Erratum for the Research Article: “Acute kidney injury promotes development of papillary renal cell adenoma and carcinoma from renal progenitor cells” by A. J. Peired, G. Antonelli, M. L. Angelotti, M. Allinovi, F. Guzzi, A. Sisti, R. Semeraro, C. Conte, B. Mazzinghi, S. Nardi, M. E. Melica, L. De Chiara, E. Lazzeri, L. Lasagni, T. Lottini, S. Landini, S. Giglio, A. Mari, F. Di Maida, A. Antonelli, F. Porpiglia, R. Schiavina, V. Ficarra, D. Facchiano, M. Gacci, S. Serni, M. Carini, G. J. Netto, R. M. Roperto, A. Magi, C. F. Christiansen, M. Rotondi, H. Liapis, H.-J. Anders, A. Minervini, M. R. Raspollini, P. Romagnani

2020 ◽  
Vol 12 (549) ◽  
pp. eabd2685
Keyword(s):  
Acute Kidney Injury ◽  
Progenitor Cells ◽  
Renal Cell ◽  
Kidney Injury ◽  
Cell Adenoma ◽  
Renal Progenitor Cells ◽  
Research Article ◽  
Renal Progenitor

scholarly journals SaO032PAPILLARY RENAL CELL CARCINOMA ORIGINATES FROM A POPULATION OF RENAL PROGENITOR CELLS AND IS PROMOTED BY ACUTE KIDNEY INJURY

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i328-i328
Author(s):  
Anna Peired ◽  
Giulia Antonelli ◽  
Maria Lucia Angelotti ◽  
Alessandro Sisti ◽  
Marco Allinovi ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Acute Kidney Injury ◽  
Cell Carcinoma ◽  
Progenitor Cells ◽  
Renal Cell ◽  
Kidney Injury ◽  
Renal Progenitor Cells ◽  
Renal Progenitor

Acute kidney injury promotes development of papillary renal cell adenoma and carcinoma from renal progenitor cells

2020 ◽  
Vol 12 (536) ◽  
pp. eaaw6003 ◽  
Author(s):  
Anna Julie Peired ◽  
Giulia Antonelli ◽  
Maria Lucia Angelotti ◽  
Marco Allinovi ◽  
Francesco Guzzi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Progenitor Cells ◽  
Renal Cell ◽  
Tissue Injury ◽  
Kidney Injury ◽  
Lineage Tracing ◽  
Cell Of Origin ◽  
Renal Progenitor Cells ◽  
Renal Progenitor

Acute tissue injury causes DNA damage and repair processes involving increased cell mitosis and polyploidization, leading to cell function alterations that may potentially drive cancer development. Here, we show that acute kidney injury (AKI) increased the risk for papillary renal cell carcinoma (pRCC) development and tumor relapse in humans as confirmed by data collected from several single-center and multicentric studies. Lineage tracing of tubular epithelial cells (TECs) after AKI induction and long-term follow-up in mice showed time-dependent onset of clonal papillary tumors in an adenoma-carcinoma sequence. Among AKI-related pathways, NOTCH1 overexpression in human pRCC associated with worse outcome and was specific for type 2 pRCC. Mice overexpressing NOTCH1 in TECs developed papillary adenomas and type 2 pRCCs, and AKI accelerated this process. Lineage tracing in mice identified single renal progenitors as the cell of origin of papillary tumors. Single-cell RNA sequencing showed that human renal progenitor transcriptome showed similarities to PT1, the putative cell of origin of human pRCC. Furthermore, NOTCH1 overexpression in cultured human renal progenitor cells induced tumor-like 3D growth. Thus, AKI can drive tumorigenesis from local tissue progenitor cells. In particular, we find that AKI promotes the development of pRCC from single progenitors through a classical adenoma-carcinoma sequence.

scholarly journals Improving outcomes of acute kidney injury using mouse renal progenitor cells alone or in combination with erythropoietin or suramin

2013 ◽  
Vol 4 (3) ◽  
pp. 74 ◽  
Author(s):  
Xiao Han ◽  
Li Zhao ◽  
Guodong Lu ◽  
Junke Ge ◽  
Yalin Zhao ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Progenitor Cells ◽  
Kidney Injury ◽  
Renal Progenitor Cells ◽  
Renal Progenitor

scholarly journals WNT/β-Catenin Signaling Is Required for Integration of CD24+Renal Progenitor Cells into Glycerol-Damaged Adult Renal Tubules

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Zhao Zhang ◽  
Diana M. Iglesias ◽  
Rachel Corsini ◽  
LeeLee Chu ◽  
Paul Goodyer
Keyword(s):  
Progenitor Cells ◽  
Kidney Injury ◽  
Perinatal Period ◽  
Renal Tubules ◽  
Adult Mice ◽  
Renal Progenitor Cells ◽  
Nephron Progenitor ◽  
Canonical Wnt ◽  
Renal Progenitor

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

scholarly journals A Porthole over AKI: Cell Dynamics in Damage and Repair

Nephron ◽  
2020 ◽  
Vol 144 (12) ◽  
pp. 650-654
Author(s):  
Luca Bordoni ◽  
Donato Sardella ◽  
Ina Maria Schiessl
Keyword(s):  
Acute Kidney Injury ◽  
Renal Cell ◽  
Kidney Injury ◽  
Cell Types ◽  
Cell Interactions ◽  
Intravital Imaging ◽  
Cell Dynamics ◽  
Powerful Technique ◽  
Increased Risk ◽  
Cell Crosstalk

Acute kidney injury (AKI) is associated with an increased risk of CKD. Injury-induced multifaceted renal cell-to-cell crosstalk can either lead to successful self-repair or chronic fibrosis and inflammation. In this mini-review, we will discuss critical renal cell types acting as victims or executioners in AKI pathology and introduce intravital imaging as a powerful technique to further dissect these cell-to-cell interactions.

scholarly journals miR-34b-5p promotes renal cell inflammation and apoptosis by inhibiting aquaporin-2 in sepsis-induced acute kidney injury

Renal Failure ◽  
2021 ◽  
Vol 43 (1) ◽  
pp. 291-301
Author(s):  
Caifa Zheng ◽  
Dansen Wu ◽  
Songjing Shi ◽  
Liming Wang
Keyword(s):  
Acute Kidney Injury ◽  
Renal Cell ◽  
Kidney Injury ◽  
Aquaporin 2

scholarly journals Endothelial progenitor cells-derived exosomal microRNA-21-5p alleviates sepsis-induced acute kidney injury by inhibiting RUNX1 expression

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Yue Zhang ◽  
Hongdong Huang ◽  
Wenhu Liu ◽  
Sha Liu ◽  
Xue Yan Wang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Renal Tissue ◽  
Endothelial Glycocalyx ◽  
Endothelial Progenitor ◽  
Marker Proteins ◽  
Related Transcription Factor

AbstractThe role of microRNA-21-5p (miR-21-5p) in sepsis-induced acute kidney injury (AKI) has been seldom discussed. Therefore, the objective of this present study was to investigate the mechanism of endothelial progenitor cells-derived exosomes (EPCs-exos) in sepsis-induced AKI via miR-21-5p/runt-related transcription factor 1 (RUNX1) axis. miR-21-5p was downregulated and RUNX1 was upregulated in the kidney of cecal ligation and puncture (CLP) rats, and miR-21-5p targeted RUNX1. Elevation of miR-21-5p improved renal function and renal tissue pathological damage, attenuated serum inflammatory response, as well as reduced apoptosis and oxidative stress response in renal tissues, and regulated endothelial glycocalyx damage marker proteins syndecan-1 and heparanase-1 in CLP rats. Overexpression of RUNX1 abolished the impacts of elevated miR-21-5p in CLP rats. Also, EPCs-exos upregulated miR-21-5p expression, and functioned similar to elevation of miR-21-5p for CLP rats. Downregulating miR-21-5p partially reversed the effects of EPCs-exos on sepsis-induced AKI. Collectively, our study suggests that EPCs release miR-21-5p-containing exosomes to alleviate sepsis-induced AKI through RUNX1 silencing.

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