration. This effect probably indicated by the production of substances by glial progenitor cells which was chemoattractants for endothelial cells line EA.hy926.
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10

Volovelsky, Oded, Thi Nguyen, Alison E. Jarmas, Alexander N. Combes, Sean B. Wilson, Melissa H. Little, David P. Witte, Eric W. Brunskill, and Raphael Kopan. "Hamartin regulates cessation of mouse nephrogenesis independently of Mtor." Proceedings of the National Academy of Sciences 115, no. 23 (May 21, 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 a 25% increase in nephron endowment with no adverse effects. Increased progenitor engraftment rates ex vivo relative to controls correlated with prolonged nephrogenesis through the fourth postnatal day. Complete loss of both Tsc1 alleles in renal progenitors led to a lethal tubular lesion. The hamartin phenotypes are not dependent on the inhibitory effect of TSC on the Mtor complex but are dependent on Raptor.
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11

Peired, Anna Julie, Giulia Antonelli, Maria Lucia Angelotti, Marco Allinovi, Francesco Guzzi, Alessandro Sisti, Roberto Semeraro, et al. "Acute kidney injury promotes development of papillary renal cell adenoma and carcinoma from renal progenitor cells." Science Translational Medicine 12, no. 536 (March 25, 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-carcinoma sequence. Among AKI-related pathways, NOTCH1 overexpression in human pRCC associated with worse outcome and was specific for type 2 pRCC. Mice overexpressing NOTCH1 in TECs developed papillary adenomas and type 2 pRCCs, and AKI accelerated this process. Lineage tracing in mice identified single renal progenitors as the cell of origin of papillary tumors. Single-cell RNA sequencing showed that human renal progenitor transcriptome showed similarities to PT1, the putative cell of origin of human pRCC. Furthermore, NOTCH1 overexpression in cultured human renal progenitor cells induced tumor-like 3D growth. Thus, AKI can drive tumorigenesis from local tissue progenitor cells. In particular, we find that AKI promotes the development of pRCC from single progenitors through a classical adenoma-carcinoma sequence.
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12

Schutgens, Frans, Maarten B. Rookmaaker, Francis Blokzijl, Ruben van Boxtel, Robert Vries, Edwin Cuppen, Marianne C. Verhaar, and Hans Clevers. "Troy/TNFRSF19 marks epithelial progenitor cells during mouse kidney development that continue to contribute to turnover in adult kidney." Proceedings of the National Academy of Sciences 114, no. 52 (December 13, 2017): E11190—E11198. http://dx.doi.org/10.1073/pnas.1714145115.

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During kidney development, progressively committed progenitor cells give rise to the distinct segments of the nephron, the functional unit of the kidney. Similar segment-committed progenitor cells are thought to be involved in the homeostasis of adult kidney. However, markers for most segment-committed progenitor cells remain to be identified. Here, we evaluate Troy/TNFRSF19 as a segment-committed nephron progenitor cell marker. Troy is expressed in the ureteric bud during embryonic development. During postnatal nephrogenesis, Troy+ cells are present in the cortex and papilla and display an immature tubular phenotype. Tracing of Troy+ cells during nephrogenesis demonstrates that Troy+ cells clonally give rise to tubular structures that persist for up to 2 y after induction. Troy+ cells have a 40-fold higher capacity than Troy− cells to form organoids, which is considered a stem cell property in vitro. In the adult kidney, Troy+ cells are present in the papilla and these cells continue to contribute to collecting duct formation during homeostasis. The number of Troy-derived cells increases after folic acid-induced injury. Our data show that Troy marks a renal stem/progenitor cell population in the developing kidney that in adult kidney contributes to homeostasis, predominantly of the collecting duct, and regeneration.
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13

Wang, Jiayi, Jianyong Zhong, Hai-Chun Yang, and Agnes B. Fogo. "Cross Talk from Tubules to Glomeruli." Toxicologic Pathology 46, no. 8 (August 29, 2018): 944–48. http://dx.doi.org/10.1177/0192623318796784.

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Tubular injury sensitizes glomeruli to injury. We review potential mechanisms of this tubuloglomerular cross talk. In the same nephron, tubular injury can cause stenosis of the glomerulotubular junction and finally result in atubular glomeruli. Tubular injury also affects glomerular filtration function through tubuloglomerular feedback. Progenitor cells, that is, parietal epithelial cells and renin positive cells, can be involved in repair of injured glomeruli and also may be modulated by tubular injury. Loss of nephrons induces additional workload and stress on remaining nephrons. Hypoxia and activation of the renin–angiotensin–aldosterone system induced by tubular injury also modulate tubuloglomerular cross talk. Therefore, effective therapies in chronic kidney disease may need to aim to interrupt this deleterious tubuloglomerular cross talk.
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14

Andrianova, Nadezda V., Marina I. Buyan, Ljubava D. Zorova, Irina B. Pevzner, Vasily A. Popkov, Valentina A. Babenko, Denis N. Silachev, Egor Y. Plotnikov, and Dmitry B. Zorov. "Kidney Cells Regeneration: Dedifferentiation of Tubular Epithelium, Resident Stem Cells and Possible Niches for Renal Progenitors." International Journal of Molecular Sciences 20, no. 24 (December 15, 2019): 6326. http://dx.doi.org/10.3390/ijms20246326.

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A kidney is an organ with relatively low basal cellular regenerative potential. However, renal cells have a pronounced ability to proliferate after injury, which undermines that the kidney cells are able to regenerate under induced conditions. The majority of studies explain yielded regeneration either by the dedifferentiation of the mature tubular epithelium or by the presence of a resident pool of progenitor cells in the kidney tissue. Whether cells responsible for the regeneration of the kidney initially have progenitor properties or if they obtain a “progenitor phenotype” during dedifferentiation after an injury, still stays the open question. The major stumbling block in resolving the issue is the lack of specific methods for distinguishing between dedifferentiated cells and resident progenitor cells. Transgenic animals, single-cell transcriptomics, and other recent approaches could be powerful tools to solve this problem. This review examines the main mechanisms of kidney regeneration: dedifferentiation of epithelial cells and activation of progenitor cells with special attention to potential niches of kidney progenitor cells. We attempted to give a detailed description of the most controversial topics in this field and ways to resolve these issues.
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15

Romagnani, Paola, and Hans-Joachim Anders. "What can tubular progenitor cultures teach us about kidney regeneration?" Kidney International 83, no. 3 (March 2013): 351–53. http://dx.doi.org/10.1038/ki.2012.437.

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16

Schwartz, John D., Francis Dumler, Jason M. Hafron, George D. Wilson, Stacy C. Wolforth, Michele T. Rooney, Wei Li, and Ping L. Zhang. "CD133 Staining Detects Acute Kidney Injury and Differentiates Clear Cell Papillary Renal Cell Carcinoma from Other Renal Tumors." ISRN Biomarkers 2013 (June 2, 2013): 1–8. http://dx.doi.org/10.1155/2013/353598.

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CD133 has recently been characterized as a progenitor cell marker in the kidney. However, the expression of this marker has not been thoroughly investigated in kidney injury and variants of renal tumors for pathology practice. We quantified CD133 expression in kidney biopsies from patients with acute renal failure and compared staining intensity with serum creatinine levels. CD133 expression levels were also evaluated in several subtypes of renal neoplasms. Normal adult renal parenchyma showed CD133 expression in parietal epithelium and in less than 5% of the epithelial cells in proximal and distal nephron tubules. However, CD133 was diffusely upregulated in the injured proximal and distal tubular epithelium and the CD133 expression scores in renal tubules were significantly correlated with serum creatinine levels. Amongst the renal tumors, CD133 was diffusely expressed in clear cell papillary renal cell carcinoma but was only focally present in other types of renal tumors. In summary, CD133 is a useful marker to detect renal tubular injury and to differentiate clear cell papillary renal cell carcinoma from other tumor types.
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17

Minuth, Will W., Lucia Denk, and Hayo Castrop. "Generation of Tubular Superstructures by Piling of Renal Stem/Progenitor Cells." Tissue Engineering Part C: Methods 14, no. 1 (March 2008): 3–13. http://dx.doi.org/10.1089/tec.2007.0230.

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18

Ebrahimi, Behzad, Zilun Li, Alfonso Eirin, Xiang-Yang Zhu, Stephen C. Textor, and Lilach O. Lerman. "Addition of endothelial progenitor cells to renal revascularization restores medullary tubular oxygen consumption in swine renal artery stenosis." American Journal of Physiology-Renal Physiology 302, no. 11 (June 1, 2012): F1478—F1485. http://dx.doi.org/10.1152/ajprenal.00563.2011.

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Renal artery stenosis (RAS) promotes microvascular rarefaction and fibrogenesis, which may eventuate in irreversible kidney injury. We have shown that percutaneous transluminal renal angioplasty (PTRA) or endothelial progenitor cells (EPC) improve renal cortical hemodynamics and function in the poststenotic kidney. The renal medulla is particularly sensitive to hypoxia, yet little is known about reversibility of medullary injury on restoration of renal blood flow. This study was designed to test the hypothesis that PTRA, with or without adjunct EPC delivery to the stenotic kidney, may improve medullary remodeling and tubular function. RAS was induced in 21 pigs using implantation of irritant coils, while another group served as normal controls ( n = 7 each). Two RAS groups were then treated 6 wk later with PTRA or both PTRA and EPC. Four weeks later, medullary hemodynamics, microvascular architecture, and oxygen-dependent tubular function of the stenotic kidneys were examined using multidetector computed tomography, microcomputed tomography, and blood oxygenation level-dependent MRI, respectively. Medullary protein expression of vascular endothelial growth factor, endothelial nitric oxide synthase, hypoxia-inducible factor-1α, and NAD(P)H oxidase p47 were determined. All RAS groups showed decreased medullary vascular density and blood flow. However, in RAS+PTRA+EPC animals, EPC were engrafted in tubular structures, oxygen-dependent tubular function was normalized, and fibrosis attenuated, despite elevated expression of hypoxia-inducible factor-1α and sustained downregulation of vascular endothelial growth factor. In conclusion, EPC delivery, in addition to PTRA, restores medullary oxygen-dependent tubular function, despite impaired medullary blood and oxygen supply. These results support further development of cell-based therapy as an adjunct to revascularization of RAS.
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Miya, Masaaki, Akito Maeshima, Keiichiro Mishima, Noriyuki Sakurai, Hidekazu Ikeuchi, Takashi Kuroiwa, Keiju Hiromura, and Yoshihisa Nojima. "Age-related decline in label-retaining tubular cells: implication for reduced regenerative capacity after injury in the aging kidney." American Journal of Physiology-Renal Physiology 302, no. 6 (March 15, 2012): F694—F702. http://dx.doi.org/10.1152/ajprenal.00249.2011.

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Recovery after acute kidney injury is impaired in the elderly, but the precise mechanism for such age-related incompetence remains unclear. By in vivo bromodeoxyuridine (BrdU) labeling, renal progenitor cells (label-retaining cells; LRCs) were identified in tubules of normal rat kidney and were shown to be the origin of proliferating cells after injury. In the present study, the involvement of LRCs in the age-related decline of tubular recovery after injury was examined. After 1 wk of BrdU labeling followed by a 2-wk chase period, ischemia-reperfusion injury was induced in 7-wk-, 7-mo-, and 12-mo-old rats. Age-related decreases in DNA synthesis and cell proliferation in renal tubules after injury were found. The number of LRCs also significantly declined with age. At 24 h after reperfusion, the number of LRCs significantly increased in all ages of rats tested. There was no significant difference in the ratio of LRC division among rats of different ages. The area of the rat endothelial cell antigen (RECA)-1-positive capillary network declined with age. When renal tubules isolated from rats treated with BrdU label were cocultured with human umbilical vein endothelial cells (HUVEC), the number of LRCs significantly increased compared with tubules cultured without HUVEC. These data suggest that the reduced capacity of tubular regeneration in the aging kidney is partly explained by the shortage of LRC reserves. The size of the LRC pool might be regulated by the surrounding peritubular capillary network.
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20

Bi, Baoyuan, Jiankan Guo, Arnaud Marlier, Shin Ru Lin, and Lloyd G. Cantley. "Erythropoietin expands a stromal cell population that can mediate renoprotection." American Journal of Physiology-Renal Physiology 295, no. 4 (October 2008): F1017—F1022. http://dx.doi.org/10.1152/ajprenal.90218.2008.

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Recent studies have demonstrated that erythropoietin (EPO) receptors are expressed on tubular epithelial cells and that EPO can protect tubular cells from injury in vitro and in vivo. Separate studies have demonstrated that marrow stromal cells (MSCs) exert a renoprotective effect in ischemia-reperfusion and cisplatin tubular injury via the secretion of factors that reduce apoptosis and increase proliferation of tubular epithelial cells. In the present study we demonstrate that MSCs express EPO receptors and that EPO can protect MSCs from serum deprivation-induced cell death and can stimulate MSC proliferation in vitro. The administration of EPO to mice resulted in the expansion of CD45-Flk1-CD105+ MSCs in the bone marrow and in the spleen and mobilized these cells as well as CD45-Flk1+ endothelial progenitor cells into the peripheral circulation. Consistent with previous reports, the administration of EPO diminished the decline in renal function associated with cisplatin administration. This effect was partially reproduced by intraperitoneal injection of cultured EPO-mobilized cells in cisplatin-treated mice. Thus the in vivo expansion and/or activation of these cells may contribute to the renoprotective effects of EPO to protect tubular cells from toxic injury.
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21

Buyan, Marina I., Nadezda V. Andrianova, Vasily A. Popkov, Ljubava D. Zorova, Irina B. Pevzner, Denis N. Silachev, Dmitry B. Zorov, and Egor Y. Plotnikov. "Age-Associated Loss in Renal Nestin-Positive Progenitor Cells." International Journal of Molecular Sciences 23, no. 19 (September 20, 2022): 11015. http://dx.doi.org/10.3390/ijms231911015.

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The decrease in the number of resident progenitor cells with age was shown for several organs. Such a loss is associated with a decline in regenerative capacity and a greater vulnerability of organs to injury. However, experiments evaluating the number of progenitor cells in the kidney during aging have not been performed until recently. Our study tried to address the change in the number of renal progenitor cells with age. Experiments were carried out on young and old transgenic nestin-green fluorescent protein (GFP) reporter mice, since nestin is suggested to be one of the markers of progenitor cells. We found that nestin+ cells in kidney tissue were located in the putative niches of resident renal progenitor cells. Evaluation of the amount of nestin+ cells in the kidneys of different ages revealed a multifold decrease in the levels of nestin+ cells in old mice. In vitro experiments on primary cultures of renal tubular cells showed that all cells including nestin+ cells from old mice had a lower proliferation rate. Moreover, the resistance to damaging factors was reduced in cells obtained from old mice. Our data indicate the loss of resident progenitor cells in kidneys and a decrease in renal cells proliferative capacity with aging.
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Moraghebi, Roksana, Roger Emanuel Rönn, Aaron Parker, Margaret Lutz, Travis Berggren, and Niels-Bjarne Woods. "Human Umbilical Cord Blood Derived IPS Cells as a Source of Hematopoietic Progenitors Cells." Blood 116, no. 21 (November 19, 2010): 4790. http://dx.doi.org/10.1182/blood.v116.21.4790.4790.

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Abstract Abstract 4790 The ability to generate hematopoietic stem cells (HSCs) from an unlimited source of cells, such as from patient derived induced pluripotent stem (iPS) cells, would enable the generation of an unlimited supply of HLA matched transplantable HSCs for therapeutic purposes. Umbilical cord blood is an ideal source of fetal/neonatal cellular material for iPS reprogramming due to the proliferative capacity of the cells as well as the reduced exposure of these cells to environmental factors compare to commonly used skin fibroblasts. In addition, it has been proposed that the cellular starting material imparts an epigenetic memory to the iPS cell line that influences lineage predisposition upon its differentiation. This project seeks to evaluate human umbilical cord blood as a starting cell source for generating iPS cells, with the ultimate goal to generate transplantable HSCs. We have isolated, cultured, and characterized an adherent cell fraction from the hemato-endothelial lineage. These cells were found to have an endothelial progenitor phenotype with CD45neg, CD133neg, VE-Cadherinhi, VEGFR2med, CD31hi, CD34hi cell surface markers as determined by FACS and formed tubules in the matrigel tubular assay. The iPS cell lines were generated using a 5-factor cocktail of inducible lentiviral vectors with an efficiency of 0.02%. The iPS cell lines were then evaluated for blood cell lineage differentiation capacity using our state-of-the-art ES/iPS-to-blood differentiation protocol. From the 5 iPS lines we tested, we saw 30 +/− 20% hematopoietic (CD45+) cells in our differentiation cultures. Moreover, the percentage of hematopoietic progenitors (CD45+ CD34+) of the hematopoietic cell fraction was 19.8+/− 0.6%, and also showed the presence of the more primitive CD45+ CD34+ CD38- progenitor fraction. Clonogenic progenitor cell counts determined by methylcellulose colony assay showed 44 +/− 3 colony forming units per 10,000 plated CD45+ cells. This is in the range of colonies obtained from umbilical cord blood mononuclear cell isolates (mean= 35+/− 2). The efficiency of hematopoietic generation for the lines ranged from 8 to 60% CD45+ suggesting that there are significant differences between the lines in terms of the completeness of reprogramming towards the pluripotent state. Further investigation into the epigenetic status of these lines is being performed. These data demonstrate the utility of human umbilical cord blood derived iPS cells for generating and expanding hematopoietic progenitors. This project advances iPS technologies towards treating life threatening hematological malignancies and diseases. Disclosures: No relevant conflicts of interest to declare.
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Tanimizu, Naoki, Atsushi Miyajima, and Keith E. Mostov. "Liver Progenitor Cells Fold Up a Cell Monolayer into a Double-layered Structure during Tubular Morphogenesis." Molecular Biology of the Cell 20, no. 9 (May 2009): 2486–94. http://dx.doi.org/10.1091/mbc.e08-02-0177.

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Bile ducts are hepatic tubular structures that are lined by cholangiocytes, a type of liver epithelial cell. Cholangiocytes first form a single layer of cells, termed the ductal plate, surrounding the portal vein, which eventually remodels into the branching tubular network of bile ducts. The process of bile duct morphogenesis is not yet clear: a conventional model where cholangiocytes proliferate to duplicate a single layer of the ductal plate before lumen formation seems inconsistent with the observation that proliferation is dramatically reduced when hepatoblasts, liver progenitor cells, differentiate into cholangiocytes. Here, we developed a new culture system in which a liver progenitor cell line, HPPL, reorganizes from a monolayer to tubular structures in response to being overlaid with a gel containing type I collagen and Matrigel. We found that some of the HPPL in the monolayer depolarized and migrated to fold up the monolayer into a double-cell layer. These morphogenetic processes occurred without cell proliferation and required phosphatidylinositol 3-kinase and Akt activity. Later in morphogenesis, luminal space was generated between the two cell layers. This process, in particular enlargement of the apical lumen, involved transcriptional activity of HNF1β. Thus, using this sandwich culture system, we could segregate tubulogenesis of bile ducts into distinct steps and found that the PI3K/Akt pathway and HNF1β regulated different steps of the morphogenesis. Although the process of tubulogenesis in culture specifically resembled early bile duct formation, involvement of these two key players suggests that the sandwich culture might help us to find common principles of tubulogenesis in general.
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Ó hAinmhire, Eoghainín, Haojia Wu, Yoshiharu Muto, Erinn L. Donnelly, Flavia G. Machado, Lucy X. Fan, Monica Chang-Panesso, and Benjamin D. Humphreys. "A conditionally immortalized Gli1-positive kidney mesenchymal cell line models myofibroblast transition." American Journal of Physiology-Renal Physiology 316, no. 1 (January 1, 2019): F63—F75. http://dx.doi.org/10.1152/ajprenal.00460.2018.

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Glioma-associated oncogene homolog-1 (Gli1)-positive resident mesenchymal stem cell-like cells are the predominant source of kidney myofibroblasts in fibrosis, but investigating Gli1-positive myofibroblast progenitor activation is hampered by the difficulty of isolating and propagating primary cultures of these cells. Using a genetic strategy with positive and negative selection, we isolated Kidney-Gli1 (KGli1) cells that maintain expression of appropriate mesenchymal stem cell-like cell markers, respond to hedgehog pathway activation, and display robust myofibroblast differentiation upon treatment with transforming growth factor-β (TGF-β). Coculture of KGli1 cells with endothelium stabilizes capillary formation. Single-cell RNA sequencing (scRNA-seq) analysis during differentiation identified autocrine ligand-receptor pair upregulation and a strong focal adhesion pathway signal. This led us to test the serum response factor inhibitor CCG-203971 that potently inhibited TGF-β-induced pericyte-to-myofibroblast transition. scRNA-seq also identified the unexpected upregulation of nerve growth factor (NGF), which we confirmed in two mouse kidney fibrosis models. The Ngf receptor Ntrk1 is expressed in tubular epithelium in vivo, suggesting a novel interstitial-to-tubule paracrine signaling axis. Thus, KGli1 cells accurately model myofibroblast activation in vitro, and the development of this cell line provides a new tool to study resident mesenchymal stem cell-like progenitors in health and disease.
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Veys, Koenraad, Sante Princiero Berlingerio, Dries David, Tjessa Bondue, Katharina Held, Ahmed Reda, Martijn van den Broek, et al. "Urine-Derived Kidney Progenitor Cells in Cystinosis." Cells 11, no. 7 (April 6, 2022): 1245. http://dx.doi.org/10.3390/cells11071245.

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Nephropathic cystinosis is an inherited lysosomal storage disorder caused by pathogenic variants in the cystinosin (CTNS) gene and is characterized by the excessive shedding of proximal tubular epithelial cells (PTECs) and podocytes into urine, development of the renal Fanconi syndrome and end-stage kidney disease (ESKD). We hypothesized that in compensation for epithelial cell losses, cystinosis kidneys undertake a regenerative effort, and searched for the presence of kidney progenitor cells (KPCs) in the urine of cystinosis patients. Urine was cultured in a specific progenitor medium to isolate undifferentiated cells. Of these, clones were characterized by qPCR, subjected to a differentiation protocol to PTECs and podocytes and assessed by qPCR, Western blot, immunostainings and functional assays. Cystinosis patients voided high numbers of undifferentiated cells in urine, of which various clonal cell lines showed a high capacity for self-renewal and expressed kidney progenitor markers, which therefore were assigned as cystinosis urine-derived KPCs (Cys-uKPCs). Cys-uKPC clones showed the capacity to differentiate between functional PTECs and/or podocytes. Gene addition with wild-type CTNS using lentiviral vector technology resulted in significant reductions in cystine levels. We conclude that KPCs present in the urine of cystinosis patients can be isolated, differentiated and complemented with CTNS in vitro, serving as a novel tool for disease modeling.
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Hermansen, Stig Eggen, Trine Lund, Trine Kalstad, Kirsti Ytrehus, and Truls Myrmel. "Adrenomedullin augments the angiogenic potential of late outgrowth endothelial progenitor cells." American Journal of Physiology-Cell Physiology 300, no. 4 (April 2011): C783—C791. http://dx.doi.org/10.1152/ajpcell.00044.2010.

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The therapeutic utility of endothelial progenitor cells (EPCs) in cardiovascular disease is potentially hampered by their low numbers in the circulation, impaired functional activity, and inhibitory factors in the recipient. These obstacles can possibly be circumvented by the use of proangiogenic cytokines and peptides. We sought to examine the effect of the endogenous vasoactive peptide adrenomedullin (AM) on the angiogenic potential of late outgrowth EPCs and their release of proangiogenic and proinflammatory cytokines/chemokines. Human peripheral blood mononuclear cells were cultured until the appearance of typical late outgrowth EPC colonies. The effect of AM on EPC proliferation was assessed using a colorimetric MTS proliferation assay while differentiation and formation of tubular structures in an EPC/fibroblast coculture or matrigel assay was used to assess the angiogenic potential of the cells. Finally, the release and mRNA transcripts of cytokines/chemokines were quantified in stimulated vs. nonstimulated EPCs using real-time PCR and a bead-based multiplex assay. The cultured EPCs possessed an endothelial phenotype and expressed the AM receptor (calcitonin receptor-like receptor/receptor activity modifying protein-2). AM stimulation induced proliferation of EPCs compared with controls ( P < 0.05). Furthermore, AM produced a 36% and 80% increase in the formation of tubular networks in the EPC/fibroblast coculture and matrigel assay, respectively ( P < 0.05). These effects seemed to be mediated through the phosphatidylinositol 3-kinase/Akt signaling pathway. AM did not seem to significantly influence the release or production of IL-6, IL-8, VEGF, stromal cell-derived factor 1, or the expression of CXCR-4 or VEGF receptor 2. In conclusion, adrenomedullin augmented the growth and angiogenic properties of late outgrowth EPCs, but did not influence their paracrine properties.
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27

Cho, E. A., L. T. Patterson, W. T. Brookhiser, S. Mah, C. Kintner, and G. R. Dressler. "Differential expression and function of cadherin-6 during renal epithelium development." Development 125, no. 5 (March 1, 1998): 803–12. http://dx.doi.org/10.1242/dev.125.5.803.

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The cadherin gene family encodes calcium-dependent adhesion molecules that promote homophilic interactions among cells. During embryogenesis, differential expression of cadherins can drive morphogenesis by stimulating cell aggregation, defining boundaries between groups of cells and promoting cell migration. In this report, the expression patterns of cadherins were examined by immunocytochemistry and in situ hybridization in the embryonic kidney, during the time when mesenchymal cells are phenotypically converted to epithelium and the pattern of the developing nephrons is established. At the time of mesenchymal induction, cadherin-11 is expressed in the mesenchyme but not in the ureteric bud epithelium, which expresses E-cadherin. The newly formed epithelium of the renal vesicle expresses E-cadherin near the ureteric bud tips and cadherin-6 more distally, suggesting that this primitive epithelium is already patterned with respect to progenitor cell types. In the s-shaped body, the cadherin expression patterns reflect the developmental fate of each region. The proximal tubule progenitors express cadherin-6, the distal tubule cells express E-cadherin, whereas the glomeruli express P-cadherin. Ultimately, cadherin-6 is down-regulated whereas E-cadherin expression remains in most, if not all, of the tubular epithelium. Antibodies generated against the extracellular domain of cadherin-6 inhibit aggregation of induced mesenchyme and the formation of mesenchyme-derived epithelium but do not disrupt ureteric bud branching in vitro. These data suggest that cadherin-6 function is required for the early aggregation of induced mesenchymal cells and their subsequent conversion to epithelium.
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Lazzeri, Elena, Maria Lucia Angelotti, Anna Julie Peired, Francesca Becherucci, Duccio Lombardi, Laura Lasagni, and Paola Romagnani. "SP181PAX2+ PROGENITOR CELLS PLAY A KEY ROLE IN TUBULAR REGENERATION AFTER ACUTE KIDNEY INJURY." Nephrology Dialysis Transplantation 31, suppl_1 (May 2016): i146. http://dx.doi.org/10.1093/ndt/gfw161.14.

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Loverre, Antonia, Carmen Capobianco, Pasquale Ditonno, Michele Battaglia, Giuseppe Grandaliano, and Francesco Paolo Schena. "Increase of Proliferating Renal Progenitor Cells in Acute Tubular Necrosis Underlying Delayed Graft Function." Transplantation 85, no. 8 (April 2008): 1112–19. http://dx.doi.org/10.1097/tp.0b013e31816a8891.

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30

Wang, Hui-ling, Nan-mei Liu, and Rui Li. "Role of adult resident renal progenitor cells in tubular repair after acute kidney injury." Journal of Integrative Medicine 12, no. 6 (November 2014): 469–75. http://dx.doi.org/10.1016/s2095-4964(14)60053-4.

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31

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 (June 1, 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 conditional deletion of AT1A receptor in the FoxD1 cell lineage in combination with global disruption of the AT1B receptor gene. These FoxD1-AT1ko mice developed normally. Their kidneys showed neither structural nor functional abnormalities compared with wild-type mice, whereas in isolated perfused FoxD1-AT1ko kidneys, the vasoconstrictor and renin inhibitory effects of ANG II were absent. In vivo, however, plasma renin concentration and renal renin expression were normal in FoxD1-AT1ko mice, as were blood pressure and glomerular filtration rate. These findings suggest that a strong reduction of AT1 receptors in renal stromal progenitors and their descendants does not disturb normal kidney development.
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Tossetta, Giovanni, Sonia Fantone, Teresa Lorenzi, Andrea Benedetto Galosi, Andrea Sagrati, Mara Fabri, Daniela Marzioni, and Manrico Morroni. "Scattered Tubular Cells Markers in Macula Densa of Normal Human Adult Kidney." International Journal of Molecular Sciences 23, no. 18 (September 10, 2022): 10504. http://dx.doi.org/10.3390/ijms231810504.

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Background: The scattered tubular cells (STCs) are a population of resident progenitor tubular cells with expansion, self-renewal and epithelial differentiation abilities. Although these cells are localized within the proximal (PTs) and distal (DTs) tubules in a normal adult kidney, their presence has never been demonstrated in human macula densa (MD). The purpose of the present study is to describe the presence of STCs in MD using specific markers such as prominin-1 (CD133), cytokeratin 7 (KRT7) and vimentin (VIM). Methods: We analyzed two sets of three consecutive serial sections for each sample. The first sections of each set were immunostained for nNOS to identify MD, the second sections were immune-stained for CD133 (specific STCs marker) while the third sections were analyzed for KRT7 (another STCs specific marker) and VIM (that stains the basal pole of the STCs) in the first and second sets, respectively, in order to study the co-expression of KRT7 and VIM with the CD133 marker. Results: CD133 was localized in some MD cells and in the adjacent DT cells. Moreover, CD133 was detected in the parietal epithelial cells of Bowman’s capsule and in some proximal tubules (PT). KRT7-positive cells were identified in MD and adjacent DT cells, while KRT7 positivity was mostly confined in both DT and collecting ducts (CD) in the other areas of the renal parenchyma. CD133 and KRT7 were co-expressed in some MD and adjacent DT cells. Some of the latter cells were positive both for CD133 and VIM. CD133 was always localized in the apical part of the cells, whereas the VIM expression was evident only in the cellular basal pole. Although some cells of MD expressed VIM or CD133, none of them co-expressed VIM and CD133. Conclusions: The presence of STCs was demonstrated in human adult MD, suggesting that this structure has expansion, self-renewal and epithelial differentiation abilities, similar to all other parts of renal tubules.
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Ciarambino, Tiziana, Pietro Crispino, and Mauro Giordano. "Gender and Renal Insufficiency: Opportunities for Their Therapeutic Management?" Cells 11, no. 23 (November 29, 2022): 3820. http://dx.doi.org/10.3390/cells11233820.

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Acute kidney injury (AKI) is a major clinical problem associated with increased morbidity and mortality. Despite intensive research, the clinical outcome remains poor, and apart from supportive therapy, no other specific therapy exists. Furthermore, acute kidney injury increases the risk of developing chronic kidney disease (CKD) and end-stage renal disease. Acute tubular injury accounts for the most common intrinsic cause of AKI. The main site of injury is the proximal tubule due to its high workload and energy demand. Upon injury, an intratubular subpopulation of proximal epithelial cells proliferates and restores the tubular integrity. Nevertheless, despite its strong regenerative capacity, the kidney does not always achieve its former integrity and function and incomplete recovery leads to persistent and progressive CKD. Clinical and experimental data demonstrate sexual differences in renal anatomy, physiology, and susceptibility to renal diseases including but not limited to ischemia-reperfusion injury. Some data suggest the protective role of female sex hormones, whereas others highlight the detrimental effect of male hormones in renal ischemia-reperfusion injury. Although the important role of sex hormones is evident, the exact underlying mechanisms remain to be elucidated. This review focuses on collecting the current knowledge about sexual dimorphism in renal injury and opportunities for therapeutic manipulation, with a focus on resident renal progenitor stem cells as potential novel therapeutic strategies.
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Shrestha, Swojani, Seema Somji, Donald A. Sens, Andrea Slusser-Nore, Divyen H. Patel, Evan Savage, and Scott H. Garrett. "Human renal tubular cells contain CD24/CD133 progenitor cell populations: Implications for tubular regeneration after toxicant induced damage using cadmium as a model." Toxicology and Applied Pharmacology 331 (September 2017): 116–29. http://dx.doi.org/10.1016/j.taap.2017.05.038.

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35

Munteanu Vlad, Adelina, Gheorghita Isvoranu, Marilena Gilca, Laura Ceafalan, Mihaela Surcel, Irina Stoian, and Gina Manda. "Sevoflurane Increases Proliferation, Adhesion on HUVEC and Incorporation in Tubular Structures of Endothelial Progenitor Cells." FASEB Journal 29 (April 2015): LB590. http://dx.doi.org/10.1096/fasebj.29.1_supplement.lb590.

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Yamashita, Shin, Akito Maeshima, and Yoshihisa Nojima. "Involvement of Renal Progenitor Tubular Cells in Epithelial-to-Mesenchymal Transition in Fibrotic Rat Kidneys." Journal of the American Society of Nephrology 16, no. 7 (May 11, 2005): 2044–51. http://dx.doi.org/10.1681/asn.2004080681.

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37

Oyake, Tatsuo, Shigeki Ito, Shugo Kowata, Kazunori Murai, Takashi Sawai, and Yoji Ishida. "Anemia of Chronic Renal Failure Is Associated with Much Higher Frequency of Apoptosis in Erythroid Progenitor in a Mouse Model." Blood 108, no. 11 (November 16, 2006): 1293. http://dx.doi.org/10.1182/blood.v108.11.1293.1293.

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Abstract Insufficient production of erythropoietin (EPO) is one of the important causes of anemia of patients with chronic renal failure (CRF). Recombinant human erythropoietin (rh-EPO) administration results in a dramatic improvement of anemia in these patients. In ASH meeting 2001, we reported that excessive apoptosis in erythroid progenitor was observed in anemia of CRF patients before rh-EPO administration. In this study, we established a mouse model of anemia of CRF to confirm the hypothesis that excessive apoptosis in erythroid progenitor induced anemia. C57B6 male mice was treated with adenine-rich diets (ADRD) for 8 weeks. Serum blood urea nitrogen (BUN), creatinine (Crt) and complete blood count (CBC) were measured every week. The frequency of apoptosis in erythroid progenitor and mature erythroblasts were evaluated by three color flow cytometric analysis. Apoptotic cells were analyzed by AnnexinV. The cell populations of erythroid progenitor were identified as CD34(+)erythropoietin-receptor (EPO-R)(+) cells and mature erythroblasts identified as CD34(-)EPO-R(+) cells. Serum BUN and Crt levels began to elevate from 2 weeks after ADRD administration (BUN; 40.1±4.6, 73.2±14.4, 150.7±11.6, 164.0±8.4, 193.0±23.3mg/dl, Crt; 0.06±0.04, 0.30±0.03, 0.51±0.07, 0.68±0.09, 0.80±0.17mg/dl, n=5: mean±SD at 0, 2, 4, 6 and 8 weeks after ADRD administration, respectively). Hb and Ht began to decrease from 6 and 4 weeks after ADRD administration (Hb; 13.6±0.4, 13.3±0.3, 13.2±0.2, 10.2±0.5, 8.3±0.5 g/dl, Ht; 52.4±1.4, 49.4±1.7, 43.6±0.2, 35.4±1.8, 30.8±1.6%, n=5: mean±SD at 0, 2, 4, 6 and 8 weeks after ADRD administration, respectively). Serum EPO levels were not elevated after ADRD administration, regardless of anemia. Much higher frequency of apoptosis was observed in erythroid progenitor from 4 to 8 weeks after ADRD administration, compared to that at 0 week (CD34(+)EPO-R(+); 18.2±7.4, 41.7±7.3, 56.0±4.8, 76.4±5.3, 70.1±6.9, 73.8±8.7%, n=5, mean±SD at 0, 4, 5, 6, 7 and 8 weeks after ADRD administration, p&lt;0.05, respectively). While, the frequency of apoptosis was not high in mature erythroblasts after ADRD administration (CD34(-)EPO-R(+); 1.58±1.4, 0.21±0.1, 0.58±0.1, 0.77±0.7, 0.49±0.2, 0.25±0.2%, n=5, mean±SD at 0, 4, 5, 6, 7 and 8 weeks after ADRD administration, N.S, respectively). Pathological examination of kidney showed that tubular damage was diffusely observed from 2 to 8 weeks after ADRD administration, and tubular necrosis was suspected as the major cause of renal failure. Our findings suggested that excessive apoptosis occurred mainly in CD34(+) erythroid progenitor by insufficient production of EPO, which induced anemia in mice with CRF.
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Mukherjee, Malini, Eric Fogarty, Madhusudhana Janga, and Kameswaran Surendran. "Notch Signaling in Kidney Development, Maintenance, and Disease." Biomolecules 9, no. 11 (November 4, 2019): 692. http://dx.doi.org/10.3390/biom9110692.

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Kidney development involves formation of nephrons intricately aligned with the vasculature and connected to a branched network of collecting ducts. Notch signaling plays multiple roles during kidney development involving the formation of nephrons composed of diverse epithelial cell types arranged into tubular segments, all the while maintaining a nephron progenitor niche. Here, we review the roles of Notch signaling identified from rodent kidney development and injury studies, while discussing human kidney diseases associated with aberrant Notch signaling. We also review Notch signaling requirement in maintenance of mature kidney epithelial cell states and speculate that Notch activity regulation mediates certain renal physiologic adaptations.
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Maeshima, A. "Identification of Renal Progenitor-Like Tubular Cells that Participate in the Regeneration Processes of the Kidney." Journal of the American Society of Nephrology 14, no. 12 (December 1, 2003): 3138–46. http://dx.doi.org/10.1097/01.asn.0000098685.43700.28.

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Ye, Yizhou, Xizhe Li, You Zhang, Zhenya Shen, and Junjie Yang. "Androgen Modulates Functions of Endothelial Progenitor Cells through Activated Egr1 Signaling." Stem Cells International 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/7057894.

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Researches show that androgens have important effects on migration of endothelial cells and endothelial protection in coronary heart disease. Endothelial progenitor cells (EPCs) as a progenitor cell type that can differentiate into endothelial cells, have a critical role in angiogenesis and endothelial protection. The relationship between androgen and the functions of EPCs has animated much interest and controversy. In this study, we investigated the angiogenic and migratory functions of EPCs after treatment by dihydrotestosterone (DHT) and the molecular mechanisms as well. We found that DHT treatment enhanced the incorporation of EPCs into tubular structures formed by HUVECs and the migratory activity of EPCs in the transwell assay dose dependently. Moreover, microarray analysis was performed to explore how DHT changes the gene expression profiles of EPCs. We found 346 differentially expressed genes in androgen-treated EPCs. Angiogenesis-related genes likeEgr-1,Vcan,Efnb2, andCdk2ap1were identified to be regulated upon DHT treatment. Furthermore, the enhanced angiogenic and migratory abilities of EPCs after DHT treatment were inhibited by Egr1-siRNA transfection. In conclusion, our findings suggest that DHT markedly enhances the vessel forming ability and migration capacity of EPCs. Egr1 signaling may be a possible pathway in this process.
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Titlbach, M., and E. Maňáková. "Development of the Rabbit Pancreas with Particular Regard to the Argyrophilic Cells." Acta Veterinaria Brno 76, no. 4 (2007): 509–17. http://dx.doi.org/10.2754/avb200776040509.

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The aim of the study was the description of the prenatal development of rabbit pancreas, cell modifications, and changes in their volume and mitotic activity. Immunohistochemical, light and electron microscopic procedures were employed. Stereological methods were used for estimation of cellular and nuclear volumes. hits on epithelial cells, tubular lumens, and endocrine progenitor cells were counted by systematic field sampling using test grid. Number of mitoses was registered in various cellular types after colchicine treatment. Data obtained were converted to 1 mm3 tissue. First granules were observed in cells on day 10 and 18 hours, however two different granular types are distinguishable by electron microscopy only on day 15, when insulin and glucagon can be detected immunohistochemically. Cellular volume increased remarkably in harmony with findings of granules in serous cells. Number of epithelial cells increased also exponentially. The increase was more rapid between days 13 and 15, later it appeared exponential. Value of mitotic index and length of cell cycle did not change considerably between days 15 and 24. Mitoses were observed in ductal, exocrine, as well as endocrine cells. The dividing endocrine cells were those that contained fine dense granules (progenitor cells). The sub-population of progenitor cells is able to divide, however, this source of cells appears insufficient for exponential growth. Results after colchicine treatment show the increase of cell population but the life-span and a period necessary for volume multiplication vary. Mitoses decrease in both sub-populations during the prenatal period. The progenitor cells arise probably by differentiation from the ducts, because their number increases proportionally to the main cell population.
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Vinsonneau, C., A. Girshovich, M. Ben M'rad, J. Perez, L. Mesnard, S. Vandermersch, S. Placier, E. Letavernier, L. Baud, and J. P. Haymann. "Intrarenal urothelium proliferation: an unexpected early event following ischemic injury." American Journal of Physiology-Renal Physiology 299, no. 3 (September 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 intrarenal urothelial cells located in the upper part of the medulla constitute a monolayered barrier and express among uroplakins only uroplakin III. However, like bladder progenitors, intrarenal urothelial cells proliferated through a FGF receptor-2 (FGFR2)-mediated process. They strongly expressed FGFR2 and proliferated in vivo after recombinant FGF7 administration to control mice. In addition, IRI led to FGFR phosphorylation together with the selective upregulation of FGF7 and FGF2. Conversely, by day 2 following IRI, renal urothelial cell proliferation was significantly inhibited by FGFR2 antisense oligonucleotide administration into an intrarenal urinary space. Of notice, no significant migration of these early dividing urothelial cells was detected in the cortex within 7 days following IRI. Thus our data show that following IRI, proliferation of urothelial cells is mediated by the FGFR2 pathway and precedes tubular cell proliferation, indicating a particular sensitivity of this structure to changes caused by the ischemic process.
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Lemos, Dario R., Graham Marsh, Angela Huang, Gabriela Campanholle, Takahide Aburatani, Lan Dang, Ivan Gomez, et al. "Maintenance of vascular integrity by pericytes is essential for normal kidney function." American Journal of Physiology-Renal Physiology 311, no. 6 (December 1, 2016): F1230—F1242. http://dx.doi.org/10.1152/ajprenal.00030.2016.

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Pericytes are tissue-resident mesenchymal progenitor cells anatomically associated with the vasculature that have been shown to participate in tissue regeneration. Here, we tested the hypothesis that kidney pericytes, derived from FoxD1+ mesodermal progenitors during embryogenesis, are necessary for postnatal kidney homeostasis. Diphtheria toxin delivery to FoxD1Cre::RsDTR transgenic mice resulted in selective ablation of >90% of kidney pericytes but not other cell lineages. Abrupt increases in plasma creatinine, blood urea nitrogen, and albuminuria within 96 h indicated acute kidney injury in pericyte-ablated mice. Loss of pericytes led to a rapid accumulation of neutral lipid vacuoles, swollen mitochondria, and apoptosis in tubular epithelial cells. Pericyte ablation led to endothelial cell swelling, reduced expression of vascular homeostasis markers, and peritubular capillary loss. Despite the observed injury, no signs of the acute inflammatory response were observed. Pathway enrichment analysis of genes expressed in kidney pericytes in vivo identified basement membrane proteins, angiogenic factors, and factors regulating vascular tone as major regulators of vascular function. Using novel microphysiological devices, we recapitulated human kidney peritubular capillaries coated with pericytes and showed that pericytes regulate permeability, basement membrane deposition, and microvascular tone. These findings suggest that through the active support of the microvasculature, pericytes are essential to adult kidney homeostasis.
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Yuan, Youcai, Xiaoke Zhang, Huan Zhang, and Bifeng Gao. "Effect of “Xiaoke Tongbi granule” on the proliferation, migration and tubule-forming ability of rat endothelial progenitor cells under high glucose conditions." Tropical Journal of Pharmaceutical Research 18, no. 10 (July 5, 2021): 2117–23. http://dx.doi.org/10.4314/tjpr.v18i10.17.

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Purpose: To investigate the effect of Xiaoke Tongbi granule (XTG) on the proliferation, migration and tubule-forming ability of endothelial progenitor cells (EPCs) of rats under high glucose conditions. Methods: Six specific pathogen-free (SPF) and twenty-four healthy rats (mean weight = 200 ± 20 g) were used in this study. Twenty-four (24) healthy rats were treated with graded concentrations of XTG (0.75 – 2.25 g/mL) for 7 days, and were thereafter euthanized to obtain serum which was later used to treat EPCs isolated from bone marrow of SPF rats. The EPCs were seeded in culture plates pre-coated with human fibronectin, and cultured at 37 °C for 72 h in a humidified atmosphere of 5 % CO2 and 95 % air. Cell viability and apoptosis were assessed using 3 (4,5 dimethyl thiazol 2 yl) 2,5 diphenyl 2H tetrazolium bromide (MTT), and flow cytometric assays, respectively. The morphology of isolated EPCs was assessed by immunofluorescence. Results: The isolated EPCs exhibited normal morphology, and were CD34-positive. Proliferation and migration of EPCs, and number of tubular structures formed were significantly suppressed under high glucose conditions, but were significantly and concentration-dependently promoted by XTG treatment (p < 0.05). Treatment with XTG also significantly improved the morphology of isolated EPCs (p < 0.05). Apoptosis was significantly promoted by high glucose conditions, but was significantly and concentration-dependently reduced by XTG treatment (p < 0.05). The incidence of tubule formation in high glucose group was 0.63 %, but was progressively increased from 1.37 to 1.52 % after treatment with graded concentrations of XTG. Conclusion: These results indicate that XTG reverses the effect of high glucose environment on EPC proliferation, migration and tubule-forming ability.
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Wang, Dai-hong, Fu-rong Li, Ying Zhang, Yi-qin Wang, and Fa-huan Yuan. "Conditioned medium from renal tubular epithelial cells stimulated by hypoxia influences rat bone marrow-derived endothelial progenitor cells." Renal Failure 32, no. 7 (July 21, 2010): 863–70. http://dx.doi.org/10.3109/0886022x.2010.494806.

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Smith, Liisa, Hannah White, Tracy Gentry, and Andrew Balber. "Human ALDH-Bright Bone Marrow Cells Produce Paracrine Factors That Protect Endothelial Cells From Hypoxic and Nutritional Stress." Blood 114, no. 22 (November 20, 2009): 3056. http://dx.doi.org/10.1182/blood.v114.22.3056.3056.

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Abstract Abstract 3056 Poster Board II-1032 Human bone marrow cell populations isolated by sorting cells on the basis of high aldehyde dehydrogenase expression (ALDHbr cells) include endothelial, mesenchymal, and other progenitor cells (Gentry et al, 2007, Cytotherapy 9, 259). These cell populations home to and are retained at ischemic endothelium, induce angiogenesis, and effect restoration of tissue perfusion in a mouse hind limb ischemia model (Cappoccia et al, 2009 Blood 113, 5340.) Critical limb ischemia patients treated with ALDHbr cells in a Phase I/II clinical trial showed increased limb perfusion. We are studying paracrine and contact dependent mechanisms by which ALDHbr cells may repair damaged endothelium by measuring the protective effects of ALDHbr cells on early passage human umbilical vein endothelial cells (HUVEC) exposed to hypoxic and nutritional stress. ALDHbr cells migrated through membrane filters in response to supernatants conditioned by hypoxic HUVECs more rapidly than to normoxic HUVEC supernatants. ALDHbr cells attached to HUVECs that had been induced to form tubular structures on Matrigel®, and more ALDHbr cells decorated HUVEC tubules under hypoxic than normoxic conditions. ALDHbr cells and HUVECs expressed several adhesion molecule-ligand pairs, including VLA-1/VCAM, that are regulated by hypoxia and could mediate these interactions. While HUVEC tubules fell apart under hypoxic conditions, adding ALDHbr cells in a transwell culture system for 24 hours preserved the branching structure of hypoxic HUVEC tubule networks. Gene array studies demonstrated that ALDHbr cells highly express several angiogenic growth factors, cytokines and matrix remodeling molecules. Expression of proteins corresponding to many of these gene products, including members of the ephrin-Eph receptor family that can direct endothelial growth, has been confirmed by flow cytometry. Additionally, 29 angiogenic factors including angiopoietin 2, VEGF-A,C, and D, and MMP2 were upregulated under hypoxic conditions. Gene array and flow cytometry showed that hypoxic HUVECs expressed surface receptors for many of the angiogenic factors expressed by ALDHbr cells. In hypoxic transwell cultures, ALDHbr cells specifically induced HUVECs to express six angiogenic factors that were not induced by hypoxia alone. ALDHbr cells protected HUVECs from apoptosis and necrosis induced by serum starvation when added to cultures at the time of or 24 hours following medium shift. Thus, in addition to providing progenitor cells that can potentially participate in angiogenesis, ALDHbr cell populations can mediate repair of ischemic injury by releasing a variety of angiogenic and protective factors at sites of endothelial damage. Disclosures Smith: Aldagen, Inc.: Employment. White:Aldagen, Inc.: Employment. Gentry:Aldagen, Inc.: Employment. Balber:Aldagen, Inc: Employment, Equity Ownership.
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Yamamoto, Kimiko, Tomono Takahashi, Takayuki Asahara, Norihiko Ohura, Takaaki Sokabe, Akira Kamiya, and Joji Ando. "Proliferation, differentiation, and tube formation by endothelial progenitor cells in response to shear stress." Journal of Applied Physiology 95, no. 5 (November 2003): 2081–88. http://dx.doi.org/10.1152/japplphysiol.00232.2003.

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Endothelial progenitor cells (EPCs), circulating in peripheral blood, migrate toward target tissue, differentiate, and contribute to the formation of new vessels. In this study, we report that shear stress generated by blood flow or tissue fluid flow can accelerate the proliferation, differentiation, and capillary-like tube formation of EPCs. When EPCs cultured from human peripheral blood were subjected to laminar shear stress, the cells elongated and oriented their long axes in the direction of flow. The cell density of the EPCs exposed to shear stress was higher, and a larger percentage of these cells were in the G2-M phase of the cell cycle, compared with EPCs cultured under static conditions. Shear stress markedly increased the EPC expression of two vascular endothelial growth factor receptors, kinase insert domain-containing receptor and fms-like tyrosine kinase-1, and an intercellular adhesion molecule, vascular endothelial-cadherin, at both the protein and mRNA levels. Assays for tube formation in the collagen gels showed that the shear-stressed EPCs formed tubelike structures and developed an extensive tubular network significantly faster than the static controls. These findings suggest that EPCs are sensitive to shear stress and that their vasculogenic activities may be modulated by shear stress.
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Sallustio, Fabio, Vincenzo Costantino, Sharon N. Cox, Antonia Loverre, Chiara Divella, Marco Rizzi, and Francesco P. Schena. "Human renal stem/progenitor cells repair tubular epithelial cell injury through TLR2-driven inhibin-A and microvesicle-shuttled decorin." Kidney International 83, no. 3 (March 2013): 392–403. http://dx.doi.org/10.1038/ki.2012.413.

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Lv, Xianhui, Zhenzhen Yu, Chunfeng Xie, Xiuliang Dai, Qing Li, Dengshun Miao, and Jianliang Jin. "Bmi-1 plays a critical role in the protection from acute tubular necrosis by mobilizing renal stem/progenitor cells." Biochemical and Biophysical Research Communications 482, no. 4 (January 2017): 742–49. http://dx.doi.org/10.1016/j.bbrc.2016.11.105.

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50

Stainier, D. Y., R. K. Lee, and M. C. Fishman. "Cardiovascular development in the zebrafish. I. Myocardial fate map and heart tube formation." Development 119, no. 1 (September 1, 1993): 31–40. http://dx.doi.org/10.1242/dev.119.1.31.

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We have analyzed the origin of cardiac progenitors in the zebrafish embryo by injection of single blastomeres with a lineage tracer dye, and examined the formation of the zebrafish heart tube by serial sectioning of immunostained embryos. At the 512-cell stage (early blastula), most cardiac progenitors lie in a marginal zone that extends from 90 degrees longitude (midway between the future dorsal and ventral axis) through 180 degrees longitude (the future ventral axis) to 270 degrees longitude. By focusing on myocardial progenitors located at 90 degrees (and 270 degrees) longitude, we found that a single cell injected in the early blastula can contribute progeny to both the atrium and ventricle. A cell injected in the midblastula contributes progeny to either the atrium or ventricle, but not both. This analysis suggests that, at least for these myocardial progenitors, the atrial and ventricular lineages separate in the midblastula. Precardiac cells involute early during gastrulation and turn towards the animal pole with other early involuting cells. These cardiogenic cells reach the embryonic axis around the 8-somite stage, and there they coalesce to form a pair of myocardial tubular primordia on either side of the midline. By the 21-somite stage, the tropomyosin-immunoreactive myocardial tubes have moved closer to each other, and a distinct group of cells, the endocardial progenitor cells, sits medially between them. The myocardial tubes then fuse to enclose the endocardial cells and form the definitive heart tube. By 22 hours postfertilization (26-somite stage), the heart tube is clearly beating. The regionalization of cardiac myosin heavy chain expression distinguishes the cardiac chambers at this stage, although they are not morphologically delineated until 36 hours. This work shows that cardiogenic regions can be identified in the early blastula, and that chamber restriction seems to arise in the midblastula. Additionally, it provides the basis for embryological perturbation at the single cell level, as well as for the genetic analysis of heart tube formation in the zebrafish.
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