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3. A genetically inducible endothelial niche enables vascularization of human kidney organoids with multilineage maturation and emergence of renin expressing cells

Author

Maggiore, Joseph C., LeGraw, Ryan, Przepiorski, Aneta, Velazquez, Jeremy, Chaney, Christopher, Vanichapol, Thitinee, Streeter, Evan, Almuallim, Zainab, Oda, Akira, Chiba, Takuto, Silva-Barbosa, Anne, Franks, Jonathan, Hislop, Joshua, Hill, Alex, Wu, Haojia, Pfister, Katherine, Howden, Sara E., Watkins, Simon C., Little, Melissa H., Humphreys, Benjamin D., Kiani, Samira, Watson, Alan, Stolz, Donna B., Davidson, Alan J., Carroll, Tom, Cleaver, Ondine, Sims-Lucas, Sunder, Ebrahimkhani, Mo R., and Hukriede, Neil A.

Published
2024
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9. Contributors

Author

Al Sayed, Zeina R., primary, Aromalaran, Kelly, additional, Azad, Priti, additional, Bernardini, Laura, additional, Chen, Zhenyu, additional, Chennappan, Saravanakkumar, additional, Clegg, Dennis O., additional, Corli, Marzia, additional, Dwivedi, Ila, additional, Ercan-Sencicek, A. Gulhan, additional, Faynus, Mohamed A., additional, Forbes, Thomas A., additional, Gutmann, David H., additional, Haddad, Gabriel G., additional, Hamazaki, Takashi, additional, Hartigan, Kelly A., additional, Hattori, Taeka, additional, Hulot, Jean-Sébastien, additional, Imitola, Jaime, additional, Julian, Katherine, additional, Kontaridis, Maria Irene, additional, Leoni, Chiara, additional, Li, Xue-Jun, additional, Little, Melissa H., additional, Masurkar, Nihar, additional, Mou, Yongchao, additional, Onesimo, Roberta, additional, Pennuto, Maria, additional, Rosati, Jessica, additional, Schurr, Sarah V., additional, Shintaku, Haruo, additional, Sireno, Laura, additional, Turco, Elisa Maria, additional, Vescovi, Angelo Luigi, additional, Wu, Wei, additional, Yao, Hang, additional, Yu, Yang, additional, Zampino, Giuseppe, additional, and Zhao, Helen, additional

Published
2022
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12. Kidney organoids reveal redundancy in viral entry pathways during ACE2-dependent SARS-CoV-2 infection

Author

Vanslambrouck, Jessica M., Neil, Jessica A., Rudraraju, Rajeev, Mah, Sophia, Tan, Ker Sin, Groenewegen, Ella, Forbes, Thomas A., Karavendzas, Katerina, Elliott, David A., Porrello, Enzo R., Subbarao, Kanta, Little, Melissa H., Vanslambrouck, Jessica M., Neil, Jessica A., Rudraraju, Rajeev, Mah, Sophia, Tan, Ker Sin, Groenewegen, Ella, Forbes, Thomas A., Karavendzas, Katerina, Elliott, David A., Porrello, Enzo R., Subbarao, Kanta, and Little, Melissa H.

Abstract

With a high incidence of acute kidney injury among hospitalized COVID-19 patients, considerable attention has been focussed on whether SARS-CoV-2 specifically targets kidney cells to directly impact renal function, or whether renal damage is primarily an indirect outcome. To date, several studies have utilized kidney organoids to understand the pathogenesis of COVID-19, revealing the ability for SARS-CoV-2 to predominantly infect cells of the proximal tubule (PT), with reduced infectivity following administration of soluble ACE2. However, the immaturity of standard human kidney organoids represents a significant hurdle, leaving the preferred SARS-CoV-2 processing pathway, existence of alternate viral receptors, and the effect of common hypertensive medications on the expression of ACE2 in the context of SARS-CoV-2 exposure incompletely understood. Utilizing a novel kidney organoid model with enhanced PT maturity, genetic- and drug-mediated inhibition of viral entry and processing factors confirmed the requirement for ACE2 for SARS-CoV-2 entry but showed that the virus can utilize dual viral spike protein processing pathways downstream of ACE2 receptor binding. These include TMPRSS- and CTSL/CTSB-mediated non-endosomal and endocytic pathways, with TMPRSS10 likely playing a more significant role in the non-endosomal pathway in renal cells than TMPRSS2. Finally, treatment with the antihypertensive ACE inhibitor, lisinopril, showed negligible impact on receptor expression or susceptibility of renal cells to infection. This study represents the first in-depth characterization of viral entry in stem cell-derived human kidney organoids with enhanced PTs, providing deeper insight into the renal implications of the ongoing COVID-19 pandemic.

Published
2024

14. Advances in our understanding of genetic kidney disease using kidney organoids

Author

Little, Melissa H. and Quinlan, Catherine

Subjects
Genetic disorders -- Models -- Usage, Tissue culture -- Usage -- Models, Kidney diseases -- Models -- Usage, Health
Abstract

A significant proportion of kidney disease presenting in childhood is likely genetic in origin with a growing number of genes implicated in its development. However, many children may have changes in previously undescribed or unrecognised genes. The recent development of methods for generating human kidney organoids from human pluripotent stem cells has the potential to substantially change the rate of diagnosis and the development of new treatments for some forms of genetic kidney disease. In this review, we discuss how accurately a kidney organoid models the human kidney, identifying the strengths and weaknesses of these potentially patient-derived models of renal disease., Author(s): Melissa H. Little [sup.1] [sup.2] [sup.3] , Catherine Quinlan [sup.1] [sup.3] [sup.4] Author Affiliations: (1) grid.1058.c, 0000 0000 9442 535X, Murdoch Children's Research Institute, , Flemington Rd., Parkville, VIC, [...]

Published
2020
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15. Vascular bioengineering of scaffolds derived from human discarded transplant kidneys using human pluripotent stem cell–derived endothelium

Author

Leuning, Daniëlle G., Witjas, Franca M.R., Maanaoui, Mehdi, de Graaf, Annemarie M.A., Lievers, Ellen, Geuens, Thomas, Avramut, Christina M., Wiersma, Loes E., van den Berg, Cathelijne W., Sol, Wendy M.P.J., de Boer, Hetty, Wang, Gangqi, LaPointe, Vanessa L.S., van der Vlag, Johan, van Kooten, Cees, van den Berg, Bernard M., Little, Melissa H., Engelse, Marten A., and Rabelink, Ton J.

Published
2019
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19. Evaluation of variability in human kidney organoids

Author

Phipson, Belinda, Er, Pei X., Combes, Alexander N., Forbes, Thomas A., Howden, Sara E., Zappia, Luke, Yen, Hsan-Jan, Lawlor, Kynan T., Hale, Lorna J., Sun, Jane, Wolvetang, Ernst, Takasato, Minoru, Oshlack, Alicia, and Little, Melissa H.

Published
2019
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25. Kidney Organoids Generated Using an Allelic Series of NPHS2 Point Variants Reveal Distinct Intracellular Podocin Mistrafficking

Author

Dorison, Aude, Ghobrial, Irene, Graham, Alison, Peiris, Thanushi, Forbes, Thomas A., See, Michael, Das, Mithun, Saleem, Moin A., Quinlan, Catherine, Lawlor, Kynan T., Ramialison, Mirana, Howden, Sara E., Little, Melissa H., Dorison, Aude, Ghobrial, Irene, Graham, Alison, Peiris, Thanushi, Forbes, Thomas A., See, Michael, Das, Mithun, Saleem, Moin A., Quinlan, Catherine, Lawlor, Kynan T., Ramialison, Mirana, Howden, Sara E., and Little, Melissa H.

Abstract

Significance Statement Missense variants of NPHS2 that cause mistrafficking of the encoded protein, PODOCIN, have been associated with steroid-resistant nephrotic syndrome. However, most studies have overexpressed such variants in 2D nonpodocyte cells. This study describes the generation and characterization of human kidney organoids representing an allelic series of homozygous NPHS2 missense variants. The strategy revealed a previously unappreciated reduction in variant PODOCIN protein, variant-specific subcellular localization, and specific effects on NEPHRIN association. All variants showed apoptosis in the absence of endoplasmic reticulum stress. Engineering endogenous NPHS2 variants to model in 3D human organoids provides a more accurate view of the pathobiology and a toolkit to screen compounds for reduction of variant protein degradation and mistrafficking. Background NPHS2 variants are the most common cause of steroid-resistant nephrotic syndrome in children >1 month old. Missense NPHS2 variants were reported to cause mistrafficking of the encoded protein, PODOCIN, but this conclusion was on the basis of overexpression in some nonpodocyte cell lines. Methods We generated a series of human induced pluripotent stem cell (iPSC) lines bearing pathogenic missense variants of NPHS2, encoding the protein changes p.G92C, p.P118L, p.R138Q, p.R168H, and p.R291W, and control lines. iPSC lines were also generated from a patient with steroid-resistant nephrotic syndrome (p.R168H homozygote) and a healthy heterozygous parent. All lines were differentiated into kidney organoids. Immunofluorescence assessed PODOCIN expression and subcellular localization. Podocytes were transcriptionally profiled and PODOCIN-NEPHRIN interaction interrogated. Results All variant lines revealed reduced levels of PODOCIN protein in the absence of reduced transcription. Although wild-type PODOCIN localized to the membrane, distinct variant prote, Significance StatementMissense variants of NPHS2 that cause mistrafficking of the encoded protein, PODOCIN, have been associated with steroid-resistant nephrotic syndrome. However, most studies have overexpressed such variants in 2D nonpodocyte cells. This study describes the generation and characterization of human kidney organoids representing an allelic series of homozygous NPHS2 missense variants. The strategy revealed a previously unappreciated reduction in variant PODOCIN protein, variant-specific subcellular localization, and specific effects on NEPHRIN association. All variants showed apoptosis in the absence of endoplasmic reticulum stress. Engineering endogenous NPHS2 variants to model in 3D human organoids provides a more accurate view of the pathobiology and a toolkit to screen compounds for reduction of variant protein degradation and mistrafficking.BackgroundNPHS2 variants are the most common cause of steroid-resistant nephrotic syndrome in children >1 month old. Missense NPHS2 variants were reported to cause mistrafficking of the encoded protein, PODOCIN, but this conclusion was on the basis of overexpression in some nonpodocyte cell lines.MethodsWe generated a series of human induced pluripotent stem cell (iPSC) lines bearing pathogenic missense variants of NPHS2, encoding the protein changes p.G92C, p.P118L, p.R138Q, p.R168H, and p.R291W, and control lines. iPSC lines were also generated from a patient with steroid-resistant nephrotic syndrome (p.R168H homozygote) and a healthy heterozygous parent. All lines were differentiated into kidney organoids. Immunofluorescence assessed PODOCIN expression and subcellular localization. Podocytes were transcriptionally profiled and PODOCIN-NEPHRIN interaction interrogated.ResultsAll variant lines revealed reduced levels of PODOCIN protein in the absence of reduced transcription. Although wild-type PODOCIN localized to the membrane, distinct variant proteins displayed unique patterns of subcellular protei

Published
2023

30. Kidney Organoids Generated Using an Allelic Series of NPHS2 Point Variants Reveal Distinct Intracellular Podocin Mistrafficking

Author

Dorison, Aude, primary, Ghobrial, Irene, additional, Graham, Alison, additional, Peiris, Thanushi, additional, Forbes, Thomas A., additional, See, Michael, additional, Das, Mithun, additional, Saleem, Moin A., additional, Quinlan, Catherine, additional, Lawlor, Kynan T., additional, Ramialison, Mirana, additional, Howden, Sara E., additional, and Little, Melissa H., additional

Published
2022
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33. List of Contributors

Author

Abecassis, Michael, primary, Abed, Ahmed, additional, Abelli, Massimo, additional, Ahmad, Sarwat, additional, Alessiani, Mario, additional, Alsharidi, Aynaa, additional, Altruda, Fiorella, additional, Amorese, Gabriella, additional, Angeletti, Andrea, additional, Angelico, Mario, additional, Angelico, Roberta, additional, Angelotti, Maria L., additional, Applegate, Robert J., additional, Atala, Anthony, additional, Attanasio, Chiara, additional, Axelrod, David, additional, Bababekov, Yanik, additional, Basu, Joydeep, additional, Becherucci, Francesca, additional, Belford, P. Matthew, additional, Benedetti, Enrico, additional, Benedetti, Valentina, additional, Benigni, Ariela, additional, Bertram, Timothy A., additional, Bestard, Oriol, additional, Blake, Joshua, additional, Boggi, Ugo, additional, Brasile, Lauren, additional, Bromberg, Jonathan S., additional, Brouard, Sophie, additional, Brovold, Matthew, additional, Burke, George W., additional, Busic, Mirela, additional, Butt, Zeeshan, additional, Caddeo, Silvia, additional, Calzone, Stefano, additional, Campistol, Josep M., additional, Carmagnola, Irene, additional, Carty, Fiona, additional, Castanares-Zapatero, Diego, additional, Chadjichristos, Christos E., additional, Chambers, Brooke E., additional, Chandran, Sindhu, additional, Chatziantoniou, Christos, additional, Chen, Ashton, additional, Chen, Linda, additional, Chen, Xiwu, additional, Chiono, Valeria, additional, Chiusa, Manuel, additional, Ciancio, Gaetano, additional, Ciardelli, Gianluca, additional, Coletti, Gino, additional, Coll, Elisabeth, additional, Collienne, Christine, additional, Colvin, Robert B., additional, Cortinovis, Monica, additional, Cosimi, A. Benedict, additional, Cravedi, Paolo, additional, D’Amico, Giuseppe, additional, Da Sacco, Stefano, additional, Danger, Richard, additional, Dantal, Jacques, additional, Davidson, Alan J., additional, De Chiara, Letizia, additional, De Fijter, Johannes W., additional, de la Rosa, Gloria, additional, Delmonico, Francis L., additional, Deng, Junhong, additional, Deurdulian, Corinne, additional, Dhal, Abritee, additional, Dionigi, Paolo, additional, Domínguez-Gil, Beatriz, additional, Drozdzik, Marek, additional, Dussaule, Jean-Claude, additional, Edgar, Lauren, additional, Egidi, Maria Francesca, additional, El Hennawy, Hany, additional, English, Karen, additional, Everly, Matthew J., additional, Fagoonee, Sharmila, additional, Famulari, Elvira Smeralda, additional, Farney, Alan C., additional, Figliuzzi, Marina, additional, Framarino-dei-Malatesta, Marialuisa, additional, Fumo, David E., additional, Gagliardini, Elena, additional, Gallon, Lorenzo, additional, Gandhi, Sanjay K., additional, Gautreaux, Michael D., additional, Geraedts, Anna, additional, Giannese, Domenico, additional, Giulianotti, Pier C., additional, Goligorsky, Michael S., additional, Griesemar, Adam, additional, Grinyó, Josep M., additional, Gruessner, Angelika C., additional, Gruessner, Rainer W.G., additional, He, Bulang, additional, Heher, Eliot, additional, Ho, Bing, additional, Hosgood, Sarah A., additional, Hotta, Kiyohiko, additional, Humar, Atul, additional, Humes, H. David, additional, Iaria, Giuseppe, additional, Imberti, Barbara, additional, Izpisua Belmonte, Juan Carlos, additional, Jochmans, Ina, additional, Katari, Ravi, additional, Kavvadas, Panagiotis, additional, Kawai, Tatsuo, additional, Kengla, Carlos, additional, Keys, Tristan, additional, Kidiyoor, Amritha, additional, Kidokoro, Kengo, additional, Kumar, Deepali, additional, Kutcher, Michael A., additional, Lai, Quirino, additional, Laterre, Pierre-François, additional, Lebbé, Céleste, additional, Legendre, Christophe, additional, Lennon, Rachel, additional, Li, Peng, additional, Lin, Jen-Jar, additional, Little, Melissa H., additional, Lu, Xiongbing, additional, Ludlow, John W., additional, Mahíllo, Beatriz, additional, Masereeuw, Rosalinde, additional, Matesanz, Rafael, additional, Matovinovic, Mirjana S., additional, Mazzinghi, Benedetta, additional, Mbiandjeu Toya, Serge Cedrick, additional, McEwen, Scott, additional, Melandro, Fabio, additional, Melchiorri, Loredana, additional, Menon, Madhav C., additional, Mirzazadeh, Majid, additional, Montag, Samantha, additional, Montgomery, Robert A., additional, Montiel, Virginie, additional, Montserrat, Nuria, additional, Morigi, Marina, additional, Morrill, Christian C., additional, Mourad, Michel, additional, Murphy, Sean V., additional, Murray, Patricia, additional, Nardo, Tiziana, additional, Netti, Paolo A., additional, Nguyen, Mark, additional, Nicholson, Michael L., additional, O’Callaghan, John M., additional, Ohler, Linda, additional, Orlando, Giuseppe, additional, Osafune, Kenji, additional, Oura, Tetsu, additional, Peired, Anna, additional, Peloso, Andrea, additional, Peng, Zhenzhen, additional, Perico, Norberto, additional, Perin, Laura, additional, Perrone, Vittorio, additional, Persad, Paul, additional, Peti-Peterdi, János, additional, Petrosyan, Astgik, additional, Pietrabissa, Andrea, additional, Pino, Christopher J., additional, Pirenne, Jacques, additional, Pisani, Francesco, additional, Ploeg, Rutger J., additional, Porrini, Esteban, additional, Pozzi, Ambra, additional, Pugliese, Alberto, additional, Pugliese, Luigi, additional, Rabelink, Ton J., additional, Rampino, Teresa, additional, Rees, Michael A., additional, Reinders, Marlies E.J., additional, Remuzzi, Andrea, additional, Remuzzi, Giuseppe, additional, Riquier-Brison, Anne, additional, Roca, Raquel G., additional, Rogers, Jeffrey, additional, Romagnani, Paola, additional, Rosales, Ivy A., additional, Rosenblum, Norman D., additional, Rota, Cinzia, additional, Ruggenenti, Piero, additional, Ruini, Francesca, additional, Sageshima, Junichiro, additional, El Salem, Fadi, additional, Sandal, Shaifali, additional, Sander, Veronika, additional, Santeramo, Ilaria, additional, Santos, Renato M., additional, Sarwal, Minnie, additional, Shah, Jigesh, additional, Shetty, Aneesha A., additional, Silengo, Lorenzo, additional, Siskind, Eric, additional, Skaro, Anton, additional, Snanoudj, Renaud, additional, Soker, Shay, additional, South, Andrew M., additional, Spasovski, Goce, additional, Stratta, Robert J., additional, Strom, Charles, additional, Stubenitsky, Bart, additional, Tamburrini, Riccardo, additional, Tang, Qizhi, additional, Tantissattamo, Ekamol, additional, Tasaki, Masayuki, additional, Tchelepi, Hisham, additional, Ticozzelli, Elena, additional, Traitanon, Opas, additional, Trillini, Matias, additional, Tzvetanov, Ivo, additional, Valentín, María O., additional, Vincenti, Flavio, additional, Vistoli, Fabio, additional, Vriend, Jelle, additional, Walker, Stephen J., additional, Wertheim, Jason A., additional, Williams, David F., additional, Wilm, Bettina, additional, Wilmer, Martijn J., additional, Wingert, Rebecca A., additional, Wittebole, Xavier, additional, Xia, Yun, additional, Xinaris, Christodoulos, additional, Yamada, Kazuhiko, additional, Yokoo, Takashi, additional, Yokote, Shinya, additional, Zandvliet, Maarten L., additional, Zent, Roy, additional, Zhang, Yuanyuan, additional, Zhao, David X., additional, Zhao, Lihui, additional, and Zhao, Susan Y., additional

Published
2017
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38. Kidney organoids from human iPS cells contain multiple lineages and model human nephrogenesis

Author

Takasato, Minoru, Er, Pei X., Chiu, Han S., Maier, Barbara, Baillie, Gregory J., Ferguson, Charles, Parton, Robert G., Wolvetang, Ernst J., Roost, Matthias S., de Sousa Lopes, Susana M. Chuva, and Little, Melissa H.

Subjects
Stem cells -- Analysis -- Health aspects, Kidneys -- Health aspects, Kidney tubules -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The human kidney contains up to 2 million epithelial nephrons responsible for blood filtration. Regenerating the kidney requires the induction of the more than 20 distinct cell types required for excretion and the regulation of pH, and electrolyte and fluid balance. We have previously described the simultaneous induction of progenitors for both collecting duct and nephrons via the directed differentiation of human pluripotent stem cells (1). Paradoxically, although both are of intermediate mesoderm in origin, collecting duct and nephrons have distinct temporospatial origins. Here we identify the developmental mechanism regulating the preferential induction of collecting duct versus kidney mesenchyme progenitors. Using this knowledge, we have generated kidney organoids that contain nephrons associated with a collecting duct network surrounded by renal interstitium and endothelial cells. Within these organoids, individual nephrons segment into distal and proximal tubules, early loops of Henle, and glomeruli containing podocytes elaborating foot processes and undergoing vascularization. When transcription profiles of kidney organoids were compared to human fetal tissues, they showed highest congruence with first trimester human kidney. Furthermore, the proximal tubules endocytose dextran and differentially apoptose in response to cisplatin, a nephrotoxicant. Such kidney organoids represent powerful models of the human organ for future applications, including nephrotoxicity screening, disease modelling and as a source of cells for therapy., The mammalian kidney is derived from intermediate mesoderm. Cells from the primitive streak (presomitic mesoderm; PSM) migrate rostrally to form the intermediate mesoderm (2). The intermediate mesoderm gives rise to [...]

Published
2015

40. Comprehensive transcriptome and immunophenotype analysis of renal and cardiac MSC-like populations supports strong congruence with bone marrow MSC despite maintenance of distinct identities

Author

Pelekanos, Rebecca A., Li, Joan, Gongora, Milena, Chandrakanthan, Vashe, Scown, Janelle, Suhaimi, Norseha, Brooke, Gary, Christensen, Melinda E., Doan, Tram, Rice, Alison M., Osborne, Geoffrey W., Grimmond, Sean M., Harvey, Richard P., Atkinson, Kerry, and Little, Melissa H.

Published
2012
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44. Contributors

Author

Al-Awqati, Qais, primary, Arts, H.H., additional, Atala, Anthony, additional, Barnes, Felicity J., additional, Benigni, Ariela, additional, Bertram, John F., additional, Black, M. Jane, additional, Bonventre, Joseph V., additional, Buffington, Deborah A., additional, Bush, Kevin T., additional, Cao, Qi, additional, Carroll, Thomas, additional, Cosgrove, Melanie, additional, Costantini, Frank, additional, Cullen-McEwen, Luise, additional, Davidson, Alan J., additional, Dekel, Benjamin, additional, Dodd, Rachel C., additional, Dressler, Gregory R., additional, Duffield, Jeremy S., additional, Dziedzic, Klaudyna, additional, Ferenbach, David A., additional, Finkelstein, Julia B., additional, Goodyer, Paul, additional, Guay-Woodford, L.M., additional, Hammerman, Marc R., additional, Harris, David C.H., additional, Hiatt, Michael J., additional, Hoy, Wendy E., additional, Hughson, Michael D., additional, Huling, Jennifer C., additional, Humes, H. David, additional, Humphreys, Benjamin D., additional, Ilagan, Roger, additional, Knoers, Nine V.A.M., additional, Kopan, Raphael, additional, Kreidberg, Jordan A., additional, Kwartler, Callie S., additional, Lasagni, Laura, additional, Lazzeri, Elena, additional, Little, Melissa H., additional, Lu, Weining, additional, Macconi, Daniela, additional, Matsell, Douglas G., additional, McMahon, Andrew P., additional, Mendelsohn, Cathy, additional, Moeller, Marcus J., additional, Moritz, Karen M., additional, Nigam, Sanjay K., additional, Nishinakamura, Ryuichi, additional, O’Connor, A.K., additional, Oliver, Juan A., additional, Osafune, Kenji, additional, Oxburgh, Leif, additional, Park, Joo-Seop, additional, Peired, Anna, additional, Pino, Christopher J., additional, Pleniceanu, Oren, additional, Presnell, Sharon, additional, Puelles, Victor G., additional, Quaggin, Susan E., additional, Rabelink, Ton J., additional, Ranghini, Egon, additional, Rapoport, Scott, additional, Reinders, Marlies E.J., additional, Remuzzi, Giuseppe, additional, Ricardo, Sharon D., additional, Romagnani, Paola, additional, Scott, Rizaldy P., additional, Sequeira Lopez, Maria Luisa S., additional, Shepherd, Benjamin, additional, Short, Kieran M., additional, Smyth, Ian M., additional, Susztak, Katalin, additional, Sutherland, Megan R., additional, Taguchi, Atsuhiro, additional, Wang, Yiping, additional, Weber, Stefanie, additional, Westover, Angela J., additional, Yokoo, Takashi, additional, Yoo, James J., additional, and Yu, Jing, additional

Published
2016
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50. Recreating kidney progenitors from pluripotent cells

Author

Takasato, Minoru, Maier, Barbara, and Little, Melissa H.

Subjects
Embryonic development -- Research, Kidneys -- Physiological aspects -- Research, Kidney tubules -- Research -- Physiological aspects -- Properties, Cell differentiation -- Research, Health
Abstract

Access to human pluripotent cells theoretically provides a renewable source of cells that can give rise to any required cell type for use in cellular therapy or bioengineering. However, successfully directing this differentiation remains challenging for most desired endpoints cell type, including renal cells. This challenge is compounded by the difficulty in identifying the required cell type in vitro and the multitude of renal cell types required to build a kidney. Here we review our understanding of how the embryo goes about specifying the cells of the kidney and the progress to date in adapting this knowledge for the recreation of nephron progenitors and their mature derivatives from pluripotent cells. Keywords Kidney development * Embryonic stem cell * Directed differentiation * Kidney progenitor, Introduction The kidney is a complex organ with a highly constrained architecture and more than 20 distinct mature cellular phenotypes, all of which are required for this organ to regulate [...]

Published
2014
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