Literatura académica sobre el tema "Renal progenitors"
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Artículos de revistas sobre el tema "Renal progenitors"
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Hasegawa, Sho, Tetsuhiro Tanaka y Masaomi Nangaku. "Recent advances in renal regeneration". F1000Research 8 (25 de febrero de 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 glomeruli with podocytes, renal tubules, and the branching ureters. Induction of the remaining renal progenitors (that is, stromal progenitors from PSCs and the further maturation of reconstructed kidneys) needs to be studied extensively to regenerate functional and sophisticated kidneys from PSCs. In addition to the proper induction of renal progenitors, new bioengineering methods such as decellularization and 3D bioprinting and the recent advancements in the regeneration of kidneys in other species are promising leads for regenerating the complex spatial arrangement of kidneys, including the vascular network and urinary excretion pathway in humans.
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Al-Marsoummi, Sarmad, Aaron A. Mehus, Swojani Shrestha, Rayna Rice, Brooke Rossow, Seema Somji, Scott H. Garrett y Donald A. Sens. "Proteasomes Are Critical for Maintenance of CD133+CD24+ Kidney Progenitor Cells". International Journal of Molecular Sciences 24, n.º 17 (27 de agosto de 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 of kidney progenitors, such as self-renewal capacity and multi-potential differentiation. In addition, a separate cell line was established, named Human Renal Epithelial Cell 24 TERT (HREC24T), which lacks CD133 expression and shows no progenitor features. To further characterize HRTPT CD133+CD24+ progenitor cells, we performed proteomic profiling which showed high proteasomal expression in HRTPT kidney progenitor cells. RT-qPCR, Western blot, and flow cytometry analysis showed that HRTPT cells possess higher proteasomal expression and activity compared to HREC24T non-progenitor cells. Importantly, inhibition of the proteasomes with bortezomib reduced the expression of progenitor markers and obliterated the potential for self-renewal and differentiation of HRTPT progenitor cells. In conclusion, proteasomes are critical in preserving progenitor markers expression and self-renewal capacity in HRTPT kidney progenitors.
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Holmes, David. "Budding renal progenitors". Nature Reviews Nephrology 10, n.º 1 (3 de diciembre de 2013): 4. http://dx.doi.org/10.1038/nrneph.2013.245.
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Sequeira-Lopez, Maria Luisa S., Eugene E. Lin, Minghong Li, Yan Hu, Curt D. Sigmund y 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, n.º 2 (15 de enero de 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, several putative progenitors marked by the expression of either the winged-forkhead transcription factor 1 (Foxd1+ progenitor), the aspartyl-protease renin (Ren+ progenitor), and/or hemangioblasts (Scl+ progenitor) are likely to differentiate and endow most of the cells of the renal arterial tree. However, the lineage relationships and the role of these distinct progenitors in renal vascular morphogenesis have not been delineated. We, therefore, designed a series of experiments to ascertain the hierarchical lineage relationships between Foxd1+ and Ren+ progenitors and the role of these two precursors in the morphogenesis and patterning of the renal arterial tree. Results show that 1) Foxd1+ cells are the precursors for all the mural cells (renin cells, smooth muscle cells, perivascular fibroblasts, and pericytes) of the renal arterial tree and glomerular mesangium, and 2) Foxd1 per se directs the origin, number, orientation, and cellular composition of the renal vessels.
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Peired, Anna Julie, Maria Elena Melica, Alice Molli, Cosimo Nardi, Paola Romagnani y Laura Lasagni. "Molecular Mechanisms of Renal Progenitor Regulation: How Many Pieces in the Puzzle?" Cells 10, n.º 1 (2 de enero de 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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Phua, Yu Leng, Kevin Hong Chen, Shelby L. Hemker, April K. Marrone, Andrew J. Bodnar, Xiaoning Liu, Andrew Clugston, Dennis Kostka, Michael B. Butterworth y Jacqueline Ho. "Loss of miR-17~92 results in dysregulation of Cftr in nephron progenitors". American Journal of Physiology-Renal Physiology 316, n.º 5 (1 de mayo de 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 transcriptome sequencing revealed that nephron progenitors lacking this cluster demonstrated increased Cftr expression. We showed that one member of the cluster, miR-19b, is sufficient to repress Cftr expression in vitro and that perturbation of Cftr activity in nephron progenitors results in impaired proliferation. Together, these data suggest that miR-19b regulates Cftr expression in nephron progenitors, with this interaction playing a role in appropriate nephron progenitor self-renewal during kidney development to generate normal nephron endowment.
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Volovelsky, Oded, Thi Nguyen, Alison E. Jarmas, Alexander N. Combes, Sean B. Wilson, Melissa H. Little, David P. Witte, Eric W. Brunskill y Raphael Kopan. "Hamartin regulates cessation of mouse nephrogenesis independently of Mtor". Proceedings of the National Academy of Sciences 115, n.º 23 (21 de mayo de 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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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, n.º 536 (25 de marzo de 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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Rymer, Christopher, Jose Paredes, Kimmo Halt, Caitlin Schaefer, John Wiersch, Guangfeng Zhang, Douglas Potoka et al. "Renal blood flow and oxygenation drive nephron progenitor differentiation". American Journal of Physiology-Renal Physiology 307, n.º 3 (1 de agosto de 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 epithelium, nephron progenitors, and nephron structures. We also analyzed nephron differentiation in normoxia compared with hypoxia. At embryonic day 13.5 (E13.5), the major vascular branches were perfused; however, smaller-caliber peripheral vessels remained unperfused. By E15.5, peripheral vessels started to be perfused as well as glomeruli. While the interior kidney vessels were perfused, the peripheral vessels (nephrogenic zone) remained unperfused. Directly adjacent and internal to the nephrogenic zone, we found differentiated nephron structures surrounded and infiltrated by perfused vessels. Furthermore, we determined that at low O2 concentration, little nephron progenitor differentiation was observed; at higher O2 concentrations, more differentiation of the nephron progenitors was induced. The formation of the developing renal vessels occurs before the onset of blood flow. Furthermore, renal blood flow and oxygenation are critical for nephron progenitor differentiation.
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Chu, Jessica Y. S., Sunder Sims-Lucas, Daniel S. Bushnell, Andrew J. Bodnar, Jordan A. Kreidberg y Jacqueline Ho. "Dicer function is required in the metanephric mesenchyme for early kidney development". American Journal of Physiology-Renal Physiology 306, n.º 7 (1 de abril de 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 as well as the renal stroma during kidney development, we conditionally ablated Dicer function in this lineage. Despite normal ureteric bud outgrowth and condensation of the metanephric mesenchyme to form nephron progenitors, early loss of miRNAs in the metanephric mesenchyme resulted in severe renal dysgenesis. Nephron progenitors are initially correctly specified in the mutant kidneys, with normal expression of several transcription factors known to be critical in progenitors, including Six2, Pax2, Sall1, and Wt1. However, there is premature loss of the nephron progenitor marker Cited1, marked apoptosis, and increased expression of the proapoptotic protein Bim shortly after the initial inductive events in early kidney development. Subsequently, there is a failure in ureteric bud branching and nephron progenitor differentiation. Taken together, our data demonstrate a previously undetermined requirement for miRNAs during early kidney organogenesis and indicate a crucial role for miRNAs in regulating the survival of this lineage.
Tesis sobre el tema "Renal progenitors"
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Hoshina, Azusa. "Development of new method to enrich human iPSC-derived renal progenitors using cell surface markers". Kyoto University, 2018. http://hdl.handle.net/2433/235064.
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Supplementary information 追加（2019-09-30)Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第21344号
医博第4402号
新制||医||1031(附属図書館)
京都大学大学院医学研究科医学専攻
(主査)教授 柳田 素子, 教授 山下 潤, 教授 江藤 浩之
学位規則第4条第1項該当
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Lund-Ricard, Yasmine. "Insights From The Small-Spotted Catshark : Kidney Development And The Persistence Of Renal Progenitor Cells In A Chondrichthyes Model". Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS130.
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Certains vertébrés peuvent régénérer des néphrons, l'unité fonctionnelle du rein. Cette capacité (la néonéphrogenèse) dépend de la présence de progéniteurs rénaux qui vont se différentier en les cellules du néphron. Pendant le développement des mammifères, les progéniteurs rénaux arrêtent de proliférer et se différencient autours de la naissance alors que d'autres vertébrés maintiennent leurs progéniteurs rénaux après le développement embryonnaire. Ainsi, après la perte de néphrons chez les mammifères, seule une réponse hypertrophique est observée. En contraste, la formation de novo de néphrons a été observée chez deux poissons cartilagineux: la petite raie, après néphrectomie partielle, et chez la petite roussette adolescente et adulte. Cette capacité de néonephrogenèse chez les poissons cartilagineux a été décrite avec des observations histologiques mais la caractérisation moléculaire et fonctionnelle des progéniteurs reste à déterminer.Avec la petite roussette Scyliorhinus canicula comme modèle, des HIS in toto pendant le développement précoce montre que Lim1 et Pax2 sont conservés comme des facteurs de transcription qui spécifient le territoire du rein. Ensuite, les progéniteurs rénaux chez S. canicula sont identifiés comme des agrégats mésenchymateux chez les embryons et juvéniles et comme exprimant des ARNm spécifiques aux progéniteurs rénaux comme Six2.L'expression de Pax2 et Wt1 est trouvée dans ces structures chez les embryons et juvéniles et les patrons sont cohérents avec les ARNm trouvés chez d'autres animaux avec la néonephrogenèse. Dans différents types de cellules souches, des niveaux bas de synthèse protéiques sont associés avec le caractère souche et des niveaux plus haut à l'activation et la différentiation. La maintenance des cellules souches pendant le développement embryonnaire et post-développement semble lié à des niveaux bas de traduction. En suivant la synthèse protéique, les agrégats mésenchymateux montrent des niveaux plus bas relatifs aux compartiments épithéliaux différentiés. Enfin, ces agrégats retiennent le BrdU (pulse); ils cyclent lentement (2 mois de chasse), ce qui est une caractéristique des cellules souches adultes. Ces résultats tentent de déchiffrer les clés derrière la maintenance des cellules souches dans les reins capables de régénérationCertain vertebrates can regenerate nephrons, the functional kidney unit of the kidney. This capacity (neonephrogenesis) relies on the presence of renal progenitor cells which differentiate into the cells that make up the nephron. During mammalian development, nephron progenitors stop propagation and differentiate within few days after birth, while other vertebrates maintain these cells after embryonic development. As such, in mammals with nephron loss, only a hypertrophic response is observed. In contrast, de novo nephron formation was reported in two adult cartilaginous fish; the little skate, after partial nephrectomy and in the adolescent and adult small-spotted catshark. The neonephrogenic capacity of cartilaginous fish was described with histological observations but molecular and functional characterization of the progenitor cells remains to be determined. Using the small-spotted catshark Scyliorhinus canicula as a model, in toto ISH during early development first show that Lim1 and Pax2 are conserved as early kidney-specifying transcription factors. Next, progenitor cells are identified as mesenchymal aggregates in embryos and juveniles for which ISH on sections revealed the expression of kidney progenitor-cell mRNAS such as Six2. Pax2 and Wt1 expression is found in these structures in embryos and juveniles and is cogent with progenitor cell mRNAs found in other animals with neonephrogenesis. In different stem cell types, low protein synthesis levels are associated with stemness and higher levels to activation and differentiation. Stem cell maintenance during embryonic development and post development seems to be linked with low rates of translation. Using a protein synthesis levels assay, the mesenchymal aggregates show lower levels relative to the differentiated epithelial compartments. Finally, these aggregates retain BrdU (pulse) labels; they are slow cycling cells (2 month chase) which is a characteristic of stemness. These exciting results intend to help decipher the keys behind stem cell maintenance in regenerative kidneys
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Cañas, Solé Laura. "Determinació de cèl·lules progenitores endotelials, malaltia renal crònica i factors de risc cardiovascular". Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/399223.
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Introducció: La malaltia cardiovascular és la principal causa de mortalitat en els pacients amb malaltia renal crònica (MRC), tant en hemodiàlisi (HD) com en els pacients trasplantats renals. Els principals factors de risc cardiovascular dels pacients amb MRC,així com els factors de risc propis de la urèmia, produeixen disfunció endotelial en aquest grup de pacients. Aquesta disfunció endotelial incrementa la morbiditat cardiovascular en aquest grup de pacients.
Les cèl.lules progenitores endotelials (CPE) són cèl·lules derivades del moll de l’os, presents en sang perifèrica i que tenen la capacitat de proliferar i diferenciar-se en cèl·lules endotelials madures, contribuint a la reendotelització i revascularització dels teixis danyats. Els pacients amb malaltia renal crònica presenten una alteració en la quantificació d’aquestes CPE, essent aquest un factor de mal pronòstic, al incrementar el risc de presentar algun episodi cardiovascular.
Objectiu: Determinar i quantificar el nombre de CPE que expressen CD34+CD133+VEGFR-2+ en sang perifèrica en pacients amb MRC, així com els factors que poden modificar el seu nombre en sang perifèrica. Avaluar la influència de l’accés vascular en la quantificació de les cèl·lules CD34+CD133+VEGFR-2+ en els pacients en HD crònica. Analitzar l’evolució de les cèl.lules CD34+CD133+VEGFR-2+ durant el primer any posttrasplantament renal (posTR) de donant viu.
Pacients i mètodes: S’han inclòs en l’estudi 36 controls sans i 86 pacients amb MRC entre els anys 2012 i 2013, dels quals 73 pacients estaven en programa d’HD crònica i 13 pacients ingressaven per a rebre un trasplantament renal de donant viu. A través de citometria de flux s’ha realitzat la quantificació de les cèl·lules CD34+ CD133+VEGFR-2+/mL de sang perifèrica. S’han recollit les dades antropomètriques, factors de risc cardiovascular, aparició d’algun episodi cardiovascular i les dades bioquímiques dels 3 grups d’estudi. Del grup trasplantament renal s’ha realitzat el seguiment durant el primer any posTR, analitzant les dades als 6 mesos i 12 mesos del trasplantament.
Resultats: Cèl·lules CD34+CD133+VEGFR-2+ dels pacients amb MRC (27,96(12,16-51,71) en comparació a controls sans (32,08(17,26-66,41), p=0,23. L’edat no interfereix en la quantificació de cèl·lules CD34+CD133+VEGFR-2+ ni en la MRC ni en els controls sans. Els pacients en tractament amb antagonistes dels canals del calci tenen menys cèl·lules CD34+CD133+VEGFR-2+ respecte els que no reben aquest tractament (p=0,018). Els pacients diabètics tenen una menor quantificació de cèl·lules CD34+CD133+VEGFR-2+ i un major risc de cardiopatia isquèmica. Els pacients que realitzen HD a través de catéter tenen menys cèl·lules CD34+CD133+VEGFR-2+ (17,50 (12,41-30,98)) que els pacients que tenen una FAVI (32,90(9,7-54,49)) (p=0,191). Els pacients que porten catéter tenen més edat (p=0,084), estan més inflamats (proteïna C reactiva) (p=0,081) i estan més desnutrits (albúmina i prealbúmina) (p=0,020 i p=0,013 respectivament), que els pacients que fan HD a través de FAVI. No podem establir diferències estadísticament significatives entre el nombre de cèl·lules CD34+CD133+VEGFR-2+ en funció de l’accés vascular i la mortalitat. En els pacients trasplantats, les cèl·lules CD34+CD133+VEGFR-2+ presenten un increment durant el primer any postTR: basal (33,87 (29,15-54,42)), 6 mesos postTR (63,35(43,40-139,90)), 12 mesos postTR (62,62(25,30-72,54)) (p=NS). El nombre de cèl·lules CD34+CD133+VEGFR-2+ als 6 i 12 mesos postTR és superior al nombre de cèl·lules que tenen els pacients que segueixen en programa d’HD crònica (p=0,008 i p=0,065 respectivament).
Conclusions: Els pacients amb MRC tenen menys cèl·lules CD34+CD133+VEGFR-2+ que la població sana, especialment els pacients diabètics. Els pacients que realitzen HD a través de catéter tunelitzat tenen menys cèl.lules CD34+CD133+VEGFR-2+, tenen més edat, estan més inflamats i desnutrits i tenen un augment de la mortalitat respecte els pacients amb FAVI. Els trasplantats renals presenten un increment del nombre de cèl·lules CD34+CD133+VEGFR-2+ durant el primer any posTR i que és superior als pacients que segueixen en HD.Introduction: Cardiovascular disease is the main cause of mortality in patients with chronic kidney disease (CKD), both hemodialysis (HD) and in kidney transplant. The main cardiovascular risk factors in CKD, as well as factors relating uremia cause endothelial dysfunction in these patients. This endothelial dysfunction increase cardiovascular morbidity in these patients. Endothelial progenitor cells (EPC) are cells derived from bone marrow, present in peripheral blood, and with the ability to proliferate and differentiate into mature endothelial cells, contributing to the reendotelization and revascularization of the damaged tissue. Patients with CKD have an alteration in the quantification of these EPC. This is a factor of poor prognosis, increasing the risk of a cardiovascular event. Aim: To determine and to quantificate the number of EPC which express CD34+CD133+VEGFR-2+ in peripheral blood in pacients with CKD, as well as the factors that may change its number in peripheral blood. To assess the influence of vascular access in quantifying CD34+CD133+VEGFR-2+ cells in patients on HD. Analysing the evolution of CD34+CD133+VEGFR-2+ cells during the first year after living donor kidney transplantation. Patients and methods: Patients included in the study: 36 healthy volunteers and 86 patients with CKD of which 73 pacients were on chronic HD and 13 were admitted to receive a living donor kidney transplant,between 2012 and 2013. The quantification of CD34+CD133+VEGFR-2+ in peripheral blood was performed by flow cytometry. We have collected anthropometric data, cardiovascular risk factors, occurrence of a cardiovascular event and biochemical data from the three groups. Kidney transplant grupo was also monitored during the first year after kidney transplantation, analyzing data at 6 and at 12 months after transplantation. Results: CD34+CD133+VEGFR-2+ cells in CKD (27,96(12,16-51,71) compared with healthy volunteers (32,08(17,26-66,41), p=0,23. Age does not interfere with the quantification of CD34+CD133+VEGFR-2+ cells in patients with CKD or in healthy people. Patients treated with calcium channel antagonists have lower quantification of CD34+CD133+VEGFR-2+ cells respect those who do not receive this treatment. Patients with diabetes have a lower quantification of CD34+CD133+VEGFR-2+ and a higher risk of ischemic heart disease. Patients on HD via catheter haver less CD34+CD133+VEGFR-2+ cells (17,50 (12,41-30,98)) than patients on HD via arteriovenous fistula (32,90(9,7-54,49)) (p=0,191). Patients on HD via catheter are older (p=0,084), they have a worse inflammation status (C reactive protein) (p=0,081) and have a worse nutritional status (albumin and prealbumin) (p=0,020 i p=0,013 respectively) than patients on HD via arteriovenous fistula. We can not establish significant differences between the number of CD34+CD133+VEGFR-2+ cells based on vascular access and mortality. In kidney transplant patients, CD34+CD133+VEGFR-2+ cells increase their quantification in peripheral blood during the first year after kidney transplantation: baseline (33,87 (29,15-54,42)), 6 months after kidney transplant (63,35(43,40-139,90)), and 12 months after kidney transplant (62,62(25,30-72,54)) (p=NS). The quantification of CD34+CD133+VEGFR-2+ cells at 6 and at 12 months after kidney transplant is higher compared to patients on chronic HD (p=0,008 i p=0,065 respectively). Conclusions: Patients with CKD have less CD34+CD133+VEGFR-2+ cells in peripheral blood compared to healthy people, specially diabetic patients. Patients on HD via catheter have less CD34+CD133+VEGFR-2+ compared to patients via arteriovenous fistula and have a worse prognosis, including a higher mortality risk. Living kidney transplant patients have an increase in the quantification of CD34+CD133+VEGFR-2+ during the first year after kidney transplant, this increase is greater than the number of cells in hemodialysis patients.
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Zanusso, Ilenia. "Acellular matrices as tool for renal progenitor differentiation studies and tissue engineering of blood vessels". Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3423024.
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AMs seem to be a very promising scaffold in TE and can be considered as temporary inductive site-appropriate templates to support the growth, differentiation, and function of the parenchymal cell population of each organ. Nowadays, TE techniques are used both to develop tissue substitutes ex vivo and as reliable tool to investigate cell behaviour, differentiation and proliferation in 3-dimentional environments.
In this work the following two different projects have investigated both potentialities using tissue-specific AMs:
1- influence of AMs on differentiation of kidney progenitor cells from amniotic fluid into mature renal cells;
2- AMs as biomaterial to develop vessel substitutes.
1- Kidney AMs (KAMs) were used to evaluate the differentiation of kidney progenitor cells from amniotic fluid into mature renal cells in order to better understand whether they could be suitable for future application in therapy. Renal progenitors were seeded into KAMs, which led them to proliferate, maintain podocyte phenotype and differentiate into tubular cells in vitro. To further evaluate the differentiative potential of KAMs, grafts composed of KAM with or without cells were intrarenal implanted into nude mice. In vivo, progenitors from amniotic fluid expressed mature renal markers, attracted inside KAMs murine cells presenting the same proteins and integrated into host structures.
2- Although autologous vascular grafts and artificial materials have been used for reconstruction of small diameter (5 mm) blood vessels, the poor availability of vessels and the occurrence of intimal hyperplasia and progressive atherosclerotic degeneration represent shortcoming of these vascular prostheses. Therefore, this study aimed to develop AM-based vascular grafts. Both AAMs alone and AAMs previously reendothelized with skin microvascular endothelial cells (ECs) were in vivo implanted and analyzed. The lack of reendothelization, leading to intimal hyperplasia and increased incidence of thrombosis observed in AAMs grafts, have indicated the need to provide in vitro an endothelial coverage of decellularized tissue. Indeed, grafts composed of AAM and skin microvasculature ECs shown good patency and no thrombi. Although these grafts appeared narrowed and a moderate hyperplasia has been detected in the inner layer, they presented two main advantages: they were obtained into a clinically relevant time frame and eliminated the need to remove healthy vessels for collecting autologous ECs.Le matrici acellulari rappresentano uno scaffold promettente per l’ingegneria tessutale. Infatti, la matrice extracellulare costituisce un supporto sito-specifico che favorisce la crescita e il differenziamento delle cellule di qualsiasi organo. Ad oggi, le tecniche dell’ingegneria tessutale sono utilizzate sia per lo sviluppo ex vivo di sostituti tessutali, che per studiare la proliferazione e la differenziazione delle cellule quando si trovano all’interno di uno scaffold tridimensionale. In questo lavoro di tesi, i due seguenti progetti sono andati a valutare entrambe le potenzialità di matrici acellulari tessuto-specifiche: 1- valutazione della capacità della matrice acellulare di indurre il differenziamento di progenitori renali da fluido amniotico in cellule renali mature; 2- valutazione della matrice acellulare per la sostituzione di vasi sanguigni. 1- La matrice acellulare renale è stata utilizzata per valutare la capacità differenziativa di progenitori renali da fluido amniotico in modo da valutarne una futura applicazione terapeutica. I progenitori renali sono stati seminati sulla matrice acellulare renale, che, in vitro, ne ha promosso la proliferazione, il mantenimento del fenotipo podocitario e la differenziazione in cellule tubulari. Per valutare in vivo il potenziale differenziativo di queste cellule, la matrice da sola o ripopolata con le cellule è stata impiantata all’interno di un rene di topo nudo. I progenitori renali si sono ulteriormente differenziati, si sono integrati all’interno delle strutture tubulari dell’ospite e hanno promosso la migrazione di cellule differenziate murine all’interno dello scaffold. 2- La matrice acellulare di aorta è stata utilizzata per lo sviluppo di sostituti vasali. Nonostante vasi autologhi o costituiti di polimeri sintetici vengano già utilizzati nella pratica clinica per la ricostruzione di vasi di piccolo diametro (5 mm), numerosi sono gli svantaggi legati al loro utilizzo, quali l’iperplasia della tonaca intima e la degenerazione arteriosclerotica. Lo scopo di questo studio è stato quello di sviluppare sostituti vasali utilizzando come scaffold vasi decellularizzati. Matrici acellulari da sole o ripopolate con cellule endoteliali da microcircolo sono state impiantate nell’aorta di ratto Lewis. Come osservato negli impianti di sola matrice acellulare, la mancanza della copertura endoteliale portava all’iperplasia dell’intima e all’aumento di incidenza dei processi trombotici, sottolineando la necessità di reendotelizzare in vitro il vaso decellularizzato prima dell’impianto in vivo. Infatti, i sostituti vasali costituiti da matrice acellulare e cellule endoteliali da microcircolo hanno dimostrato di avere una buona resistenza al flusso e non presentavano trombi al loro interno. Sebbene questi vasi fossero assottigliati e mostrassero una leggera iperplasia della tonaca intima, questo approccio presentava due principali vantaggi: permetteva di ottenere sostituti vasali in un tempo clinicamente utile ed eliminava la necessità di rimuovere vasi sani per ottenere cellule endoteliali autologhe.
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Borges, Francielly Pinheiro da Silva. "Citomegalovírus em pacientes submetidos a transplante de células progenitoras hematopoiéticas". Universidade Federal de Goiás, 2016. http://repositorio.bc.ufg.br/tede/handle/tede/5801.
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Fundação de Amparo à Pesquisa do Estado de Goiás - FAPEG
The Human Cytomegalovirus (HCMV) is an important cause of morbi-mortality in recipients of allogeneic hematopoietic stem cell transplantation (AloHSCT). However, there is not a consensus on which protocol to use for monitoring the infection by HCMV and, data on the frequency and clinical manifestations of the infection in this group population are quite variable among the distinct transplant centers in the world. Thus, the main objective of the present study was to proceed the monitoring of active HCMV infection in patients undergoing AloHSCT by three different methodologies: antigenemia (AGM), nested-PCR (nPCR) and real-time PCR (qPCR) and determine viral load, correlating active infection with the clinical manifestations and prognosis of patients. For this, 21 patients undergoing AloHSCT were monitored (from pre-transplant period -5 days prior to transplantation- until one year after transplantation). For HCMV detection three methodologies were used: AGM, nPCR and qPCR, and for molecular detection a comparison was made between detection of HCMV in DNA extracted from pellet (buffy coat) and serum, in a paired manner. The results showed that the active HCMV infection was detected by at least one of three methodologies in 95.2% (20/21) of patients and 45% (9/20) of these were positive in pre-transplantation period, having been observed good agreement between the results of AGM and qPCR (kappa = 0.65). Of the 20 patients positive for active HCMV infection, 85% (17/20) were positive for the three methods and only 15% (3/20) were positive for AGM and qPCR, and negative by nPCR. Regarding the type of clinical sample, molecular techniques showed higher sensitivity to the pellet over the serum. The main alteration of patients was pancytopenia and the main complication was graft-versus-host disease. Six patients died during the study period, however, it was not possible to confirm if HCMV active infection was directly associated with the cause of death. The obtained data reveal a high positivity index and the occurrence of HCMV syndrome in patients submitted to aloHSCT. We hope that the results may assist in the therapeutical measures, as well as in the methodology of choice and the type of clinical sample for detection of active HCMV infection, in order to contribute for the inclusion of HCMV monitoring is included in the routine testing of patients.
O Citomegalovírus Humano (HCMV) constitui importante causa de morbi-mortalidade em receptores de transplantes de células progenitoras hematopoiéticas do tipo alogênico (AloTCPH). Entretanto, não existe ainda um consenso sobre que protocolo utilizar para o monitoramento da infecção por HCMV e, dados sobre a frequência e manifestações clínicas da infecção neste grupo populacional são bastante variáveis entre os diferentes centros de transplante em todo o mundo. Dessa forma, o principal objetivo do presente estudo foi realizar o monitoramento da infecção ativa por HCMV em pacientes submetidos ao AloTCPH por três metodologias distintas: antigenemia (AGM), nested-PCR (nPCR) e PCR em tempo real (qPCR), bem como determinar a carga viral, correlacionando a infecção ativa ao quadro clínico e prognóstico dos pacientes. Para tanto, foram monitorados (desde o período pré-transplante -5 dias antes do transplante- até um ano após o transplante) 21 pacientes submetidos ao AloTCPH. A pesquisa de HCMV foi realizada utilizando as metodologias de AGM, nPCR e qPCR, sendo que para as técnicas moleculares, houve comparação da detecção do HCMV em DNA extraído de pellet (creme leucocitário) e soro, de forma pareada. Os resultados mostraram que a infecção ativa pelo HCMV foi detectada por pelo menos uma das três metodologias em 95,2% (20/21) dos pacientes e 45% (9/20) destes foram positivos no período pré-transplante, tendo sido observada um boa concordância entre os resultados de AGM e qPCR (kappa = 0,65). Dos 20 pacientes positivos para infecção ativa por HCMV, 85% (17/20) foram positivos pelas três metodologias e 15% (3/20) foram positivos apenas por AGM e qPCR e negativos por nPCR. Em relação ao tipo de amostra clínica, as técnicas moleculares apresentaram maior sensibilidade em amostras de pellet, em comparação ao soro. A principal alteração apresentada pelos pacientes foi a pancitopenia e a principal intercorrência, a doença do enxerto contra o hospedeiro. Seis pacientes foram a óbito durante o período de estudo, entretanto, não foi possível confirmar se a infecção ativa por HCMV estava diretamente associada à causa mortis. Os dados obtidos revelam um elevado índice de positividade e síndrome de HCMV em pacientes submetidos ao AloTCPH. Esperamos que os resultados possam auxiliar na tomada de medidas terapêuticas, bem como na escolha da melhor metodologia assim como o tipo de amostra clínica para detecção da infecção ativa por HCMV de forma a contribuir para que a pesquisa de HCMV seja incluída na rotina de exames desses pacientes.
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Chang, Claudia Veiga. "Análise de marcadores de células-tronco/progenitoras em hipófises de modelos animais com hipopituitarismo". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-03122013-115816/.
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Introdução: As células-tronco apresentam capacidade de proliferação, autorrenovação, potencial de diferenciação e já foram descritas na hipófise estando envolvidas na renovação celular e regulação homeostática, porém pouco se sabe sobre o seu perfil de expressão nos quadros de hipopituitarismo. Dentre os marcadores de células-tronco descritos previamente na hipófise, destacam-se os genes Sox2, Nanog, Nestina, Cd44 e Oct4. Outro marcador, o gene Nr2e1 (Tlx), encontrado em células-tronco neuronais, apresenta-se elevado durante a embriogênese e na vida adulta no cérebro de camundongos, mas, até o momento, não foi caracterizado na hipófise. Objetivo: Analisar a imunolocalização do SOX2 e o padrão de expressão de marcadores de células-tronco/progenitoras, fatores de transcrição precoce, marcadores de apoptose e proliferação celular na hipófise de três linhagens de camundongos com hipopituitarismo de causa genética por alteração em fatores precoces de diferenciação glandular, as linhagens Ames (Prop1) e Snell (Pou1f1), e por fator tardio de conjugação dos hormônios glicoproteicos, a linhagem alfaGSU, nocaute do gene Cga. Material e Métodos: Foram coletadas hipófises nos tempos P0 (ao nascimento), P7 (final da primeira onda de crescimento glandular), 4 semanas (4S-período da puberdade) e 8 semanas (8S-vida adulta). Nas três linhagens de animais, realizou-se imuno-histoquímica com SOX2 e RT-qPCR com os marcadores de células-tronco/progenitoras Sox2, Nanog, Nestina, Cd44, Oct4 e Nr2e1, fatores de transcrição precoces (Hesx1, Hes1 e Otx2), fator de proliferação celular (Ki67), fatores de diferenciação celular (S100beta e Sox9) e marcadores de apoptose (Caspases 3 e 7). A quantificação relativa dos genes-alvo nos animais mutantes teve como calibrador os seus respectivos selvagens. Resultados: A imunolocalização do SOX2 foi observada na zona que circunda a fenda de Rathke (camada marginal) e em nichos difusos pela glândula nas três linhagens estudadas. Na linhagem alfaGSU, evidenciou-se uma redução de Nanog, Nr2e1, Oct4, e Hesx1 em 4S e de Nestina em 8S. Na linhagem Snell, observou-se aumento na expressão de Sox2, Nanog, Cd44, Nr2e1, Hesx1, Hes1, Otx2, S100beta e Sox9 em 4S e aumento de Sox2, Cd44, Hesx1, Otx2 e Sox9 em 8S, associado à redução de Ki67 em ambos os períodos. Na linhagem Ames, evidenciou-se aumento de Sox2, Nanog, Cd44, Hesx1, Hes1, Otx2, S100beta e Sox9 em 4S e 8S. O gene Nr2e1 esteve hiperexpresso em todos os tempos. Houve redução do Ki67 em 4S. As caspases 3 e 7 não se apresentaram alteradas em nenhuma linhagem e/ou tempo. Discussão e conclusão: O padrão de imunolocalização de SOX2 encontrado nas três linhagens estudadas foi semelhante ao descrito em animais sem hipopituitarismo. A evidência da presença do Nr2e1 o coloca como um novo marcador de células-tronco/progenitoras na hipófise. A expressão elevada dos marcadores de células-tronco/progenitoras nas linhagens Ames e Snell sugere que a ausência dos fatores de transcrição precoces não permitiria que a célula tronco/progenitora iniciasse o processo de diferenciação celular, enquanto o oposto ocorreria na linhagem alfaGSU. Adicionalmente, estes achados justificam a hipoplasia hipofisária observada em animais com defeitos em fatores de transcrição expressos no início da diferenciação hipofisária, nos quais o acúmulo de células-tronco pode ser um indicador da indiferenciação hipofisáriaIntroduction: The role of stem cells, with their capacity for proliferation, self-renewal, and differentiation, has already been described in the cell turnover and homeostatic regulation of the pituitary gland. However, little is known about the expression profiles of these markers in hypopituitarism. Among the stem cell markers previously described in the pituitary include the genes for Sox2, Nanog, nestin, CD44 and Oct4. Another gene marker, Nr2e1 (Tlx), found in neural stem cells, is highly expressed during embryogenesis and adulthood, but so far has not been characterized in the pituitary. Objective: To analyze the immunohistochemical profile of SOX2, as well as the pattern of expression of various markers of stem/progenitor cells, early transcription factors, apoptosis factors and cell proliferation in three pituitary strains of mice with a genetic cause of hypopituitarism. Strains studied with hypopituitarism due to changes in factors of precocious glandular differentiation, include the Ames (Prop1) and Snell (Pou1f1) lineages; hypopituitarism due to the delayed conjugation of glycoprotein hormones include the alfaGSU strain, which is caused by the knockout of the Cga gene. Material and Methods: We collected pituitaries at four time points including P0 (birth), P7 (considered the end of the first wave of growth glandular), 4 weeks (4S - puberty period) and 8 weeks (8S - adulthood). All three strains were subjected to immunohistochemical analysis of SOX2 and RT-qPCR of markers of stem/progenitor cells Sox2, Nanog, Nestin, Cd44, Oct4 and Nr2e1, early transcription factors (Hesx1, Otx2 and Hes1), cell proliferation (Ki67), cell differentiation factors (S100beta and Sox9) and apoptosis (caspases 3 and 7) markers. Relative quantification of target genes in mutant animals was normalized to their respective wild type littermate. Results: The immunolocalization of SOX2 was observed in the area surrounding the Rathke cleft (marginal layer), as well as in diffuse niches throughout the gland in all three strains studied. The alfaGSU strain showed a reduction of Nanog, Nr2e1, Oct4 and Hesx1 at 4S, and Nestin at 8S. The Snell mice exhibited an increase of expression in Sox2, Nanog, Cd44, Nr2e1, Hesx1, Hes1, Otx2, S100beta and Sox9 in at 4S and increased Sox2, Cd44, Hesx1, Otx2 and Sox9 at 8S, associated with the reduction of Ki67 in both periods. The Ames strain showed an increase of Sox2, Nanog, Cd44, Hesx1, Hes1, Otx2, S100beta and Sox9 at 4S and 8S; the gene Nr2e1 was over expressed at all times; and there was reduction in Ki67 at 4S. Caspases 3 and 7 had not changed in any strain, at any time. Discussion and Conclusion: The pattern of immunolocalization of SOX2 found in the three strains studied was similar to that described in animals without hypopituitarism. The presence of Nr2e1 in our study suggests it as a new marker of stem/progenitor cells in the pituitary. The high expression of markers of stem/progenitor cells in the Ames and Snell strains suggests that the absence of early transcription factors Prop1 and Pou1f1 do not allow the stem/ progenitors cells to start the process of cell differentiation, while the opposite occurs in the alfaGSU lineage. Additionally, these findings explain the pituitary hypoplasia observed in animals with defects in early transcription factors, as indicated by the accumulation of stem cells in the Snell and Ames lineages, preventing the initiation of pituitary differentiation
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Jian, Motamedi Fariba. "Les fonctions vitales de WT1 au cours de la vie des cellules progénitrices du rein embryonnaire". Thesis, Nice, 2015. http://www.theses.fr/2015NICE4099.
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Le développement du rein est un exemple intriguant d’un équilibre délicat entre la prolifération des cellules progénitrices, la différentiation et l’apoptose. Le gène Wt1 est indispensable pour la survie des cellules progénitrices. Le but de cette thèse a été de définir les voies de signalisation activées par Wt1 pendant le développement du rein. En utilisant les souris Wt1 KO, nous avons démontré que WT1 coordonne l’action de deux voies de signalisation opposées : Fgf et Bmp/Smad intervenant dans la survie des cellules progénitrices rénales. Dans une deuxième étude, nous avons analysé le rôle du modificateur épigénétique, le gène Phf19 pendant le développement du rein. Nous avons démontré que l’expression de ce gène est Wt1-dependant et il est exclusivement exprimé dans les cellules progénitrices rénales au cours du développement et que son inactivation dans le rein embryonnaire en culture, conduit à l’apoptose des cellules progénitrices. Nous avons généré des souris knockout de Phf19 par l’approche de CRISPR/Cas9. Dans le cas d’une létalité précoce des embryons homozygotes, nous opterons pour la production du model animal knockout conditionnel et procéderons à la caractérisation de leur profile épigénétique. Cette thèse a permis d’une part, de découvrir deux voies de signalisation antagonistes, régulées par le Wt1et impliquées dans le contrôle de la survie des cellules progénitrices rénales et d’autre part de nous orienter vers le contrôle de la survie et la prolifération de ces cellules par modifications épigénétiques. Ceci nous permettra de contribuer à la connaissance de l’étiologie d’une grande proportion des malformations rénales restant à ce jour inconnuesKidney organogenesis requires the tight control of proliferation, differentiation and apoptosis of renal progenitor cells. The Wilms’ tumour suppressor Wt1 is required for renal progenitor survival. The aim of this thesis was to elucidate the molecular cause for renal agenesis in Wt1 mutant mouse. Here we demonstrate that lack of Wt1 abolishes FGF and induces BMP/pSMAD signaling within the metanephric mesenchyme. We further show that recombinant BMP4, but not BMP7, induces an apoptotic response within the early kidney that can be suppressed by simultaneous addition of FGFs. These data reveal an unknown sensitivity of early renal progenitors to pSMAD signalling, establishes FGF and pSMAD signalling as antagonistic forces in early kidney development and places WT1 as a key regulator of pro-survival FGF signalling pathway genes. In a second study, we demonstrated, that Phf19, an epigenetic modifier, is essential both for maintaining Wt1 expression in renal progenitor cells and their survival in an ex-vivo culture. We further generated a Phf19 knockout mouse by CRISPR/Cas9. The homozygous embryos will be analyzed to further decipher the contribution of Phf19 to potential kidney malformations and the epigenetic profile of renal progenitor cells will be characterized. Overall, the new insights into the molecular mechanisms controlling the survival of renal progenitor cells, reported in this thesis, provide one more step in our understanding of renal malformations. In addition, our results conducted us toward the epigenetique modifications that could open up promising new avenue of understanding the etiology of an important proportion of renal malformation that remains unknown
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NARDI, SARA. "Studio dell'effetto di un danno renale acuto sulla formazione di carcinoma renale". Doctoral thesis, 2019. http://hdl.handle.net/2158/1154908.
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Lo studio affrontato in questa tesi ha evidenziato come il danno renale acuto possa influire sullo sviluppo di carcinoma renale, e in particolare delle forme papillari di carcinoma, agendo sulla via di segnalazione di Notch. Abbiamo preso in considerazione una popolazione di progenitori renali localizzati tra le cellule epiteliali parietali (PEC) e le cellule epiteliali tubulari (TEC), la cui proliferazione e differenziazione è controllata dalla via di segnalazione di Notch.
Abbiamo lavorato in vivo allestendo linee murine transgeniche in cui i progenitori renali sono identificati dal marcatore Pax2. Per valutare come il danno renale acuto influisse sullo sviluppo neoplastico abbiamo sottoposto gli animali ad ischemia/riperfusione.
Lo studio ha identificato i tumori papillari come clonali e ha identificato nelle cellule Pax2+ la popolazione che, in seguito ad una aberrante espressione di Notch1, dà origine ad adenomi e carcinomi papillari. Inoltre identifica il danno renale acuto come un fattore di rischio per lo sviluppo di tumori papillari nel topo.
The study dealt with in this thesis has shown that acute kidney injury can affect the development of renal carcinoma, and in particular papillary carcinoma, acting on the Notch signaling pathway. We considered a population of renal progenitors located between parietal epithelial cells (PEC) and tubular epithelial cells (TEC), whose proliferation and differentiation is controlled by the Notch signaling pathway.
We worked in vivo setting up transgenic murine lines in which the renal progenitors are identified by the Pax2 marker. To assess how acute kidney injury affected neoplastic development, we subjected the animals to ischemia / reperfusion injury.
The study identified papillary tumors as clonal and identified Pax2 + cells as the population that, following an aberrant expression of Notch1, gives rise to papillary adenomas and carcinomas.
It also identifies acute kidney injury as a risk factor for the development of papillary tumors in the mouse.
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Antonelli, Giulia. "Studio delle pathways che promuovono la trasformazione del progenitore renale in cellula di origine del carcinoma renale papillare". Doctoral thesis, 2022. http://hdl.handle.net/2158/1263955.
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Questo studio ha dimostrato che il carcinoma renale papillare (pRCC), uno dei 3 più frequenti tipi di RCC, origina dall’espansione clonale di una popolazione di cellule staminali residenti nel rene, i progenitori renali . In seguito ad un danno renale acuto , queste cellule sono in grado di rigenerare la porzione di tubulo renale danneggiata. Tuttavia, in seguito al danno si ha l’alterazione di alcune pathways che possono promuovere la loro trasformazione in cellula staminale tumorale (CSC, cancer stem cell). In particolare, abbiamo dimostrato con questo lavoro di tesi che l’overespressione della pathway di NOTCH1, è specifica per il pRCC di tipo 2 ed è associata ad una prognosi sfavorevole nell’uomo . Infine, abbiamo dimostrato che NOTCH1 promuove la trasformazione del progenitore renale, sia in vivo che in vitro promuovendone la proliferazione clonale incontrollata favorendo delle mitosi aberranti. I risultati di questo studio rappresentano un’importante scoperta dal punto di vista clinico, per la diagnosi e il trattamento dei pazienti con questo tipo di tumore.
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Conte, Carolina. "Studio del ruolo dei progenitori renali nell’eziopatogenesi della preeclampsia". Doctoral thesis, 2022. http://hdl.handle.net/2158/1263956.
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I progenitori renali hanno un ruolo di primaria importanza nella capacità del rene di far fronte allo stress da filtrazione glomerulare e di ripristinare prontamente i podociti danneggiati durante la gravidanza. La stimolazione estrogenica guida tale adattamento e se carente può fare la differenza tra il successo della gravidanza e l’insorgenza di complicanze quali la preeclampsia. Questi risultati aggiungono un tassello in più verso l a comprensione
dell’eziopatogenesi della preeclampsia, in quanto pongono il rene, in particolare la capacità dei progenitori renali di generare nuovi podociti, in risposta agli estrogeni, tra le cause che predispongono alla patologia. In vitro colture primarie di progenitori renali umani risultano essere sensibili alla stimolazione estrogenica che agisce attraverso il recettore ER α . Questo effetto trova riscontro negli esperimenti in vivo , attraverso cui è stato possibile dimostrare che la carenza del recettore α degli estrogeni sui progenitori renali ha effetti sulla loro capacità di differenziare in podociti. Il che predispone ad un maladattamento funzionale del rene alla gravidanza.
Libros sobre el tema "Renal progenitors"
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Pleniceanu, Oren y Benjamin Dekel. Kidney stem cells. Editado por Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0344.
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End-stage renal failure is a major cause of death with currently only dialysis and transplantation available as therapeutic options, each with its own limitations and drawbacks. To allow regenerative medicine-based kidney replacement therapies and due to the fact that neither haematopoietic stem cells nor mesenchymal stem cells, the most accessible human stem cells, can be used to derive genuine nephron progenitors, much attention has been given to finding adult renal stem cells. Several candidates for this have been described, but their true identity as stem or progenitor cells and their potential use in therapy has not yet been shown. However, the analysis of embryonic renal stem cells, specifically stem/progenitor cells that are induced into the nephrogenic pathway to form nephrons until the 34th week of gestation, has been much more conclusive.
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Weinberger, Christopher. Imaginary Worlds and Real Ethics in Japanese Fiction. Bloomsbury Publishing Inc, 2024. http://dx.doi.org/10.5040/9798765105429.
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Can novels contribute to the ethical lives of readers? What responsibilities might they bear in representing others? Are we ethically accountable for how we read fiction? s study takes up modern Japanese fiction and metafiction, subjects overwhelmingly ignored by Anglophone scholarship on novel ethics, to discover pioneering answers to these and other questions. Each chapter offers new readings of major works of modern Japanese literature (1880s through 1920s) that experiment with the capacity of novel narration to involve readers in ethically freighted encounters. Christopher Weinberger shows that Mori Ogai and Akutagawa Ryunosuke help to address key issues in new ethical theories today: debates about the roles that identification and empathy play in novel ethics; concerns about the representation of “otherness” and alterity in novels; divergence between cognitive and affective theories of ethics; widespread disagreement about what novel ethics obtain in the experience of reading, the effects of reading, or the form or content of novel representation; and, finally, concerns with bias and appropriation in the study of world literature. Concluding with a jump to the present, Imaginary Worlds and Real Ethics in Japanese Fiction puts on display a startling continuity between the methods of Japan’s modern novel progenitors and those of novelists at the forefront of global literature today, especially Haruki Murakami. Ultimately, this book models an original approach to ethical criticism while demonstrating the relevance of modern Japanese fiction for rethinking contemporary theories of the novel.
Capítulos de libros sobre el tema "Renal progenitors"
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Zhang, Ping L. y Olaf Kroneman. "Evolving Understanding of Renal Progenitor (Stem) Cells in Renal Physiology and Pathophysiology". En Handbook of Stem Cell Applications, 1–25. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-0846-2_23-1.
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Sallustio, Fabio, Angela Picerno, Francesca Giannuzzi, Francesca Montenegro, Rossana Franzin y Loreto Gesualdo. "The Regenerative Potential of Human Adult Renal Stem/Progenitor Cells". En Handbook of Stem Cell Applications, 1–27. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-0846-2_24-1.
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Bussolati, Benedetta y Giovanni Camussi. "New Insights into the Renal Progenitor Cells and Kidney Diseases by Studying CD133". En Advances in Experimental Medicine and Biology, 113–23. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5894-4_8.
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Minuth, Will W. y Lucia Denk. "Advanced Fixation for Transmission Electron Microscopy Unveils Special Extracellular Matrix Within the Renal Stem/Progenitor Cell Niche". En Methods in Molecular Biology, 21–37. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/7651_2014_93.
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Jacobi, Angela, Philipp Rosendahl, Martin Kräter, Marta Urbanska, Maik Herbig y Jochen Guck. "Analysis of Biomechanical Properties of Hematopoietic Stem and Progenitor Cells Using Real-Time Fluorescence and Deformability Cytometry". En Stem Cell Mobilization, 135–48. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9574-5_11.
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Balistreri, Carmela Rita. "Endothelial Progenitor Cells: A Real Hope or an Unrealizable Dream? Which Measures or Strategies Are Necessary for making EPCs a clinical reality? Focus on a Potential Roadmap". En UNIPA Springer Series, 67–78. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55107-4_3.
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Lasagni, Laura, Elena Lazzeri, Anna Peired y Paola Romagnani. "Evidence for Renal Progenitors in the Human Kidney". En Kidney Development, Disease, Repair and Regeneration, 395–406. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-800102-8.00029-1.
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Yamaleyeva, L. M., S. H. Mirmalek-Sani, A. Atala y J. J. Yoo. "Renal progenitor and stem cell biology and therapy". En Progenitor and Stem Cell Technologies and Therapies, 443–62. Elsevier, 2012. http://dx.doi.org/10.1533/9780857096074.3.443.
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Pertica, Nicoletta, Cataldo Abaterusso, Antonio Lupo y Giovanni Gambaro. "Endothelial Progenitor Cells in Acute Renal Injury". En Critical Care Nephrology, 221–24. Elsevier, 2009. http://dx.doi.org/10.1016/b978-1-4160-4252-5.50044-7.
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Cinelli, Steven A. "Real Estate Crowdfunding". En Foreign Direct Investments, 720–47. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-2448-0.ch031.
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Like a juggernaut, “crowdfunding” has hit the media, the financial markets and the common narrative by storm. Incipient in many ways, the intermediation of financing transactions online has become a billion-dollar industry. As technology has advanced, even recreated, industries, there seems none more primed than “finance”, an inherently information business. By creating improved efficiency, both art and science of finance are enriched. A 21st century vestige of the 1980's syndication business, real estate seems to be enjoying the fruits of the crowd, with $1 billion of property financings conducted online in 2014, with an expected $2.5 billion this year. For sponsors and investors, there appears legitimacy to the online approach, underscored by the level of venture capital now finding home in this burgeoning sector. Yet, like its progenitor, might real estate crowdfinance find legislative, regulatory, and practical headwinds, stunting its progress? Still early, with business models, scalability and sustainability still suspect, the current momentum seems promising.
Actas de conferencias sobre el tema "Renal progenitors"
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Whited, Bryce M., Matthias C. Hofmann, Chris G. Rylander, Aaron S. Goldstein, Joseph W. Freeman, Mark Furth, Shay Soker, Ge Wang, Yong Xu y Marissa N. Rylander. "Non-Destructive Real-Time Imaging of Cell Seeded Tissue Engineered Scaffolds". En ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53721.
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The use of tissue engineered scaffolds in combination with progenitor cells has emerged as a promising strategy to restore or replace tissues damaged by disease or trauma. In addition to being biocompatible and exhibiting appropriate mechanical properties, scaffolds must be designed to sustain cell attachment, proliferation, and differentiation to ultimately produce the desired tissue once implanted in the patient [1]. Conventional techniques used to assess successful scaffold design include cell viability stains, DNA assays, and histological sectioning/staining. While significant information can be gained from using these methodologies, they are destructive to the sample and only provide snapshots of scaffold and cell development at a limited number of time points. Consequently, key temporal and spatial information relating to tissue regeneration in the scaffold is lost utilizing these techniques. Thus, the ability to non-destructively monitor cell viability, proliferation, and differentiation in real-time is of great importance for scaffold design and tissue engineering [2].
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Chechetka, Vladimir Vladimirovich. "Invention of the MP3 format as one of the most successful projects in the digital history of Germany". En All-Russian Scientific and Practical Conference, chair Aleksei Viacheslavovich Bredikhin. Publishing house Sreda, 2023. http://dx.doi.org/10.31483/r-108831.
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The creation of the famous format for storing and broadcasting audio data – mp3 solved at one time the problem of high-precision transmission of human speech via telephone lines. But soon a real revolution took place in the world of telecommunications – a fiber-optic cable and an ISDN digital communication network were created. The developers switched to another idea – efficient encoding and compression of audio signals. The scientist who first drew attention to the fact that optimal compression of audio content is impossible without taking into account the features of the human hearing aid was Karlheinz Brandenburg, the "progenitor" of the mp3 format.
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Farace, Françoise, Marine Gross - Goupil, Elodie Tournay, Melissa Taylor, Catherine Hill y Bernard Escudier. "Abstract 372: Circulating endothelial progenitor cell levels predict survival benefit in metastatic renal cell cancer patients treated with antiangiogenic agents". En Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-372.
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Medica, Davide, Vincenzo Cantaluppi, Rossana Franzin, Alessandra Stasi, Giuseppe Castellano, Massimiliano Migliori, Vincenzo Panichi y Giovanni Camussi. "Extracellular Vesicles derived from Endothelial Progenitor Cells inhibit complement- and cytokine-mediated injury of renal glomerular endothelial cells and podocytes". En Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08932.
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Farace, Françoise, Claire Cropet, Ellen Blanc, David Pérol, Sylvie Négrier y Bernard Escudier. "Abstract 4127: Levels of circulating CD45dimCD34+VEGFR2+ progenitor cells correlate with outcome in metastatic renal cell carcinoma patients treated with targeted therapies". En Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4127.
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MEIRELLES, KARINE PERES y JOÃO GABRIEL TAVARES BRUNO. "PRINCIPAIS COMPLICAÇÕES CLÍNICAS CAUSADAS PELA HIPERTENSÃO ARTERIAL CRÔNICA NO PERÍODO GESTACIONAL". En I Congresso Brasileiro de Doenças Crônicas On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/cronics/7535.
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Introdução: A Hipertensão Arterial é uma das condições médicas de maior incidência mundial, sendo responsável por cerca de 50 mil mortes maternas mundial por ano, e no Brasil, é considerada a primeira causa de mortalidade materna, correspondendo a 37% dos óbitos. Importante ressaltar, que para ser considerada crônica, deve ser diagnosticada até a 20ª semana gestacional e com pressão arterial sustentada 140 x 90 mmHg. Durante a gestação, quando não há o monitoramento e tratamento adequado da HAC, pode-se desencadear uma série de complicações clínicas graves que comprometem a manutenção da vitalidade materna e fetal. Objetivos: O objetivo consiste em reunir e analisar as principais complicações da Hipertensão Arterial Crônica durante o período gestacional. Metodologia: Para a realização deste estudo descritivo e qualitativo, foram realizadas buscas bibliográficas, nas plataformas digitais UptoDate, PubMed e SciELO disponibilizadas de forma eletrônica em um espaço amostral de 2005 a 2019, nos idiomas português e inglês. Resultados: Os artigos que serviram como base para a discussão dos resultados, demonstraram que entre as principais complicações maternas da Hipertensão Arterial Crônica durante a gestação encontram-se a toxemia gravídica (3 a 10% das gestações), descolamento prematura de placenta (15,6 a cada 1000 gestantes), diabetes gestacional, Insuficiência Renal, edema pulmonar, Encefalopatia hipertensiva. Contudo, estudos comprovam que, apesar da HAC durante a gestação ser controlada, a mulher ainda possui um risco de 10-20% de desenvolver pré-eclâmpsia, e quando não há nenhum tipo de tratamento este risco aumenta em 50%. Por outro lado, as complicações fetais também são resultado de uma HAC desenvolvida pela progenitora na gravidez, podendo ser citados a restrição do crescimento fetal, parto prematuro e óbito fetal. Conclusão: Sendo assim, através dos dados reunidos fica evidente que a Hipertensão Arterial Crônica é um importante fator de risco para complicações clínicas maternas e fetais. Com isso, é essencial que haja uma detecção precoce, monitoramento e tratamento dessa condição clínica a fim de reduzir os riscos e melhorar o prognóstico materno e do feto.