Perfluorocarbon solutions limit tubular epithelial cell injury and promote CD133+ kidney progenitor differentiation: potential use in renal assist devices for sepsis-associated acute kidney injury and multiple organ failure

Cantaluppi, Vincenzo; Medica, Davide; Quercia, Alessandro Domenico; Dellepiane, Sergio; Figliolini, Federico; Virzì, Grazia Maria; Brocca, Alessandra; Quaglia, Marco; Marengo, Marita; Olivieri, Carlo; Senzolo, Mara; Garzotto, Francesco; Corte, Francesco Della; Castellano, Giuseppe; Gesualdo, Loreto; Camussi, Giovanni; Ronco, Claudio

doi:10.1093/ndt/gfx328

Cited by 11 publications

(12 citation statements)

References 44 publications

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“…A large body of preclinical work has investigated several pathways to potentially intervene and prevent or treat SA-AKI, and although this work has focused on molecules such as the caspase and interleukin inhibitors, to date it has not translated into human investigations of SA-AKI 162163164165Table 5. summarizes several clinical trials that have investigated novel and traditional agents in the setting of SA-AKI.…”

Section: Prevention and Medical Treatmentmentioning

confidence: 99%

Sepsis associated acute kidney injury

Poston

Koyner

2019

BMJ

443

381

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Sepsis is defined as organ dysfunction resulting from the host’s deleterious response to infection. One of the most common organs affected is the kidneys, resulting in sepsis associated acute kidney injury (SA-AKI) that contributes to the morbidity and mortality of sepsis. A growing body of knowledge has illuminated the clinical risk factors, pathobiology, response to treatment, and elements of renal recovery that have advanced our ability to prevent, detect, and treat SA-AKI. Despite these advances, SA-AKI remains an important concern and clinical burden, and further study is needed to reduce the acute and chronic consequences. This review summarizes the relevant evidence, with a focus on the risk factors, early recognition and diagnosis, treatment, and long term consequences of SA-AKI. In addition to literature pertaining to SA-AKI specifically, pertinent sepsis and acute kidney injury literature relevant to SA-AKI was included.

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Section: Prevention and Medical Treatmentmentioning

confidence: 99%

Sepsis associated acute kidney injury

Poston

Koyner

2019

BMJ

443

381

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“…A recent publication by Cantaluppi et al (2018) reported that the addition of PFCs to viable renal tubular epithelial cells in a renal-assist device led to the differentiation of those cells toward renal progenitor cells.…”

Section: Scs: Specifications Peculiarities and Limitationsmentioning

confidence: 99%

Artificial Oxygen Carriers—Past, Present, and Future—a Review of the Most Innovative and Clinically Relevant Concepts

Ferenz

Steinbicker

2019

J Pharmacol Exp Ther

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“…The kidney is one of the most vulnerable organs in sepsis and sepsis associated acute kidney injury (SAKI) is determined to be closely related to poor prognosis and progress to chronic kidney disease (CKD) [5][6][7][8]. Renal tubular epithelial cell (TEC) acts as a central role in the occurrence and development of SAKI [9][10][11]. Epithelium injury and dysfunction caused by adaptive and/or maladaptive responses were attributed as increasing importance as the mechanisms of such process.…”

Section: Introductionmentioning

confidence: 99%

MiR-21-3p Plays a Crucial Role in Metabolism Alteration of Renal Tubular Epithelial Cells during Sepsis Associated Acute Kidney Injury via AKT/CDK2-FOXO1 Pathway

Lin

Liu

Wang

et al. 2019

BioMed Research International

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Objective. Sepsis and associated acute kidney injury (SAKI) are determined to be closely related to poor prognosis. Because the metabolic alterations of tubular epithelial cells (TECs) are crucial for the occurrence and development of SAKI, we carried out this present study to identify the metabolism changes of TECs during SAKI and relevant mechanisms. Methods. Rat SAKI model and rat tubular epithelial cell line were used in our study. ELISA was used to determine the serum cytokines levels. Protein expressions were examined with Western-Blotting and the transcriptions of RNAs were determined with qRT-PCR. ADP/ATP assay and Oil Red O staining were used to examine the energy and lipid metabolism, respectively. Dual-luciferase reporter assay was carried out to determine the interactions between miRNA and specific proteins. Cell cycle arrest and apoptosis were determined with flow cytometry. Results. Sepsis and AKI were induced 12 h after CLP. Energy and lipid metabolism reduced significantly while FOXO1 levels increased remarkably in TECs during SAKI. The expressions of both AKT and CDK2 and the transcriptions of relevant mRNAs reduced significantly in TECs during SAKI while miR-21-3p expression increased remarkably. Both AKT and CDK2 were determined as the direct targets of miR-21-3p. Furthermore, by in vitro experiments, it was demonstrated that FOXO1 levels were regulated by miR-21-3p in TECs via AKT/CDK2 and AKT/CDK2-FOXO1 pathway was crucial in the regulations of miR-21-3p on lipid metabolism, cell cycle arrest, and apoptosis of TECs. Conclusions. MiR-21-3p mediates metabolism and cell fate alterations of TECs via manipulating AKT/CDK2-FOXO1 pathway, and that is crucial in the regulation of energy metabolism of TECs during SAKI.

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Perfluorocarbon solutions limit tubular epithelial cell injury and promote CD133+ kidney progenitor differentiation: potential use in renal assist devices for sepsis-associated acute kidney injury and multiple organ failure

Abstract: PFCs improved the viability and metabolic function of TECs seeded within a polysulphone hollow fibre and subjected to plasma from septic AKI patients. Additionally, PFCs promoted differentiation towards a tubular/epithelial phenotype of CD133+ renal progenitor cells.

Cited by 11 publications

References 44 publications

Sepsis associated acute kidney injury

Sepsis associated acute kidney injury

Artificial Oxygen Carriers—Past, Present, and Future—a Review of the Most Innovative and Clinically Relevant Concepts

MiR-21-3p Plays a Crucial Role in Metabolism Alteration of Renal Tubular Epithelial Cells during Sepsis Associated Acute Kidney Injury via AKT/CDK2-FOXO1 Pathway

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