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Journal articles on the topic 'Renal stem cell'

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Published: 9 March 2023

Last updated: 10 March 2023

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1

Bussolati, Benedetta, Akito Maeshima, Janos Peti-Peterdi, Takashi Yokoo, and Laura Lasagni. "Renal Stem Cells, Tissue Regeneration, and Stem Cell Therapies for Renal Diseases." Stem Cells International 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/302792.

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2

Jin, Meiling, Yuansheng Xie, Qinggang Li, and Xiangmei Chen. "Stem Cell-Based Cell Therapy for Glomerulonephritis." BioMed Research International 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/124730.

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Glomerulonephritis (GN), characterized by immune-mediated inflammatory changes in the glomerular, is a common cause of end stage renal disease. Therapeutic options for glomerulonephritis applicable to all cases mainly include symptomatic treatment and strategies to delay progression. In the attempt to yield innovative interventions fostering the limited capability of regeneration of renal tissue after injury and the uncontrolled pathological process by current treatments, stem cell-based therapy has emerged as novel therapy for its ability to inhibit inflammation and promote regeneration. Many basic and clinical studies have been performed that support the ability of various stem cell populations to ameliorate glomerular injury and improve renal function. However, there is a long way before putting stem cell-based therapy into clinical practice. In the present article, we aim to review works performed with respect to the use of stem cell of different origins in GN, and to discuss the potential mechanism of therapeutic effect and the challenges for clinical application of stem cells.

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3

Park, Hyeong-Cheon, Kaoru Yasuda, Mei-Chuan Kuo, Jie Ni, Brian Ratliff, Praveen Chander, and Michael S. Goligorsky. "Renal capsule as a stem cell niche." American Journal of Physiology-Renal Physiology 298, no. 5 (May 2010): F1254—F1262. http://dx.doi.org/10.1152/ajprenal.00406.2009.

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Renal resident stem cells were previously reported within the renal tubules and papillary area. The aim of the present study was to determine whether renal capsules harbor stem cells and whether this pool can be recruited to the renal parenchyma after ischemic injury. We demonstrated the presence of label-retaining cells throughout the renal capsule, at a density of ∼10 cells/mm2, and their close apposition to the blood vessels. By flow cytometry, in vitro cultured cells derived from the renal capsule were positive for mesenchymal stem cell (MSC) markers (CD29+, vimentin+, Sca-1+, nestin+) but did not express hematopoietic and endothelial stem cell markers. Moreover, renal capsule-derived cells also exhibited self-renewal, clonogenicity, and multipotency in differentiation conditions, all favoring stem cell characteristics and identifying them with MSC. In situ labeling of renal capsules with CM-DiI CellTracker demonstrated in vivo a directed migration of CM-DiI-labeled cells to the ischemic renal parenchyma, with the rate of migration averaging 30 μm/h. Decapsulation of the kidneys during ischemia resulted in a modest, but statistically significant, deceleration of recovery of plasma creatinine compared with ischemic kidneys with intact renal capsule. Comparison of these conditions allows the conclusion that renal capsular cells may contribute ∼25–30% of the recovery from ischemia. In conclusion, the data suggest that the renal capsule may function as a novel stem cell niche harboring MSC capable of participating in the repair of renal injury.

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4

Mollura, Daniel J., Joshua M. Hare, and Hamid Rabb. "Stem-cell therapy for renal diseases." American Journal of Kidney Diseases 42, no. 5 (November 2003): 891–905. http://dx.doi.org/10.1016/j.ajkd.2003.07.018.

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5

Bregni, Marco, Wolfgang Herr, and Didier Blaise. "Allogeneic stem cell transplantation for renal cell carcinoma." Expert Review of Anticancer Therapy 11, no. 6 (June 2011): 901–11. http://dx.doi.org/10.1586/era.11.12.

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6

Childs, Richard, and Darrel Drachenberg. "Allogeneic stem cell transplantation for renal cell carcinoma." Current Opinion in Urology 11, no. 5 (September 2001): 495–502. http://dx.doi.org/10.1097/00042307-200109000-00008.

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7

Hayes-Lattin, Brandon M., Richard T. Maziarz, and Tomasz M. Beer. "Allogeneic stem-cell transplantation in renal-cell carcinoma." Current Oncology Reports 3, no. 5 (October 2001): 433–37. http://dx.doi.org/10.1007/s11912-001-0030-7.

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8

Osmanov, Y. I., E. А. Kogan, V. I. Shchekin, G. А. Demyashkin, and A. V. Kaem. "FEATURES OF EXPRESSION OF STEM CELL MARKERS IN RENAL CELL CARCINOMAS." Crimea Journal of Experimental and Clinical Medicine 10, no. 2 (2020): 29–39. http://dx.doi.org/10.37279/2224-6444-2020-10-2-29-39.

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Intensive studies of recent decades have been devoted to identifying a population of cancer stem cells among the renal tubule epithelial cells. To date, a broad spectrum of genes involved in the molecular pathogenesis of renal cell carcinoma has been investigated in search of potential cancer stem cells of renal cell carcinoma. Among them, ALDH 1, CD133, CXCR4, CD24, CD82 and SOX2 can be distinguished. The aim of the study was to comparative characteristics of stem marker expression – ALDH1A1, CXCR4, CD24, CD82, CD133 and SOX2 in histological variants of renal cell carcinoma and determination of their prognostic signifi- cance. Subject and method. The study was performed on surgical material from 225 patients with renal cell carcinoma. As a comparison group, biopsy samples from 46 patients with renal oncocytoma were studied. Immunohistochemi- cal staining for the detection of antigens in the paraffin-embedded slices was made using the antibodies to ALDHA1, CD82, CD133, CXCR4, SOX2 («Abcam») and CD24 («Invitrogen»). To identify differences between the compared groups, the nonparametric Pearson’s criterion (ч2) were employed. Results. Expression of ALDHA1 was detected in 103 (45.8%) cases, CXCR4 in 105 (46.7%) cases. A positive reaction to CD24 occurred in 98 (43.6%) samples, SOX2 in 106 (47.1%) tumors. Among the variants of renal cell car- cinoma, CD133 expression is most often observed in clear cell papillary renal cell carcinoma. A higher expression rate of CD82 is observed in chromophobic renal cell carcinoma. Conclusion. Reliable associations between stem cell marker expressions and clinical parameters were revealed depending on the histological variant of renal cell carcinoma.

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9

Maeshima, Akito, Masao Nakasatomi, and Yoshihisa Nojima. "Regenerative Medicine for the Kidney: Renotropic Factors, Renal Stem/Progenitor Cells, and Stem Cell Therapy." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/595493.

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The kidney has the capacity for regeneration and repair after a variety of insults. Over the past few decades, factors that promote repair of the injured kidney have been extensively investigated. By using kidney injury animal models, the role of intrinsic and extrinsic growth factors, transcription factors, and extracellular matrix in this process has been examined. The identification of renal stem cells in the adult kidney as well as in the embryonic kidney is an active area of research. Cell populations expressing putative stem cell markers or possessing stem cell properties have been found in the tubules, interstitium, and glomeruli of the normal kidney. Cell therapies with bone marrow-derived hematopoietic stem cells, mesenchymal stem cells, endothelial progenitor cells, and amniotic fluid-derived stem cells have been highly effective for the treatment of acute or chronic renal failure in animals. Embryonic stem cells and induced pluripotent stem cells are also utilized for the construction of artificial kidneys or renal components. In this review, we highlight the advances in regenerative medicine for the kidney from the perspective of renotropic factors, renal stem/progenitor cells, and stem cell therapies and discuss the issues to be solved to realize regenerative therapy for kidney diseases in humans.

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10

YAN, XINLONG, LIXIN SHI, GUANGFU CHEN, XU ZHANG, BING LIU, WEN YUE, XUETAO PEI, and SHENGKUN SUN. "Mesenchymal stem cell-like cells in classic renal angiomyolipoma." Oncology Letters 4, no. 3 (June 14, 2012): 398–402. http://dx.doi.org/10.3892/ol.2012.760.

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11

Czarnecka, Anna, and Cezary Szczylik. "Renal Cell Carcinoma Cancer Stem Cells as Therapeutic Targets." Current Signal Transduction Therapy 8, no. 3 (April 2014): 203–9. http://dx.doi.org/10.2174/1574362409666140206222251.

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12

An, JH, KB Kim, SC Kwon, HJ Kim, MO Ryu, YI Oh, JO Ahn, and HY Youn. "Canine adipose tissue-derived mesenchymal stem cell therapy in a dog with renal Fanconi syndrome." Veterinární Medicína 67, No. 4 (February 16, 2022): 206–11. http://dx.doi.org/10.17221/213/2020-vetmed.

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Renal Fanconi syndrome (RFS) affects the proximal tubular resorption in the nephrons. This causes excessive loss of key solutes through the urine. In a canine patient, we successfully managed the renal tubular acidosis and proteinuria caused by RFS via transplantation of canine adipose tissue-derived mesenchymal stem cells (cAT-MSCs). cAT-MSCs were administered ten times at intervals of 2–4 weeks. The post-therapy check-up revealed that the cAT-MSC treatment improved the renal tubular acidosis and proteinuria. Hence, a cAT-MSC transplant may be considered as an adjuvant therapy in veterinary medicine to initiate and maintain relief of RFS-induced acidosis and proteinuria.

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13

Fang, Pengchao, Liuting Zhou, Lee Y. Lim, Hualin Fu, Zhi-xiang Yuan, and Juchun Lin. "Targeting Strategies for Renal Cancer Stem Cell Therapy." Current Pharmaceutical Design 26, no. 17 (June 8, 2020): 1964–78. http://dx.doi.org/10.2174/1381612826666200318153106.

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Renal cell carcinoma (RCC) is an intractable genitourinary malignancy that accounts for approximately 4% of adult malignancies. Currently, there is no approved targeted therapy for RCC that has yielded durable remissions, and they remain palliative in intent. Emerging evidence has indicated that renal tumorigenesis and RCC treatment-resistance may originate from renal cancer stem cells (CSCs) with tumor-initiating capacity (CSC hypothesis). A better understanding of the mechanism underlying renal CSCs will help to dissect RCC heterogeneity and drug treatment efficiency, to promote more personalized and targeted therapies. In this review, we summarized the stem cell characteristics of renal CSCs. We outlined the targeting strategies and challenges associated with developing therapies that target renal CSCs angiogenesis, immunosuppression, signaling pathways, surface biomarkers, microRNAs and nanomedicine. In conclusion, CSCs are an important role in renal carcinogenesis and represent a valid target for treatment of RCC patients.

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14

Inaguma, Yosuke, Hiroshi Kaito, Atsuro Saito, Daiichiro Hasegawa, Yoshiyuki Kosaka, and Ryojiro Tanaka. "Renal outcome after hemopoietic stem cell transplantation." Japanese journal of pediatric nephrology 33, no. 2 (2020): 115–22. http://dx.doi.org/10.3165/jjpn.oa.2020.0177.

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15

Pode-Shakked, Naomi, and Benjamin Dekel. "Wilms tumor—a renal stem cell malignancy?" Pediatric Nephrology 26, no. 9 (September 2011): 1535–43. http://dx.doi.org/10.1007/s00467-011-1858-1.

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16

Wang, Hao, Jose A. Gomez, Sabine Klein, Zhiping Zhang, Barbara Seidler, Yanqiang Yang, Jeffrey Schmeckpeper, et al. "Adult Renal Mesenchymal Stem Cell–Like Cells Contribute to Juxtaglomerular Cell Recruitment." Journal of the American Society of Nephrology 24, no. 8 (June 6, 2013): 1263–73. http://dx.doi.org/10.1681/asn.2012060596.

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17

Sorg, R., Z. Özcan, A. Obaje, P. Wernet, and R. Ackermann. "26 RENAL CELL CARCINOMA-DERIVED CELL LINES SHARE CHARACTERISTICS WITH STEM CELLS." European Urology Supplements 6, no. 2 (March 2007): 29. http://dx.doi.org/10.1016/s1569-9056(07)60026-8.

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18

El Aggan, Hayam Abdel Meguid, Mona Abdel Kader Salem, Nahla Mohamed Gamal Farahat, Ahmad Fathy El-Koraie, and Ghaly Abd Al-Rahim Mohammed Kotb. "Role of bone marrow-derived stem cells, renal progenitor cells and stem cell factor in chronic renal allograft nephropathy." Alexandria Journal of Medicine 49, no. 3 (September 1, 2013): 235–47. http://dx.doi.org/10.1016/j.ajme.2013.01.002.

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19

Yang, Juhong, Lei Yang, Shen Li, and Ning Hu. "HGF/c-Met Promote Renal Carcinoma Cancer Stem Cells Enrichment Through Upregulation of Cir-CCDC66." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303381990111. http://dx.doi.org/10.1177/1533033819901114.

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Increasing studies have suggested that circular RNAs play an important function in the process of numerous cancers. We aimed to investigate the possible role of cir-CCDC66 in renal carcinoma cancer. As cancer stem cells are responsible for the renal carcinoma cancer tumor growth and resistance to conventional therapy, we focus on the cir-CCDC66 influence on renal carcinoma cancer stem cells. In this study, we performed experiments in human renal tubular epithelial cell HK2 cells and several renal carcinoma cancer cancer cell lines. The results showed that cir-CCDC66 was upregulated not only in renal carcinoma cancer cancer cell lines but also in cancer stem cell spheres. What’s more, the results showed that cir-CCDC66 enhanced the cancer stem cell enrichment. Further mechanistic studies showed that hepatocyte growth factor/c-Met pathway was activated in cancer stem cell enrichment and responsible for the cir-CCDC66 upregulation. Inhibition of hepatocyte growth factor/c-Met could block cir-CCDC66-induced cancer stem cell enrichment. In conclusion, our research revealed a novel mechanism between hepatocyte growth factor/c-Met/cir-CCDC66 and cancer stem cell enrichment. We verified that cir-CCDC66 could be a promising biomarker and therapy target for renal carcinoma cancer treatment.

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20

Bonsib, Stephen M. "Renal Tubular Cell Recruitment and Plasticity of Hematopoietic Stem Cells." Advances in Anatomic Pathology 11, no. 1 (January 2004): 66–67. http://dx.doi.org/10.1097/00125480-200401000-00009.

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21

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

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According to the cancer stem cell hypothesis tumors are maintained by a cancer stem cell population which is able to initiate and maintain tumors. Tumor-initiating stem cells display stem or progenitor cell properties such as self-renewal and capacity to re-establish tumors that recapitulate the tumor of origin. In this paper, we discuss data relative to the presence of cancer stem cells in human renal carcinoma and their possible origin from normal resident stem cells. The cancer stem cells identified in human renal carcinomas are not derived from the normal CD133+progenitors of the kidney, but rather from a more undifferentiated population that retains a mesenchymal phenotype. This population is able to self-renewal, clonogenicity, and in vivo tumor initiation. Moreover, they retain pluripotent differentiation capability, as they can generate not only the epithelial component of the tumor, but also tumor endothelial cells. This suggests that renal cancer stem cells may contribute to the intratumor vasculogenesis.

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22

Omori, So, Tomoaki Fujioka, Yoko Ono, Hideharu Numaoka, and Yoji Ishida. "REDUCED INTENSITY STEM CELL TRANSPLANTATION FOR METASTATIC RENAL CELL CARCINOMA." Japanese Journal of Urology 95, no. 3 (2004): 583–87. http://dx.doi.org/10.5980/jpnjurol1989.95.583.

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23

Bregni, Marco, Fabio Ciceri, and Jacopo Peccatori. "Allogeneic Stem Cell Transplantation for Metastatic Renal Cell Cancer (RCC)." Journal of Cancer 2 (2011): 347–49. http://dx.doi.org/10.7150/jca.2.347.

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24

Nguyen, Lisa, Lucas-Sebastian Spitzhorn, and James Adjaye. "Constructing an Isogenic 3D Human Nephrogenic Progenitor Cell Model Composed of Endothelial, Mesenchymal, and SIX2-Positive Renal Progenitor Cells." Stem Cells International 2019 (May 2, 2019): 1–11. http://dx.doi.org/10.1155/2019/3298432.

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Urine has become the source of choice for noninvasive renal epithelial cells and renal stem cells which can be used for generating induced pluripotent stem cells. The aim of this study was to generate a 3D nephrogenic progenitor cell model composed of three distinct cell types—urine-derived SIX2-positive renal progenitor cells, iPSC-derived mesenchymal stem cells, and iPSC-derived endothelial cells originating from the same individual. Characterization of the generated mesenchymal stem cells revealed plastic adherent growth and a trilineage differentiation potential to adipocytes, chondrocytes, and osteoblasts. Furthermore, these cells express the typical MSC markers CD73, CD90, and CD105. The induced endothelial cells express the endothelial cell surface marker CD31. Upon combination of urine-derived renal progenitor cells, induced mesenchymal stem cells, and induced endothelial cells at a set ratio, the cells self-condensed into three-dimensional nephrogenic progenitor cells which we refer to as 3D-NPCs. Immunofluorescence-based stainings of sectioned 3D-NPCs revealed cells expressing the renal progenitor cell markers (SIX2 and PAX8), podocyte markers (Nephrin and Podocin), the endothelial marker (CD31), and mesenchymal markers (Vimentin and PDGFR-β). These 3D-NPCs share kidney progenitor characteristics and thus the potential to differentiate into podocytes and proximal and distal tubules. As urine-derived renal progenitor cells can be easily obtained from cells shed into urine, the generation of 3D-NPCs directly from renal progenitor cells instead of pluripotent stem cells or kidney biopsies holds a great potential for the use in nephrotoxicity tests, drug screening, modelling nephrogenesis and diseases.

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25

Roks, Anton J. M. "Angiotensin II, oxidative stress and stem cell therapy: a matter of delicacy." Clinical Science 128, no. 11 (March 17, 2015): 749–50. http://dx.doi.org/10.1042/cs20150082.

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Optimization of stem cell therapy after cardiovascular and renal injury depends on many factors, among which is stem cell donor health. The renin–angiotensin system (RAS) plays an important role in cardiovascular and renal homoeostasis and pathophysiology. It is becoming increasingly clear that the RAS affects the therapeutic performance of stem cells. In this issue of Clinical Science, Kankuri et al. dig deeper into the consequences of excessive angiotensin II signalling and reactive oxygen species (ROS) formation in the stem cell donor, applying a model of regenerative medicine after renal injury.

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26

Wiwanitkit, Viroj. "Stem cell therapy for renal failure: present considerations." European Journal of Clinical and Experimental Medicine 17, no. 3 (2019): 201–2. http://dx.doi.org/10.15584/ejcem.2019.3.0.

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27

Morales, Elvin E. "Renal stem cell reprogramming: Prospects in regenerative medicine." World Journal of Stem Cells 6, no. 4 (2014): 458. http://dx.doi.org/10.4252/wjsc.v6.i4.458.

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28

Yokoo, T., K. Sakurai, T. Ohashi, and T. Kawamura. "Stem Cell Gene Therapy for Chronic Renal Failure." Current Gene Therapy 3, no. 5 (October 1, 2003): 387–94. http://dx.doi.org/10.2174/1566523034578221.

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29

Eirin, Alfonso, and Lilach O. Lerman. "Mesenchymal stem cell treatment for chronic renal failure." Stem Cell Research & Therapy 5, no. 4 (2014): 83. http://dx.doi.org/10.1186/scrt472.

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30

Troxell, Megan L., John P. Higgins, and Neeraja Kambham. "Renal Pathology Associated With Hematopoietic Stem Cell Transplantation." Advances In Anatomic Pathology 21, no. 5 (September 2014): 330–40. http://dx.doi.org/10.1097/pap.0000000000000034.

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31

&NA;. "Stem cell transplantation feasible for metastatic renal cancer?" Inpharma Weekly &NA;, no. 1256 (September 2000): 16. http://dx.doi.org/10.2165/00128413-200012560-00038.

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32

Choi, Soo Jeong, Jin Kuk Kim, and Seung Duk Hwang. "Mesenchymal stem cell therapy for chronic renal failure." Expert Opinion on Biological Therapy 10, no. 8 (July 13, 2010): 1217–26. http://dx.doi.org/10.1517/14712598.2010.500284.

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33

Tsuji, Kenji, and Shinji Kitamura. "Trophic Factors from Tissue Stem Cells for Renal Regeneration." Stem Cells International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/537204.

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Stem cell therapies against renal injury have been advancing. The many trials for renal regeneration are reported to be effective in many kinds of renal injury models. Regarding the therapeutic mechanism, it is believed that stem cells contribute to make regeneration via not only direct stem cell differentiation in the injured space but also indirect effect via secreted factors from stem cells. Direct differentiation from stem cells to renal composed cells has been reported. They differentiate to renal composed cells and make functions. However, regarding renal regeneration, stem cells are discussed to secrete many kinds of growth factors, cytokines, and chemokines in paracrine or autocrine manner, which protect against renal injury, too. In addition, it is reported that stem cells have the ability to communicate with nearby cells via microvesicle-related RNA and proteins. Taken together from many reports, many secreted factors from stem cells were needed for renal regeneration orchestrally with harmony. In this review, we focused on the effects and insights of stem cells and regenerative factors from stem cells.

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34

Huang, Bin, Yi Jun Huang, Zhi Jun Yao, Xu Chen, Sheng Jie Guo, Xiao Peng Mao, Dao Hu Wang, Jun Xing Chen, and Shao Peng Qiu. "Cancer Stem Cell-Like Side Population Cells in Clear Cell Renal Cell Carcinoma Cell Line 769P." PLoS ONE 8, no. 7 (July 11, 2013): e68293. http://dx.doi.org/10.1371/journal.pone.0068293.

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35

Pan, Binbin, and Guoping Fan. "Stem cell-based treatment of kidney diseases." Experimental Biology and Medicine 245, no. 10 (April 11, 2020): 902–10. http://dx.doi.org/10.1177/1535370220915901.

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Kidney dysfunction, including chronic kidney disease and acute kidney injury, is a globally prevalent health problem. However, treatment regimens are still lacking, especially for conditions involving kidney fibrosis. Stem cells hold great promise in the treatment of chronic kidney disease and acute kidney injury, but success has been hampered by insufficient incorporation of the stem cells in the injured kidney. Thus, new approaches for the restoration of kidney function after acute or chronic injury have been explored. Recently, kidney organoids have emerged as a useful tool in the treatment of kidney diseases. In this review, we discuss the mechanisms and approaches of cell therapy in acute kidney injury and chronic kidney disease, including diabetic kidney disease and lupus nephritis. We also summarize the potential applications of kidney organoids in the treatment of kidney diseases. Impact statement Stem cells hold great promise in regenerative medicine. Pluripotent stem cells have been differentiated into kidney organoids to understand human kidney development and to dissect renal disease mechanisms. Meanwhile, recent studies have explored the treatment of kidney diseases using a variety of cells, including mesenchymal stem cells and renal derivatives. This mini-review discusses the diverse mechanisms underlying current renal disease treatment via stem cell therapy. We postulate that clinical applications of stem cell therapy for kidney diseases can be readily achieved in the near future.

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36

Rota, Cinzia, Marina Morigi, and Barbara Imberti. "Stem Cell Therapies in Kidney Diseases: Progress and Challenges." International Journal of Molecular Sciences 20, no. 11 (June 7, 2019): 2790. http://dx.doi.org/10.3390/ijms20112790.

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The prevalence of renal diseases is emerging as a public health problem. Despite major progress in supportive therapy, mortality rates among patients remain high. In an attempt to find innovative treatments to stimulate kidney regeneration, stem cell-based technology has been proposed as a potentially promising strategy. Here, we summarise the renoprotective potential of pluripotent and adult stem cell therapy in experimental models of acute and chronic kidney injury and we explore the different mechanisms at the basis of stem cell-induced kidney regeneration. Specifically, cell engraftment, incorporation into renal structures, or paracrine activities of embryonic or induced pluripotent stem cells as well as mesenchymal stem cells and renal precursors are analysed. We also discuss the relevance of stem cell secretome-derived bioproducts, including soluble factors and extracellular vesicles, and the option of using them as cell-free therapy to induce reparative processes. The translation of the experimental results into clinical trials is also addressed, highlighting the safety and feasibility of stem cell treatments in patients with kidney injury.

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37

Hong, Dae Sik, Seongkyu Park, Jong-Ho Won, Chan Kyu Kim, Sang Chul Lee, Kyu Taeg Lee, Sang Byung Bae, and Hee Sook Park. "The Effect of Mesenchymal Stem Cells as a Cell Therapy in Renal Ischemia." Blood 112, no. 11 (November 16, 2008): 4756. http://dx.doi.org/10.1182/blood.v112.11.4756.4756.

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Abstract Introduction: The most commonly used therapeutic targets in nephrology are the reduction of injury, the delay of progression, or renal replacement therapy. Many animal and human studies demonstrated the role of stem cells in repair and regenerations of kidney. Mesenchymal stem cells (MSCs) have shown to improve outcome of acute renal injury models. It is controversial whether MSCs can reduce injury following a toxic/ischemic event and delay renal failure in chronic kidney disease. We evaluated the hypothesis that the treatment with MSCs could improve renal function and attenuate injury in chronic renal failure (CRF). Materials and methods: Sprague-Dawley female rats (8 weeks old, 182.2 ± 7.2g) were underwent modified 5/6 nephrectomy. Rats in the MSC group received an injection of MSCs (1 × 106 cells) via tail vein 1 day after nephrectomy. Blood and urine samples were collected after 7 days and every month thereafter. The kidneys of rats were removed for histologic evaluation after 24-hr urine collection and blood sampling. The Y-chromosome stain using fluorescent in situ hybridization was performed to verify the presence of male MSCs in the kidney of female recipients. Results: No significant differences in blood urea nitrogen and creatinine concentration were observed between MSC group and untreated CRF group. However, the weight gain and creatinine clearance in the MSC group were greater than those of the CRF group. Proteinuria in the MSC group was less after 4 months. Y chromosome was detected in the kidney of MSC group. Although no significances were observed between two groups, the histologic analysis suggests that MSCs have positive effect against glomerulosclerosis. Conclusions: These results suggest that MSCs help preserve renal function and attenuate renal injury in CRF.

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38

Sawinski, Deirdre. "Kidney Disease Associated with Hematopoietic Stem Cell Transplant." Journal of Onco-Nephrology 1, no. 1 (January 2017): 24–29. http://dx.doi.org/10.5301/jo-n.5000011.

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Hematopoietic stem cell transplantation in the USA is growing, and stem cell transplant recipients are at risk for both acute and chronic renal injury. Some etiologies of acute kidney injury are shared with the general population, such as prerenal azotemia and acute tubular necrosis, while others are unique to aspects of the stem cell procedure and include hepatic veno-occlusive disease and BK cystitis. Long-term hematopoietic stem cell transplant survivors are also at increased risk for chronic kidney disease, and important etiologies include calcineurin inhibitor toxicity, nephrotic syndrome, and thrombotic microangiopathy. Stem cell transplant patient survival on chronic dialysis is poor, but well-selected patients can have excellent outcomes with renal transplantation.

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39

Stokman, Geurt, Jaklien C. Leemans, Nike Claessen, Jan J. Weening, and Sandrine Florquin. "Hematopoietic Stem Cell Mobilization Therapy Accelerates Recovery of Renal Function Independent of Stem Cell Contribution." Journal of the American Society of Nephrology 16, no. 6 (April 13, 2005): 1684–92. http://dx.doi.org/10.1681/asn.2004080678.

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40

Gassenmaier, Maximilian, Dong Chen, Alexander Buchner, Lynette Henkel, Matthias Schiemann, Brigitte Mack, Dolores J. Schendel, Wolfgang Zimmermann, and Heike Pohla. "CXC Chemokine Receptor 4 is Essential for Maintenance of Renal cell Carcinoma-Initiating Cells and Predicts Metastasis." STEM CELLS 31, no. 8 (August 2013): 1467–76. http://dx.doi.org/10.1002/stem.1407.

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41

CZARNECKA, ANNA M., WOJCIECH SOLAREK, ANNA KORNAKIEWICZ, and CEZARY SZCZYLIK. "Tyrosine kinase inhibitors target cancer stem cells in renal cell cancer." Oncology Reports 35, no. 3 (December 24, 2015): 1433–42. http://dx.doi.org/10.3892/or.2015.4514.

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Lucarelli, Giuseppe, Vanessa Galleggiante, Monica Rutigliano, Antonio Vavallo, Pasquale Ditonno, and Michele Battaglia. "Isolation and Characterization of Cancer Stem Cells in Renal Cell Carcinoma." Urologia Journal 82, no. 1 (November 25, 2014): 46–53. http://dx.doi.org/10.5301/uro.5000099.

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Hu, Junping, Qing Zhu, Pin-Lan Li, Weili Wang, Fan Yi, and Ningjun Li. "Stem Cell Conditioned Culture Media Attenuated Albumin-Induced Epithelial-Mesenchymal Transition in Renal Tubular Cells." Cellular Physiology and Biochemistry 35, no. 5 (2015): 1719–28. http://dx.doi.org/10.1159/000373984.

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Background: Proteinuria-induced epithelial-mesenchymal transition (EMT) plays an important role in progressive renal tubulointerstitial fibrosis in chronic renal disease. Stem cell therapy has been used for different diseases. Stem cell conditioned culture media (SCM) exhibits similar beneficial effects as stem cell therapy. The present study tested the hypothesis that SCM inhibits albumin-induced EMT in cultured renal tubular cells. Methods: Rat renal tubular cells were treated with/without albumin (20 µmg/ml) plus SCM or control cell media (CCM). EMT markers and inflammatory factors were measured by Western blot and fluorescent images. Results: Albumin induced EMT as shown by significant decreases in levels of epithelial marker E-cadherin, increases in mesenchymal markers fibroblast-specific protein 1 and a-smooth muscle actin, and elevations in collagen I. SCM inhibited all these changes. Meanwhile, albumin induced NF-κB translocation from cytosol into nucleus and that SCM blocked the nuclear translocation of NF-κB. Albumin also increased the levels of pro-inflammatory factor monocyte chemoattractant protein-1 (MCP)-1 by nearly 30 fold compared with control. SCM almost abolished albumin-induced increase of MCP-1. Conclusion: These results suggest that SCM attenuated albumin-induced EMT in renal tubular cells via inhibiting activation of inflammatory factors, which may serve as a new therapeutic approach for chronic kidney diseases.

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Liu, Yang, and Sydney C. W. Tang. "Recent Progress in Stem Cell Therapy for Diabetic Nephropathy." Kidney Diseases 2, no. 1 (December 5, 2015): 20–27. http://dx.doi.org/10.1159/000441913.

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Background: Diabetic nephropathy (DN) represents the leading cause of end-stage renal disease. Current therapeutic strategies for DN are very limited, and none of them can stop end-stage renal disease progression. Stem cell-based therapy showed encouraging outcomes in kidney disease, including experimental DN. Summary: Both podocytes and proximal tubular epithelial cells play key roles in the pathogenesis of DN and, accordingly, could be regarded as treatment targets. Multiple kinds of stem cells contribute to the regeneration of the injured kidney, including embryonic stem cells (ESCs), mesenchymal stem cells, and induced pluripotent stem cells (iPSCs). Stem cells exert reparatory effects mainly by homing to injured sites, directing differentiation, paracrine action, and immunoregulation. However, poor survival after transplantation under diabetic conditions and unsatisfactory animal models of advanced DN are major obstacles for achieving an efficacious therapeutic effect from stem cell transplantation. Recently, remarkable progress has been made both in the direct differentiation of human ESCs and iPSCs into renal cells and in the generation of tissue- and patient-specific iPSCs, offering a powerful tool to investigate DN mechanisms and to identify the ideal candidate cell for future clinical application. Key Message: This review provides updated information on recent progress and limitations of stem cell-based therapy for DN.

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Roigas, Jan, Manfred Johannsen, Martin Ringsdorf, and Gero Massenkeil. "Allogeneic stem cell transplantation for patients with metastatic renal cell carcinoma." Expert Review of Anticancer Therapy 6, no. 10 (October 2006): 1449–58. http://dx.doi.org/10.1586/14737140.6.10.1449.

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Yun, Tak, Keun-Wook Lee, Eun-Gi Song, Im-Il Na, Hyun-Chun Shin, Sung-Soo Yoon, Seon-Yang Park, et al. "Non-myeloablative allogeneic stem cell transplantation for metastatic renal cell carcinoma." Clinical Transplantation 21, no. 3 (May 2007): 337–43. http://dx.doi.org/10.1111/j.1399-0012.2007.00646.x.

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Bahnson, R., H. Shawn Hu, and Nicholas J. Vogelzang. "Non-myeloablative allogeneic stem cell transplantation for metastatic renal cell carcinoma." Urologic Oncology: Seminars and Original Investigations 21, no. 1 (January 2003): 79–81. http://dx.doi.org/10.1016/s1078-1439(01)00181-8.

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RINI, BRIAN I., TODD M. ZIMMERMAN, THOMAS F. GAJEWSKI, WALTER M. STADLER, and NICHOLAS J. VOGELZANG. "ALLOGENEIC PERIPHERAL BLOOD STEM CELL TRANSPLANTATION FOR METASTATIC RENAL CELL CARCINOMA." Journal of Urology 165, no. 4 (April 2001): 1208–9. http://dx.doi.org/10.1016/s0022-5347(05)66479-8.

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Satoh, Makoto, Koichi Miyamura, Minami Yamada, Shigeto Ishidoya, Richard W. Childs, and Yoichi Arai. "Haploidentical, non-myeloablative stem-cell transplantation for advanced renal-cell carcinoma." Lancet Oncology 5, no. 2 (February 2004): 125–26. http://dx.doi.org/10.1016/s1470-2045(04)01387-7.

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Park, Eun Jae, Hyung Suk Kim, Yu Jeong Kang, Hye Jin Lee, Hye Won Jun, Hong Kyung Lee, Jin Tae Hong, Youngsoo Kim, and Sang-Bae Han. "Effect of mesenchymal stem cell in adriamycin-induced renal nephropathy." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 79.25. http://dx.doi.org/10.4049/jimmunol.204.supp.79.25.

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Abstract Mesenchymal stem cells (MSCs) are multi-potent progenitor cells able to differentiate into osteoblasts, chondrocytes, and adipocytes. MSCs secrete various soluble factors that are advantageous for tissue repair, anti-apoptosis, anti-fibrosis, and immunomodulation. Recently, MSCs improve the renal inflammation in adriamycin (ADR)-, adenine-, and cisplatin-induced animal model, but the mechanisms underlying their efficacy are unclear. In this study, we examined effect of MSCs in ADR-induced renal nephropathy. MSCs prolonged survival, restored body weight, and decreased serum creatinine and proteinuria levels in ADR-induced animal model. MSCs also inhibited renal fibrosis and podocyte damage by decreasing the expression of fibronectin, α-smooth muscle actin, and collagen 1α1. MSCs inhibited renal inflammation by decreasing the expression of CCL4, CCL7, CCL19, IFN-α/β, TNF-α, TGF-β and chitinase 3-like 1. Taken together, our data suggest that MSCs improve renal injury by decreasing inflammatory factor in ADR-induced nephropathy.

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