Journal articles: 'Kidney cells'

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Yokote, Shinya, Shuichiro Yamanaka, and Takashi Yokoo. "De NovoKidney Regeneration with Stem Cells." Journal of Biomedicine and Biotechnology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/453519.

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Recent studies have reported on techniques to mobilize and activate endogenous stem-cells in injured kidneys or to introduce exogenous stem cells for tissue repair. Despite many recent advantages in renal regenerative therapy, chronic kidney disease (CKD) remains a major cause of morbidity and mortality and the number of CKD patients has been increasing. When the sophisticated structure of the kidneys is totally disrupted by end stage renal disease (ESRD), traditional stem cell-based therapy is unable to completely regenerate the damaged tissue. This suggests that whole organ regeneration may be a promising therapeutic approach to alleviate patients with uncured CKD. We summarize here the potential of stem-cell-based therapy for injured tissue repair andde novowhole kidney regeneration. In addition, we describe the hurdles that must be overcome and possible applications of this approach in kidney regeneration.

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Law, Becker M. P., Ray Wilkinson, Xiangju Wang, Katrina Kildey, Kurt Giuliani, Kenneth W. Beagley, Jacobus Ungerer, Helen Healy, and Andrew J. Kassianos. "Human Tissue-Resident Mucosal-Associated Invariant T (MAIT) Cells in Renal Fibrosis and CKD." Journal of the American Society of Nephrology 30, no. 7 (June 11, 2019): 1322–35. http://dx.doi.org/10.1681/asn.2018101064.

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BackgroundMucosal-associated invariant T (MAIT) cells represent a specialized lymphocyte population associated with chronic inflammatory disorders. Little is known, however, about MAIT cells in diseases of the kidney, including CKD.MethodsTo evaluate MAIT cells in human native kidneys with tubulointerstitial fibrosis, the hallmark of CKD, we used multicolor flow cytometry to identify, enumerate, and phenotype such cells from human kidney tissue biopsy samples, and immunofluorescence microscopy to localize these cells. We cocultured MAIT cells and human primary proximal tubular epithelial cells (PTECs) under hypoxic (1% oxygen) conditions to enable examination of mechanistic tubulointerstitial interactions.ResultsWe identified MAIT cells (CD3+ TCR Vα7.2+ CD161hi) in healthy and diseased kidney tissues, detecting expression of tissue-resident markers (CD103/CD69) on MAIT cells in both states. Tissue samples from kidneys with tubulointerstitial fibrosis had significantly elevated numbers of MAIT cells compared with either nonfibrotic samples from diseased kidneys or tissue samples from healthy kidneys. Furthermore, CD69 expression levels, also an established marker of lymphocyte activation, were significantly increased on MAIT cells from fibrotic tissue samples. Immunofluorescent analyses of fibrotic kidney tissue identified MAIT cells accumulating adjacent to PTECs. Notably, MAIT cells activated in the presence of human PTECs under hypoxic conditions (modeling the fibrotic microenvironment) displayed significantly upregulated expression of CD69 and cytotoxic molecules perforin and granzyme B; we also observed a corresponding significant increase in PTEC necrosis in these cocultures.ConclusionsOur findings indicate that human tissue-resident MAIT cells in the kidney may contribute to the fibrotic process of CKD via complex interactions with PTECs.

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Valiño-Rivas, Lara, Leticia Cuarental, Mateo Agustin, Holger Husi, Pablo Cannata-Ortiz, Ana B. Sanz, Harald Mischak, Alberto Ortiz, and Maria Dolores Sanchez-Niño. "MAGE genes in the kidney: identification of MAGED2 as upregulated during kidney injury and in stressed tubular cells." Nephrology Dialysis Transplantation 34, no. 9 (December 11, 2018): 1498–507. http://dx.doi.org/10.1093/ndt/gfy367.

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Abstract Background Mutations in Melanoma Antigen-encoding Gene D2 (MAGED2) promote tubular dysfunction, suggesting that MAGE proteins may play a role in kidney pathophysiology. We have characterized the expression and regulation of MAGE genes in normal kidneys and during kidney disease. Methods The expression of MAGE genes and their encoded proteins was explored by systems biology multi-omics (kidney transcriptomics and proteomics) in healthy adult murine kidneys and following induction of experimental acute kidney injury (AKI) by a folic acid overdose. Changes in kidney expression during nephrotoxic AKI were validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blot and immunohistochemistry. Factors regulating gene expression were studied in cultured tubular cells. Results Five MAGE genes (MAGED1, MAGED2, MAGED3, MAGEH1, MAGEE1) were expressed at the mRNA level in healthy adult mouse kidneys, as assessed by RNA-Seq. Additionally, MAGED2 was significantly upregulated during experimental AKI as assessed by array transcriptomics. Kidney proteomics also identified MAGED2 as upregulated during AKI. The increased kidney expression of MAGED2 mRNA and protein was confirmed by qRT-PCR and western blot, respectively, in murine folic acid- and cisplatin-induced AKI. Immunohistochemistry located MAGED2 to tubular cells in experimental and human kidney injury. Tubular cell stressors [serum deprivation and the inflammatory cytokine tumour necrosis factor-like weak inducer of apoptosis (TWEAK)] upregulated MAGED2 in cultured tubular cells. Conclusions MAGED2 is upregulated in tubular cells in experimental and human kidney injury and is increased by stressors in cultured tubular cells. This points to a role of MAGED2 in tubular cell injury during kidney disease that should be dissected by carefully designed functional approaches.

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Baban, Babak, Jun Yao Liu, and Mahmood S. Mozaffari. "Aryl hydrocarbon receptor agonist, leflunomide, protects the ischemic-reperfused kidney: role of Tregs and stem cells." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 11 (December 1, 2012): R1136—R1146. http://dx.doi.org/10.1152/ajpregu.00315.2012.

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The aryl hydrocarbon receptor (AHR) has emerged as a major modulator of inflammatory processes. We tested the hypothesis that AHR activation protects the ischemic-reperfused kidney in association with the suppression of the inflammatory response. Accordingly, male mice were treated with the nondioxin AHR agonist, leflunomide (40 mg/kg ip); vehicle-treated animals served as controls. Thereafter, the right kidney was subjected to an ischemia (45 min)-reperfusion (4 h) insult, while the left kidney served as a sham control. Renal cells prepared from ischemic-reperfused kidneys of leflunomide-treated mice displayed preservation of mitochondrial membrane potential (Ψm) and decreased apoptosis and necrosis compared with vehicle-treated ischemic-reperfused kidneys. Leflunomide treatment increased regulatory T cells (Tregs; forkhead box P3+) and IL-10-positive cells but reduced IL-17- and IL-23-expressing cells in both the peripheral blood and kidney cells, indicative of down-regulation of inflammatory responses. Leflunomide treatment also increased mobilization of stems cells subsets (i.e., mesenchymal and hematopoietic stem cells and endothelial progenitor cells) in the peripheral blood and promoted their recruitment into the ischemic-reperfused kidney. Collectively, the results indicate that AHR stimulation may represent a novel renoprotective mechanism likely involving mobilization and recruitment of Tregs and stem cells into the damaged kidney.

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Kim, Bo Hye, Do Yeon Kim, Yejin Ahn, Eun Ji Lee, Hyunjoo Park, Meeyoung Park, and Jong Hoon Park. "Semaphorin-3C Is Upregulated in Polycystic Kidney Epithelial Cells and Inhibits Angiogenesis of Glomerular Endothelial Cells." American Journal of Nephrology 51, no. 7 (2020): 556–64. http://dx.doi.org/10.1159/000508263.

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Background: Polycystic kidney disease (PKD) is a hereditary disease characterized by cyst formation in the kidneys bilaterally. It has been observed that semaphorin-3C (SEMA3C) is overexpressed in polycystic kidney epithelial cells. It is hypothesized that upregulated SEMA3C would contribute to survival of polycystic kidney epithelial cells. Furthermore, as the kidney is a highly vascularized organ, the secreted SEMA3C from PKD epithelial cells will affect glomerular endothelial cells (GECs) in a paracrine manner. Methods: To evaluate the effect of SEMA3C on renal cells, siSEMA3C-treated PKD epithelial cells were used for further analysis, and GECs were exposed to recombinant SEMA3C (rSEMA3C). Also, co-culture and treatment of conditioned media were employed to confirm whether PKD epithelial cells could influence on GECs via SEMA3C secretion. Results: SEMA3C knockdown reduced proliferation of PKD epithelial cells. In case of GECs, exposure to rSEMA3C decreased angiogenesis, which resulted from suppressed migratory ability not cell proliferation. Conclusions: This study indicates that SEMA3C is the aggravating factor in PKD. Thus, it is proposed that targeting SEMA3C can be effective to mitigate PKD.

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Zhang, Zhu-Xu, Jifu Jiang, Xuyan Huang, Ziqin Yin, Weihua Liu, Bertha Garcia, and Anthony Jevnikar. "NK cells mediate chronic kidney allograft injury (169.26)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 169.26. http://dx.doi.org/10.4049/jimmunol.186.supp.169.26.

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Abstract Chronic allograft injury remains the leading cause of kidney graft loss after transplantation and no-specific therapy currently exist. We have recently demonstrated that NK cells can kill syngeneic tubular epithelial cells (TEC) and participate in kidney ischemia-reperfusion injury. In this study, we investigated the capacity of NK cells to mediate kidney injury in transplantion. C57BL/6 (B6, H-2b) kidneys were transplanted into nephrectomized F1 (B6 x BALB/c, CB6F1) mice. Serum creatinine levels increased from baseline (22+5 uM, n=8) to 38±6 uM (n=6, P<0.001) at 60 days post transplant, demonstrating a clear loss of kidney function. Infiltrates and low grade renal tubular cell injury were consistently present in B6-to-CB6F1transplants suggesting a non T cell pathway. This was supported by results using a B6-Rag-/--to- CB6F1Rag-/- (B6Rag-/-xBALB/cRag-/-) F1 kidney transplant that eliminates T and B cell but not NK cell participation. Similar levels of kidney dysfunction (creatinine: 34+8 uM, n=6, p<0.01) and histological injury were observed 65 days post transplant. Finally depletion of NK cells prevented kidney injury (25±6 vs 34+8 uM in no antibody injection, n=6, p<0.05) as well as improved histology. In conclusion, these data demonstrate for the first time a critical role for NK cells in mediating chronic kidney injury, which is independent of T and B cells. NK cells are newly appreciated and formidable effectors to chronic kidney injury and graft loss.

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Jang, Hee-Seong, Jee In Kim, Sang Jun Han, and Kwon Moo Park. "Recruitment and subsequent proliferation of bone marrow-derived cells in the postischemic kidney are important to the progression of fibrosis." American Journal of Physiology-Renal Physiology 306, no. 12 (June 15, 2014): F1451—F1461. http://dx.doi.org/10.1152/ajprenal.00017.2014.

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Acute kidney injury (AKI) is an independent risk factor of the development of chronic kidney disease. Kidney fibrosis is a typical feature of chronic kidney disease and is characterized as an expansion of the interstitium due to increases in extracellular matrix molecules and interstitial cells caused by accumulations of extrarenal cells and by the proliferation or differentiation of intrarenal cells. However, the role of bone marrow-derived cells (BMDCs) in AKI-induced kidney fibrosis remains to be defined. Here, we investigated the role of BMDCs in kidney fibrosis after ischemia-reperfusion injury (IRI)-induced AKI in green fluorescent protein (GFP)-expressing bone marrow chimeric mice. IRI resulted in severe fibrotic changes in kidney tissues and dramatically increased interstitial cell numbers. Furthermore, GFP-expressing BMDCs accounted for >80% of interstitial cells in fibrotic kidneys. Interstitial GFP-expressing cells expressed α-smooth muscle actin (a myofibroblast marker), fibroblast-specific protein-1 (a fibroblast marker), collagen type III, and F4/80 (a macrophage marker). Over 20% of interstitial cells were bromodeoxyuridine-incorporating (proliferating) cells, and of these, 80% cells were GFP-expressing BMDCs. Daily treatment of IRI mice with apocynin (a NADPH oxidase inhibitor that functions as an antioxidant) from the day after surgery until euthanization slightly inhibited these changes with a small reduction of fibrosis. Taken together, our findings show that BMDCs make a major contribution to IRI-induced fibrosis due to their infiltration, subsequent differentiation, and proliferation in injured kidneys, suggesting that BMDCs be considered an important target for the treatment of kidney fibrosis.

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Du, Ao-Ling, Dan Liu, Wen-Hui Zhang, and Sheng-Hua Chen. "The Development of Endothelial Cells in Revascularization of Blood Vessels in Kidney Scaffolds." Journal of Biomaterials and Tissue Engineering 9, no. 9 (September 1, 2019): 1167–78. http://dx.doi.org/10.1166/jbt.2019.2122.

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The kidney is an important organ of the human body. However, the morbidity and mortality of endstage renal disease (ESRD) have been increasing year after year. Currently, the best treatment for ESRD is kidney transplantation. However, the extreme lack of donor kidneys causes many people to die in queues waiting for a kidney source. Fortunately, recent advances in bioengineering, stem cells, and regenerative medicine have raised new hopes that there may be a viable way to form new transplantable kidneys. Kidney scaffolds have had all cellular components removed, but retain intact extracellular matrix (ECM). However, there are still many challenges, such as thrombosis, before this potential therapy can be used in clinical patients. Vascularization is a key part of the success of tissue engineering and a vital factor for maintaining organ function. Endothelial cells are crucial in the formation of vessels in kidney scaffolds. The primary challenge of recellularized kidney scaffolds is to re-endothelialize the renal vasculature. Unfortunately, until now, there have been no report demonstrating successful vascularization in bioengineering kidney scaffolds, such as uniform endothelial cell coverage of vascular walls, no thrombosis and blood flow maintenance for a long time. Hence, this review mainly discusses the development of endothelial cells in the re-endothelialized vasculature of renal scaffolds.

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Salcido-Ochoa, Francisco, Susan Swee-Shan Hue, Doreen Haase, Jason Chon Jun Choo, Nurhashikin Yusof, Reiko Lixiang Li, John Carson Allen, Jabed Iqbal, Alwin Hwai Liang Loh, and Olaf Rotzschke. "Analysis of T Cell Subsets in Adult Primary/Idiopathic Minimal Change Disease: A Pilot Study." International Journal of Nephrology 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/3095425.

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Aim. To characterise infiltrating T cells in kidneys and circulating lymphocyte subsets of adult patients with primary/idiopathic minimal change disease. Methods. In a cohort of 9 adult patients with primary/idiopathic minimal change recruited consecutively at disease onset, we characterized (1) infiltrating immune cells in the kidneys using immunohistochemistry and (2) circulating lymphocyte subsets using flow cytometry. As an exploratory analysis, association of the numbers and percentages of both kidney-infiltrating immune cells and the circulating lymphocyte subsets with kidney outcomes including deterioration of kidney function and proteinuria, as well as time to complete clinical remission up to 48 months of follow-up, was investigated. Results. In the recruited patients with primary/idiopathic minimal change disease, we observed (a) a dominance of infiltrating T helper 17 cells and cytotoxic cells, comprising cytotoxic T cells and natural killer cells, over Foxp3+ Treg cells in the renal interstitium; (b) an increase in the circulating total CD8+ T cells in peripheral blood; and (c) an association of some of these parameters with kidney function and proteinuria. Conclusions. In primary/idiopathic minimal change disease, a relative numerical dominance of effector over regulatory T cells can be observed in kidney tissue and peripheral blood. However, larger confirmatory studies are necessary.

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Ko, Gang Jee, Douglas Linfert, Hye Ryoun Jang, Elizabeth Higbee, Tonya Watkins, Chris Cheadle, Manchang Liu, Lorraine Racusen, Dmitry N. Grigoryev, and Hamid Rabb. "Transcriptional analysis of infiltrating T cells in kidney ischemia-reperfusion injury reveals a pathophysiological role for CCR5." American Journal of Physiology-Renal Physiology 302, no. 6 (March 15, 2012): F762—F773. http://dx.doi.org/10.1152/ajprenal.00335.2011.

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Although T cells have been shown to play a direct role in kidney ischemia-reperfusion injury (IRI), little is known about the underlying mechanisms. We hypothesized that studying the transcriptional responses in kidney-infiltrating T cells would help elucidate novel therapeutic targets for kidney IRI. Unilateral renal pedicle clamping for 45 min was performed in male C57BL/6 mice, and CD3+ T cells were isolated from the kidney and purified. Transcriptional activities of T cell were measured by array-based PCR compared between ischemic kidneys and contralateral nonischemic kidneys. Among total of 89 genes analyzed, 24, 22, 24, and 37 genes were significantly changed at 6 h, day 3, day 10, and day 28 after IRI. Genes associated with cytokines, chemokines, and costimulatory molecules were upregulated. Pathway analysis identified CC motif chemokine receptor 5 (CCR5) as a candidate pathophysiological pathway. CCR5 upregulation was validated at the protein level, and CCR5 blockade improved renal function after kidney IRI. Using discovery techniques to identify transcriptional responses in purified kidney-infiltrating cells enabled the elucidation of novel mechanisms and therapeutic targets for IRI.

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Rambe, Tri Putra Rahmad Ramadani, and M. Hidayat Surya Atmaja. "Kidney cancer with complications in Dr. Soetomo Regional Public Hospital, Surabaya, Indonesia." International journal of health sciences 6, S1 (March 22, 2022): 1832–41. http://dx.doi.org/10.53730/ijhs.v6ns1.4944.

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Kidney cancer is a disease in which kidney cells become malignant and grow uncontrollably, forming a mass or tumor. Before discussing further kidney cancer, it is important to briefly know the kidneys. The kidneys are two bean-shaped organs located in the lower abdomen on the left and right of the spine. The primary function of the kidneys is to excrete and excrete water, salt, and other unnecessary substances and turn them into urine. The urine collects in the renal pelvis (the funnel-shaped part of each kidney), then travels to the ureters (the tube between the kidneys and bladder), and finally to the bladder, where it is stored before urination. Another function of the kidneys is to help control blood pressure by making the renin hormone and forming red blood cells by forming the hormone erythropoietin. In the United States, an estimated 76,080 adults were diagnosed with kidney cancer, and 13,780 of them died from the disease in 2021. Meanwhile, a total of 2,394 new cases of kidney cancer were found in Indonesia with 1,358 total deaths in 2020. More than half of patients with kidney cancer are diagnosed at an advanced stage.

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Kelley, Rusty, Eric S. Werdin, Andrew T. Bruce, Sumana Choudhury, Shay M. Wallace, Roger M. Ilagan, Bryan R. Cox, et al. "Tubular cell-enriched subpopulation of primary renal cells improves survival and augments kidney function in rodent model of chronic kidney disease." American Journal of Physiology-Renal Physiology 299, no. 5 (November 2010): F1026—F1039. http://dx.doi.org/10.1152/ajprenal.00221.2010.

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Established chronic kidney disease (CKD) may be identified by severely impaired renal filtration that ultimately leads to the need for dialysis or kidney transplant. Dialysis addresses only some of the sequelae of CKD, and a significant gap persists between patients needing transplant and available organs, providing impetus for development of new CKD treatment modalities. Some postulate that CKD develops from a progressive imbalance between tissue damage and the kidney's intrinsic repair and regeneration processes. In this study we evaluated the effect of kidney cells, delivered orthotopically by intraparenchymal injection to rodents 4–7 wk after CKD was established by two-step 5/6 renal mass reduction (NX), on the regeneration of kidney function and architecture as assessed by physiological, tissue, and molecular markers. A proof of concept for the model, cell delivery, and systemic effect was demonstrated with a heterogeneous population of renal cells (UNFX) that contained cells from all major compartments of the kidney. Tubular cells are known contributors to kidney regeneration in situ following acute injury. Initially tested as a control, a tubular cell-enriched subpopulation of UNFX (B2) surprisingly outperformed UNFX. Two independent studies (3 and 6 mo in duration) with B2 confirmed that B2 significantly extended survival and improved renal filtration (serum creatinine and blood urea nitrogen). The specificity of B2 effects was verified by direct comparison to cell-free vehicle controls and an equivalent dose of non-B2 cells. Quantitative histological evaluation of kidneys at 6 mo after treatment confirmed that B2 treatment reduced severity of kidney tissue pathology. Treatment-associated reduction of transforming growth factor (TGF)-β1, plasminogen activator inhibitor (PAI)-1, and fibronectin (FN) provided evidence that B2 cells attenuated canonical pathways of profibrotic extracellular matrix production.

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Munk, Anders, Christina Søndergaard Duvald, Michael Pedersen, Stine Lohmann, Anna Krarup Keller, Bjarne Kuno Møller, Steffen Ringgaard, Niels Henrik Buus, Bente Jespersen, and Marco Eijken. "Dosing Limitation for Intra-Renal Arterial Infusion of Mesenchymal Stromal Cells." International Journal of Molecular Sciences 23, no. 15 (July 27, 2022): 8268. http://dx.doi.org/10.3390/ijms23158268.

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The immunomodulatory and regenerative properties of mesenchymal stromal cells (MSCs) make MSC therapy a promising therapeutic strategy in kidney disease. A targeted MSC administration via the renal artery offers an efficient delivery method with limited spillover to other organs. Although local administration alleviates safety issues with MSCs in systemic circulation, it introduces new safety concerns in the kidneys. In a porcine model, we employed intra-renal arterial infusion of ten million allogenic adipose tissue-derived MSCs. In order to trigger any potential adverse events, a higher dose (hundred million MSCs) was also included. The kidney function was studied by magnetic resonance imaging after the MSC infusion and again at two weeks post-treatment. The kidneys were assessed by single kidney glomerular filtration rate (skGFR) measurements, histology and inflammation, and fibrosis-related gene expression. None of the measured parameters were affected immediately after the administration of ten million MSCs, but the administration of one hundred million MSCs induced severe adverse events. Renal perfusion was reduced immediately after MSC administration which coincided with the presence of microthrombi in the glomeruli and signs of an instant blood-mediated inflammatory reaction. At two weeks post-treatment, the kidneys that were treated with one hundred million MSCs showed reduced skGFR, signs of tissue inflammation, and glomerular and tubular damage. In conclusions, the intra-renal administration of ten million MSCs is well-tolerated by the porcine kidney. However, higher concentrations (one hundred million MSCs) caused severe kidney damage, implying that very high doses of intra-renally administered MSCs should be undertaken with caution.

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Veys, Koenraad, Sante Princiero Berlingerio, Dries David, Tjessa Bondue, Katharina Held, Ahmed Reda, Martijn van den Broek, et al. "Urine-Derived Kidney Progenitor Cells in Cystinosis." Cells 11, no. 7 (April 6, 2022): 1245. http://dx.doi.org/10.3390/cells11071245.

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Nephropathic cystinosis is an inherited lysosomal storage disorder caused by pathogenic variants in the cystinosin (CTNS) gene and is characterized by the excessive shedding of proximal tubular epithelial cells (PTECs) and podocytes into urine, development of the renal Fanconi syndrome and end-stage kidney disease (ESKD). We hypothesized that in compensation for epithelial cell losses, cystinosis kidneys undertake a regenerative effort, and searched for the presence of kidney progenitor cells (KPCs) in the urine of cystinosis patients. Urine was cultured in a specific progenitor medium to isolate undifferentiated cells. Of these, clones were characterized by qPCR, subjected to a differentiation protocol to PTECs and podocytes and assessed by qPCR, Western blot, immunostainings and functional assays. Cystinosis patients voided high numbers of undifferentiated cells in urine, of which various clonal cell lines showed a high capacity for self-renewal and expressed kidney progenitor markers, which therefore were assigned as cystinosis urine-derived KPCs (Cys-uKPCs). Cys-uKPC clones showed the capacity to differentiate between functional PTECs and/or podocytes. Gene addition with wild-type CTNS using lentiviral vector technology resulted in significant reductions in cystine levels. We conclude that KPCs present in the urine of cystinosis patients can be isolated, differentiated and complemented with CTNS in vitro, serving as a novel tool for disease modeling.

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Nam, Sun Ah, Eunjeong Seo, Jin Won Kim, Hyung Wook Kim, Hong Lim Kim, Kyuryung Kim, Tae-Min Kim, et al. "Graft immaturity and safety concerns in transplanted human kidney organoids." Experimental & Molecular Medicine 51, no. 11 (November 2019): 1–13. http://dx.doi.org/10.1038/s12276-019-0336-x.

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AbstractFor chronic kidney disease, regeneration of lost nephrons with human kidney organoids derived from induced pluripotent stem (iPS) cells is proposed to be an attractive potential therapeutic option. It remains unclear, however, whether organoids transplanted into kidneys in vivo would be safe or functional. Here, we purified kidney organoids and transplanted them beneath the kidney capsules of immunodeficient mice to test their safety and maturity. Kidney organoid grafts survived for months after transplantation and became vascularized from host mouse endothelial cells. Nephron-like structures in grafts appeared more mature than kidney organoids in vitro, but remained immature compared with the neighboring mouse kidney tissue. Ultrastructural analysis revealed filtration barrier-like structures, capillary lumens, and tubules with brush border in the transplanted kidney organoids, which were more mature than those of the kidney organoids in vitro but not as organized as adult mammalian kidneys. Immaturity was a common feature of three separate differentiation protocols by immunofluorescence analysis and single cell RNA sequencing. Stroma of transplanted kidney organoid grafts were filled with vimentin-positive mesenchymal cells, and chondrogenesis, cystogenesis, and stromal expansion were observed in the long term. Transcription profiles showed that long-term maintenance after kidney organoid transplantation induced transcriptomic reprogramming with prominent suppression of cell-cycle-related genes and upregulation of extracellular matrix organization. Our data suggest that kidney organoids derived from iPS cells may be transplantable but strategies to improve nephron differentiation and purity are required before they can be applied in humans as a therapeutic option.

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Robert, B., P. L. St John, D. P. Hyink, and D. R. Abrahamson. "Evidence that embryonic kidney cells expressing flk-1 are intrinsic, vasculogenic angioblasts." American Journal of Physiology-Renal Physiology 271, no. 3 (September 1, 1996): F744—F753. http://dx.doi.org/10.1152/ajprenal.1996.271.3.f744.

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Renal glomerular capillary tufts have been believed to arise from angiogenic ingrowth of extrinsic vessels. We found, however, that when embryonic day 12 (E12) mouse kidneys were maintained in culture for 6 days and then grafted into anterior eye chambers of adult transgenic ROSA26 host mice (which carry the beta-galactosidase transgene), glomerular endothelial cells within the grafts were predominantly of intrinsic, kidney origin. To identify potential endothelial precursors, we immunolabled kidneys with antibodies against the vascular endothelial growth factor receptor, flk-1. Numerous discrete cells expressing flk-1 were scattered throughout the nephrogenic mesenchyme of both E12 and newborn kidneys, and with development these cells became concentrated in microvessels, glomerular vascular clefts, and glomerular tufts. In adults, flk-1 was weakly expressed in glomeruli but absent elsewhere. To examine abilities of flk-1-positive cells to establish glomeruli, E12 kidneys were grafted into kidney cortices of adult and newborn ROSA26 hosts. Grafts into adults resulted in few glomeruli containing host-derived endothelium, whereas a majority of glomeruli grafted into newborns contained host cells. Cells of graft origin were found in vessels forming in renal cortices of newborn hosts, but not in adults. Our findings indicate that embryonic kidney cells expressing flk-1 are angioblasts that create microvessels and glomeruli by vasculogenesis.

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Miranda, Cláudia C., Mariana Ramalho Gomes, Mariana Moço, Joaquim M. S. Cabral, Frederico Castelo Ferreira, and Paola Sanjuan-Alberte. "A Concise Review on Electrospun Scaffolds for Kidney Tissue Engineering." Bioengineering 9, no. 10 (October 14, 2022): 554. http://dx.doi.org/10.3390/bioengineering9100554.

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Chronic kidney disease is one of the deadliest diseases globally and treatment methods are still insufficient, relying mostly on transplantation and dialysis. Engineering of kidney tissues in vitro from induced pluripotent stem cells (iPSCs) could provide a solution to this medical need by restoring the function of damaged kidneys. However, implementation of such approaches is still challenging to achieve due to the complexity of mature kidneys in vivo. Several strategies have been defined to obtain kidney progenitor endothelial and epithelial cells that could form nephrons and proximal tube cells, but these lack tissue maturity and vascularisation to be further implemented. Electrospinning is a technique that has shown promise in the development of physiological microenvironments of several tissues and could be applied in the engineering of kidney tissues. Synthetic polymers such as polycaprolactone, polylactic acid, and poly(vinyl alcohol) have been explored in the manufacturing of fibres that align and promote the proliferation and cell-to-cell interactions of kidney cells. Natural polymers including silk fibroin and decellularised extracellular matrix have also been explored alone and in combination with synthetic polymers promoting the differentiation of podocytes and tubular-specific cells. Despite these attempts, further work is still required to advance the applications of electrospun fibres in kidney tissue engineering and explore this technique in combination with other manufacturing methods such as bioprinting to develop more organised, mature and reproducible kidney organoids.

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Breton, Sylvie, and Dennis Brown. "Novel Proinflammatory Function of Renal Intercalated Cells." Annals of Nutrition and Metabolism 72, Suppl. 2 (2018): 11–16. http://dx.doi.org/10.1159/000488303.

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Background: Serious and often fatal acute kidney injury (AKI) is frequently seen after major surgery, local and remote organ damage, and sepsis. It is associated with uncontrolled inflammation, and is usually diagnosed only after the kidneys have gone through significant and often irreversible damage. Summary: During our work involving another type of kidney disease that leads to acid-base disorders of the blood, we unexpectedly found high levels of a protein called the P2Y14 “purinergic” receptor, in specialized kidney epithelial cells called intercalated cells (ICs). These cells are responsible for maintaining whole body acid-base balance by regulating the secretion of excess protons into the urine, which normalizes blood pH. However, it turns out that the P2Y14 receptor in these cells responds to a molecule called uridine diphosphate (UDP)-glucose, which is a danger signal released by damaged cells anywhere in the body. When UDP-glucose reaches the kidney, it stimulates ICs to produce chemoattractant cytokines; this results in renal inflammation and contributes to the onset of AKI. Key Message: Thus, our work now points to ICs as key mediators of renal inflammation and AKI, following surgery and/or damage to remote organs, sepsis, and also local insults to the kidney itself. The link between the proton secreting ICs of the kidney and AKI is an example of how a fundamental research project with a defined aim, in this case understanding acid-base homeostasis, can lead to a novel observation that has unexpected but major implications in another area of human health.

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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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Monastirskiy, V. M., and V. I. Pivtorak. "MORPHOFUNCTIONAL STATE OF A SINGLE KIDNEY REMAINING AFTER CONTRALATERAL NEPHRECTOMY (LITERATURE REVIEW AND OWN RESEARCH)." Reports of Vinnytsia National Medical University 22, no. 4 (December 28, 2018): 743–51. http://dx.doi.org/10.31393/reports-vnmedical-2018-22(4)-30.

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The study of the structural and functional basis of compensatory and adaptive processes in the kidneys is one of the fundamental problems of biology and medicine. The purpose of the work: to highlight modern views on the question of compensation of structure and function in the loss of one kidney. There is a discussion about the mechanisms and patterns of development of compensatory processes in the surgical removal of one kidney, as well as at the birth of a child with kidney agenesis in the scientific literature. Previously, it was believed that the kidney, after it was formed and grown, does not regenerate and is a static organ, and the replacement of dead cells occurs only by increasing other cells in size. As scientists have now found out that not only stem cells of the kidneys, but also ordinary cells of the epithelium and other renal tissues are able to divide. The kidney is restored throughout human life. Also, authors' own research concerning changes of topographic anatomy of the kidney after radical nephrectomies of the contralateral kidney is given in the article. With the help of mathematical modelling, it is proved that with increasing the mass of the kidney, provided that the width, length and thickness of the kidney increases proportionally, the movement of the kidney is due to its rotation in the plane of material symmetry in a clockwise direction. The characteristics of the position of a single kidney, after contralateral nephrectomy, in the frontal, sagittal and horizontal planes in patients of various somatotypes based on magnetic resonance imaging, are presented.

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Watanabe, Hirofumi, Robert L. Paxton, Matthew R. Tolerico, Vidya K. Nagalakshmi, Shinji Tanaka, Mark D. Okusa, Shin Goto, et al. "Expression of Acsm2, a kidney-specific gene, parallels the function and maturation of proximal tubular cells." American Journal of Physiology-Renal Physiology 319, no. 4 (October 1, 2020): F603—F611. http://dx.doi.org/10.1152/ajprenal.00348.2020.

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The acyl-CoA synthetase medium-chain family member 2 ( Acsm2) gene was first identified and cloned by our group as a kidney-specific “ KS” gene. However, its expression pattern and function remain to be clarified. In the present study, we found that the Acsm2 gene was expressed specifically and at a high level in normal adult kidneys. Expression of Acsm2 in kidneys followed a maturational pattern: it was low in newborn mice and increased with kidney development and maturation. In situ hybridization and immunohistochemistry revealed that Acsm2 was expressed specifically in proximal tubular cells of adult kidneys. Data from the Encyclopedia of DNA Elements database revealed that the Acsm2 gene locus in the mouse has specific histone modifications related to the active transcription of the gene exclusively in kidney cells. Following acute kidney injury, partial unilateral ureteral obstruction, and chronic kidney diseases, expression of Acsm2 in the proximal tubules was significantly decreased. In human samples, the expression pattern of ACSM2A, a homolog of mouse Acsm2, was similar to that in mice, and its expression decreased with several types of renal injuries. These results indicate that the expression of Acsm2 parallels the structural and functional maturation of proximal tubular cells. Downregulation of its expression in several models of kidney disease suggests that Acms2 may serve as a novel marker of proximal tubular injury and/or dysfunction.

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Vincent, Isaah, Stefan Moscalu, Christopher Chhoun, Hong Ye, Liping Huang, Sun-Sang Sung, and Mark Okusa. "Natural killer (NK) cells but not NK T cells attenuate renal fibrosis after acute kidney injury (AKI). (IRC8P.480)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 190.8. http://dx.doi.org/10.4049/jimmunol.192.supp.190.8.

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Abstract Renal fibrosis is the common pathway of various kidney diseases that lead to progressive renal failure and end stage renal disease. NK and NK T cells have been linked to regulating fibrosis in several different organ systems. However, there is debate as to whether they are pro-fibrotic or anti-fibrotic. To determine their role in renal fibrosis, mice were administered PK136 mAb (200μg i.p), which depletes both NK and NKT cells, twice weekly for 14 days starting 5 days after 26 minutes of unilateral kidney ischemia-reperfusion (uIRI) or folic acid (250 mg/kg, i.p.). In both models, compared to IgG-treated mice, kidneys of mice treated with PK136 had increased fibrosis as assessed by Masson’s Trichrome and mRNA expression of collagen 1 and α-SMA. This suggests that NK/NKT depletion increases extracellular matrix deposition and myofibroblast number. This may be due to changes in the kidney microenvironment as kidneys of PK136-depleted mice had decreased expression of IFN-γ and increased expression of IL-10 and TGF-β compared to IgG-treated mice. We next subjected Jα18-/- and CD1d-/- mice to unilateral IRI to determine the specific role of NKT cells in renal fibrosis. Compared to wild-type mice, Jα18-/- and CD1d-/- mice subjected to uIRI demonstrated no increase in fibrosis, thus we conclude that the that NK but not NKT cells attenuate renal fibrosis after AKI. Further investigation will focus on determining the mechanism by which NK cells regulate fibrosis within the kidney.

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Liu, Hongbao, Weihui Liu, Shuibing Liu, Qiuhong Meng, Ning Zhang, Hanmin Wang, Rong Li, Limin Wang, Peng Zhang, and Shiren Sun. "Reconstitution of Kidney Side Population Cells after Ischemia-Reperfusion Injury by Self-Proliferation and Bone Marrow-Derived Cell Homing." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/370961.

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The aim of this study was to examine the contribution of side population (SP) cells from kidney and bone marrow for reconstitution of kidney SP pools after ischemia-reperfusion injury (IRI). The SP and non-SP cells in kidneys following IRI were isolated and serially assessed by fluorescence-activated cell sorting. The apoptosis, proliferation, phenotype, and paracrine actions of SP cells were evaluatedin vitroandin vivo. Results indicated that the SP cells from ischemic kidney were acutely depleted within one day following renal IRI and were progressively restored to baseline within 7 days after IRI, through both proliferation of remaining kidney SP cells and homing of bone marrow-derived cells to ischemic kidney. Either hypoxia or serum deprivation alone increased apoptosis of SP cells, and a combination of both further aggravated it. Furthermore, hypoxiain vivoandin vitroinduced the increase in the secretion of vascular endothelial growth factor, insulin-like growth factor 1, hepatocyte growth factor, and stromal cell-derived factor-1αin kidney SP but not non-SP cells. In summary, these results suggest that following renal IRI, kidney SP cells are acutely depleted and then progressively restored to baseline levels by both self-proliferation and extrarenal source, that is, bone marrow-derived cell homing.

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Kuehn, E. Wolfgang, Kwon Moo Park, Stefan Somlo, and Joseph V. Bonventre. "Kidney injury molecule-1 expression in murine polycystic kidney disease." American Journal of Physiology-Renal Physiology 283, no. 6 (December 1, 2002): F1326—F1336. http://dx.doi.org/10.1152/ajprenal.00166.2002.

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Kidney injury molecule-1 (Kim-1) is a type 1 membrane protein maximally upregulated in proliferating and dedifferentiated tubular cells after renal ischemia. Because epithelial dedifferentiation, proliferation, and local ischemia may play a role in the pathophysiology of autosomal dominant polycystic kidney disease, we investigated Kim-1 expression in a mouse model of this disease. In the Pkd2WS25/− mouse model for autosomal dominant polycystic kidney disease, cystic kidneys show markedly upregulated Kim-1 levels compared with noncystic control kidneys. Kim-1 is present in a subset of cysts of different sizes and segmental origins and in clusters of proximal tubules near cysts. Kim-1-expressing tubular cells show decreased complexity and quantity of basolateral staining for Na-K-ATPase. Other changes in polarity characteristic of ischemic injury are not present in Kim-1-expressing pericystic tubules. Polycystin-2 expression is preserved in Kim-1-expressing tubules. The interstitium surrounding Kim-1-expressing tubules shows high proliferative activity and staining for smooth muscle α-actin, characteristic of myofibroblasts. Although the functional role of the protein in cysts remains unknown, Kim-1 expression in tubules is strongly associated with partial dedifferentiation of epithelial cells and may play a role in the development of interstitial fibrosis.

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Zhang, Zhu-Xu, Kelvin Shek, Shuang Wang, Xuyan Huang, Ziqin Yin, Hongtao Sun, Weihua Liu, Bertha Garcia, Susan Rittling, and Anthony Jevnikar. "OPN expression by epithelial tubular cells regulates NK cell-mediated kidney ischemia reperfusion injury (98.30)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 98.30. http://dx.doi.org/10.4049/jimmunol.182.supp.98.30.

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Abstract Renal ischemia reperfusion injury (IRI) is a major cause of acute injury in both native and transplanted kidneys. This type of kidney injury is considered an antigen-independent inflammatory condition that involves multiple factors leading to tubular and endothelial dysfunction. We have recently found that NK cells induce apoptosis in tubular epithelial cells (TEC) and contribute to renal IRI. Kidney can express osteopontin (OPN) during injury. Therefore we examined the role OPN in NK cell function and kidney IRI. We have found that TEC expressed high levels of OPN in vitro and in vivo after injury. Kidneys in OPN-/- mice had less severity of IRI compared to wild-type mice (P<0.05). Interestingly, recombinant OPN could activate NK cells that express high levels of perforin and granzyme and could mediate TEC apoptotic death. Importantly, we have found that NK cell migrate towards OPN protein as well as OPN-producing TEC in the transwell assay. Whereas, less NK cell migration was seen towards OPN-/- TEC (P<0.01). Further more, Kidneys in OPN-/- mice had less NK cell infiltration after IRI compared to WT mice (P<0.02). Taken together, our study results support a previously unrecognized role for TEC expression of OPN in NK cell-mediated kidney injury. TEC expression of OPN promotes early kidney inflammatory and IRI, and limiting OPN expression may improve kidney function and graft survival.

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Satriano, Joseph, Hadi Mansoury, Aihua Deng, Kumar Sharma, Volker Vallon, Roland C. Blantz, and Scott C. Thomson. "Transition of kidney tubule cells to a senescent phenotype in early experimental diabetes." American Journal of Physiology-Cell Physiology 299, no. 2 (August 2010): C374—C380. http://dx.doi.org/10.1152/ajpcell.00096.2010.

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Diabetic nephropathy is the commonest cause of end-stage renal disease. Inordinate kidney growth and glomerular hyperfiltration at the very early stages of diabetes are putative antecedents to this disease. The kidney is the only organ that grows larger with the onset of diabetes mellitus, yet there remains confusion about the mechanism and significance of this growth. Here we show that kidney proximal tubule cells in culture transition to senescence in response to oxidative stress. We further determine the temporal expression of G1 phase cell cycle components in rat kidney cortex at days 4 and 10 of streptozotocin diabetes to evaluate changes in this growth response. In diabetic rats we observe increases in kidney weight-to-body weight ratios correlating with increases in expression of the growth-related proteins in the kidney at day 4 after induction of diabetes. However, at day 10 we find a decrease in this profile in diabetic animals coincident with increased cyclin-dependent kinase inhibitor expressions. We observe no change in caspase-3 expression in the diabetic kidneys at these early time points; however, diabetic animals demonstrate reduced kidney connexin 43 and increased plasminogen activator inhibitor-1 expressions and increased senescence-associated β-galactosidase activity in cortical tubules. In summary, diabetic kidneys exhibit an early temporal induction of growth phase components followed by their suppression concurrent with the induction of cyclin-dependent kinase inhibitors and markers of senescence. These data delineate a phenotypic change in cortical tubules early in the pathogenesis of diabetes that may contribute to further downstream complications of the disease.

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Alexander, Jessy J., Alexander Jacob, Anthony Chang, Richard J. Quigg, and James N. Jarvis. "Double negative T cells, a potential biomarker for systemic lupus erythematosus." Precision Clinical Medicine 3, no. 1 (January 20, 2020): 34–43. http://dx.doi.org/10.1093/pcmedi/pbaa001.

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Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease that is a challenge to diagnose and treat. There is an urgent need for biomarkers to help define organ involvement, and more effective therapies. A unique population of T cells, the CD3+CD4−CD8− (DNeg) cells, is significantly increased in lupus patients. Twenty-seven cases (53%) of pediatric SLE patients had elevated DNeg cells in their peripheral blood, which correlated with kidney function (R2 = 0.54). Significant infiltration of DNeg cells was observed in both adult and pediatric lupus kidneys by immunofluorescence. For the first time, this study provides direct evidence that DNeg cells facilitate kidney injury in preclinical 8-week-old MRL/lpr lupus mice. In lupus mice, the increase in DNeg cells tracked with worsening disease and correlated with kidney function (R2 = 0.85). Our results show that DNeg cells per se can cause kidney dysfunction, increase in number with increase in disease pathology, and could serve as a potential biomarker.

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Bellini, Maria Irene, Francesco Tortorici, Maria Ida Amabile, and Vito D’Andrea. "Assessing Kidney Graft Viability and Its Cells Metabolism during Machine Perfusion." International Journal of Molecular Sciences 22, no. 3 (January 23, 2021): 1121. http://dx.doi.org/10.3390/ijms22031121.

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Kidney transplantation is the golden treatment for end-stage renal disease. Static cold storage is currently considered the standard method of preservation, but dynamic techniques, such as machine perfusion (MP), have been shown to improve graft function, especially in kidneys donated by extended criteria donors and donation after circulatory death. With poor organ quality being a major reason for kidneys not being transplanted, an accurate, objective and reliable quality assessment during preservation could add value and support to clinicians’ decisions. MPs are emerging technologies with the potential to assess kidney graft viability and quality, both in the hypothermic and normothermic scenarios. The aim of this review is to summarize current tools for graft viability assessment using MP prior to implantation in relation to the ischemic damage.

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Lin, Tien-An, Victor Chien-Chia Wu, and Chao-Yung Wang. "Autophagy in Chronic Kidney Diseases." Cells 8, no. 1 (January 16, 2019): 61. http://dx.doi.org/10.3390/cells8010061.

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Autophagy is a cellular recycling process involving self-degradation and reconstruction of damaged organelles and proteins. Current evidence suggests that autophagy is critical in kidney physiology and homeostasis. In clinical studies, autophagy activations and inhibitions are linked to acute kidney injuries, chronic kidney diseases, diabetic nephropathies, and polycystic kidney diseases. Oxidative stress, inflammation, and mitochondrial dysfunction, which are implicated as important mechanisms underlying many kidney diseases, modulate the autophagy activation and inhibition and lead to cellular recycling dysfunction. Abnormal autophagy function can induce loss of podocytes, damage proximal tubular cells, and glomerulosclerosis. After acute kidney injuries, activated autophagy protects tubular cells from apoptosis and enhances cellular regeneration. Patients with chronic kidney diseases have impaired autophagy that cannot be reversed by hemodialysis. Multiple nephrotoxic medications also alter the autophagy signaling, by which the mechanistic insights of the drugs are revealed, thus providing the unique opportunity to manage the nephrotoxicity of these drugs. In this review, we summarize the current concepts of autophagy and its molecular aspects in different kidney cells pathophysiology. We also discuss the current evidence of autophagy in acute kidney injury, chronic kidney disease, toxic effects of drugs, and aging kidneys. In addition, we examine therapeutic possibilities targeting the autophagy system in kidney diseases.

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TUFRO, ALDA, VICTORIA F. NORWOOD, ROBERT M. CAREY, and R. ARIEL GOMEZ. "Vascular Endothelial Growth Factor Induces Nephrogenesis and Vasculogenesis." Journal of the American Society of Nephrology 10, no. 10 (October 1999): 2125–34. http://dx.doi.org/10.1681/asn.v10102125.

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Abstract. The expression of vascular endothelial growth factor (VEGF) and its receptors Flt-1 and Flk-1 in the rat kidney was examined during ontogeny using Northern blot analysis and immunocytochemistry. In prevascular embryonic kidneys (embryonic day 14 [E14]), immunoreactive Flt-1 and Flk-1 were observed in isolated angioblasts, whereas VEGF was not detected. Angioblasts aligned forming cords before morphologically differentiating into endothelial cells. In late fetal kidneys (E19), immunoreactive VEGF was detected in glomerular epithelial and tubular cells, whereas Flt-1 and Flk-1 were expressed in contiguous endothelial cells. To determine whether VEGF induces endothelial cell differentiation and vascular development in the kidney, the effect of recombinant human VEGF (5 ng/ml) was examined on rat metanephric organ culture, a model known to recapitulate nephrogenesis in the absence of vessels. After 6 d in culture in serum-free, defined media, metanephric kidney growth and morphology were assessed. DNA content was higher in VEGF-treated explants (1.9 ± 0.17 μg/kidney, n = 9) than in paired control explants (1.4 ± 0.10 μg/kidney, n = 9) (P < 0.05). VEGF induced proliferation of tubular epithelial cells, as indicated by an increased number of tubules and tubular proliferating cell nuclear antigen-containing cells. VEGF induced upregulation of Flk-1 and Flt-1 expression, as assessed by Western blot analysis. Developing endothelial cells were identified and localized using immunocytochemistry and electron microscopy. Flt-1, Flk-1, and angiotensin-converting enzyme-containing cells were detected in VEGF-treated explants, whereas control explants were negative. These studies confirmed previous reports indicating that the expression of VEGF and its receptors is temporally and spatially associated with kidney vascularization and identified angioblasts expressing Flt-1 and Flk-1 in prevascular embryonic kidneys. The data indicate that VEGF expression is downregulated in standard culture conditions and that VEGF stimulates growth of embryonic kidney explants by expanding both endothelium and epithelium, resulting in vasculogenesis and enhanced tubulogenesis. These data suggest that VEGF plays a critical role in renal development by promoting endothelial cell differentiation, capillary formation, and proliferation of tubular epithelia.

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Little, Melissa H., Lorna J. Hale, Sara E. Howden, and Santhosh V. Kumar. "Generating Kidney from Stem Cells." Annual Review of Physiology 81, no. 1 (February 10, 2019): 335–57. http://dx.doi.org/10.1146/annurev-physiol-020518-114331.

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Human kidney tissue can now be generated via the directed differentiation of human pluripotent stem cells. This advance is anticipated to facilitate the modeling of human kidney diseases, provide platforms for nephrotoxicity screening, enable cellular therapy, and potentially generate tissue for renal replacement. All such applications will rely upon the accuracy and reliability of the model and the capacity for stem cell–derived kidney tissue to recapitulate both normal and diseased states. In this review, we discuss the models available, how well they recapitulate the human kidney, and how far we are from application of these cells for use in cellular therapies.

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Sallam, May, Anwar A. Palakkan, Christopher G. Mills, Julia Tarnick, Mona Elhendawi, Lorna Marson, and Jamie A. Davies. "Differentiation of a Contractile, Ureter-Like Tissue, from Embryonic Stem Cell–Derived Ureteric Bud and Ex Fetu Mesenchyme." Journal of the American Society of Nephrology 31, no. 10 (August 21, 2020): 2253–62. http://dx.doi.org/10.1681/asn.2019101075.

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BackgroundThere is intense interest in replacing kidneys from stem cells. It is now possible to produce, from embryonic or induced pluripotent stem cells, kidney organoids that represent immature kidneys and display some physiologic functions. However, current techniques have not yet resulted in renal tissue with a ureter, which would be needed for engineered kidneys to be clinically useful.MethodsWe used a published sequence of growth factors and drugs to induce mouse embryonic stem cells to differentiate into ureteric bud tissue. We characterized isolated engineered ureteric buds differentiated from embryonic stem cells in three-dimensional culture and grafted them into ex fetu mouse kidney rudiments.ResultsEngineered ureteric buds branched in three-dimensional culture and expressed Hoxb7, a transcription factor that is part of a developmental regulatory system and a ureteric bud marker. When grafted into the cortex of ex fetu kidney rudiments, engineered ureteric buds branched and induced nephron formation; when grafted into peri-Wolffian mesenchyme, still attached to a kidney rudiment or in isolation, they did not branch but instead differentiated into multilayer ureter-like epithelia displaying robust expression of the urothelial marker uroplakin. This engineered ureteric bud tissue also organized the mesenchyme into smooth muscle that spontaneously contracted, with a period a little slower than that of natural ureteric peristalsis.ConclusionsMouse embryonic stem cells can be differentiated into ureteric bud cells. Grafting those UB-like structures into peri-Wolffian mesenchyme of cultured kidney rudiments can induce production of urothelium and organize the mesenchyme to produce rhythmically contracting smooth muscle layers. This development may represent a significant step toward the goal of renal regeneration.

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Sequeira Lopez, Maria Luisa S., Ellen S. Pentz, Barry Robert, Dale R. Abrahamson, and R. Ariel Gomez. "Embryonic origin and lineage of juxtaglomerular cells." American Journal of Physiology-Renal Physiology 281, no. 2 (August 1, 2001): F345—F356. http://dx.doi.org/10.1152/ajprenal.2001.281.2.f345.

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To define the embryonic origin and lineage of the juxtaglomerular (JG) cell, transplantation of embryonic kidneys between genetically marked and wild-type mice; labeling studies for renin, smooth muscle, and endothelial cells at different developmental stages; and single cell RT-PCR for renin and other cell identity markers in prevascular kidneys were performed. From embryonic kidney day 12 to day 15 ( E12 to E15), renin cells did not yet express smooth muscle or endothelial markers. At E16 renin cells acquired smooth muscle but not endothelial markers, indicating that these cells are not related to the endothelial lineage, and that the smooth muscle phenotype is a later event in the differentiation of the JG cell. Prevascular genetically labeled E12 mouse kidneys transplanted into the anterior chamber of the eye or under the kidney capsule of adult mice demonstrated that renin cell progenitors originating within the metanephric blastema differentiated in situ to JG cells. We conclude that JG cells originate from the metanephric mesenchyme rather than from an extrarenal source. We propose that renin cells are less differentiated than (and have the capability to give rise to) smooth muscle cells of the renal arterioles.

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Wong, Wei. "Pressuring kidney cells into endocytosis." Science 370, no. 6514 (October 15, 2020): 305.1–305. http://dx.doi.org/10.1126/science.370.6514.305-a.

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Kreidberg, Jordan A. "WT1 and kidney progenitor cells." Organogenesis 6, no. 2 (April 2010): 61–70. http://dx.doi.org/10.4161/org.6.2.11928.

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Yokoo, Takashi. "Stem cells and kidney organogenesis." Frontiers in Bioscience 13, no. 13 (2008): 2814. http://dx.doi.org/10.2741/2888.

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John, Rohan, and Peter J. Nelson. "Dendritic Cells in the Kidney." Journal of the American Society of Nephrology 18, no. 10 (September 5, 2007): 2628–35. http://dx.doi.org/10.1681/asn.2007030273.

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Al-Awqati, Qais, and Juan A. Oliver. "Stem cells in the kidney." Kidney International 61, no. 2 (February 2002): 387–95. http://dx.doi.org/10.1046/j.1523-1755.2002.00164.x.

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39

Yokote, Shinya, and Takashi Yokoo. "Stem Cells in Kidney Regeneration." Current Medicinal Chemistry 19, no. 35 (December 1, 2012): 6009–17. http://dx.doi.org/10.2174/092986712804485890.

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Yokote, Shinya, and Takashi Yokoo. "Stem Cells in Kidney Regeneration." Current Medicinal Chemistry 19, no. 35 (November 29, 2012): 6009–17. http://dx.doi.org/10.2174/0929867311209066009.

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HISHIKAWA, Keiichi, and Toshiro FUJITA. "Stem Cells and Kidney Disease." Hypertension Research 29, no. 10 (2006): 745–49. http://dx.doi.org/10.1291/hypres.29.745.

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42

Ausiello, Dennis A., Karl L. Skorecki, Alan S. Verkman, and Joseph V. Bonventre. "Vasopressin signaling in kidney cells." Kidney International 31, no. 2 (February 1987): 521–29. http://dx.doi.org/10.1038/ki.1987.31.

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Wilm, Bettina, Riccardo Tamburrini, Giuseppe Orlando, and Patricia Murray. "Autologous Cells for Kidney Bioengineering." Current Transplantation Reports 3, no. 3 (June 9, 2016): 207–20. http://dx.doi.org/10.1007/s40472-016-0107-8.

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Chou, Yu-Hsiang, Szu-Yu Pan, Chian-Huei Yang, and Shuei-Liong Lin. "Stem cells and kidney regeneration." Journal of the Formosan Medical Association 113, no. 4 (April 2014): 201–9. http://dx.doi.org/10.1016/j.jfma.2013.12.001.

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Oberleithner, H., U. Vogel, and U. Kersting. "Madin-Darby canine kidney cells." Pfl�gers Archiv European Journal of Physiology 416, no. 5 (July 1990): 526–32. http://dx.doi.org/10.1007/bf00382685.

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Oberleithner, H., U. Vogel, U. Kersting, and W. Steigner. "Madin-Darby canine kidney cells." Pfl�gers Archiv European Journal of Physiology 416, no. 5 (July 1990): 533–39. http://dx.doi.org/10.1007/bf00382686.

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Oberleithner, H., W. Steigner, S. Silbernagl, U. Vogel, G. Gstraunthaler, and W. Pfaller. "Madin-Darby canine kidney cells." Pfl�gers Archiv European Journal of Physiology 416, no. 5 (July 1990): 540–47. http://dx.doi.org/10.1007/bf00382687.

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Kuberka, M., G. Rau, and B. Glasmacher. "CRYOPRESERVATION OF EPITHELIAL KIDNEY CELLS." Biomedizinische Technik/Biomedical Engineering 48, s1 (2003): 322–23. http://dx.doi.org/10.1515/bmte.2003.48.s1.322.

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Vigneau, Cecile, Feng Zheng, Katalin Polgar, Patricia D. Wilson, and Gary Striker. "Stem cells and kidney injury." Current Opinion in Nephrology and Hypertension 15, no. 3 (May 2006): 238–44. http://dx.doi.org/10.1097/01.mnh.0000222689.76841.db.

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Laurini, R. N. "ENDOCRINE CELLS IN THE KIDNEY." Acta Pathologica Microbiologica Scandinavica Section A Pathology 83A, no. 1 (August 15, 2009): 191–92. http://dx.doi.org/10.1111/j.1699-0463.1975.tb01373.x.

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Journal articles on the topic 'Kidney cells'

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