scholarly journals Renal progenitors derived from human iPSCs engraft and restore function in a mouse model of acute kidney injury

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Barbara Imberti ◽  
Susanna Tomasoni ◽  
Osele Ciampi ◽  
Anna Pezzotta ◽  
Manuela Derosas ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Mouse Model ◽  
Kidney Injury ◽  
Human Ipscs ◽  
Renal Progenitors

scholarly journals Untargeted Metabolomics Reveals the Protective Effect of a Traditional Chinese Herbal Decoction on Cisplatin-Induced Acute Kidney Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yuyan Li ◽  
Xinhui Liu ◽  
Siqi Liu ◽  
Jiandong Lu ◽  
Jianping Chen ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Mouse Model ◽  
High Performance ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Lysine Biosynthesis ◽  
Chinese Herbal ◽  
Flight Mass Spectrometry ◽  
Herbal Decoction ◽  
Group A

Our previous studies have demonstrated that Jian-Pi-Yi-Shen formula (JPYSF), a traditional Chinese herbal decoction, has a renoprotective effect in 5/6 nephrectomy-induced chronic kidney injury. However, the role and potential mechanisms of JPYSF in the treatment of acute kidney injury (AKI) remain unknown. This study was designed to test the beneficial effect of JPYSF in an AKI mouse model and to investigate the underlying mechanism by using metabolomics analysis. The AKI mouse model was induced by a single intraperitoneal injection of cisplatin at a dose of 20 mg/kg. The mice in the treatment group were pretreated orally with JPYSF (18.35 g/kg/d) for 5 days before cisplatin injection. Seventy-two hours after cisplatin injection, serum and kidney samples were collected for biochemical and histological examination. Ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UHPLC-QTOF/MS) was applied to analyze metabolic profiling variations in the kidney. The results showed that pretreatment with JPYSF obviously reduced the levels of serum creatinine and blood urea nitrogen and alleviated renal pathological injury in AKI mice. Orthogonal partial least-squares discriminant analysis (OPLS-DA) score plot revealed a clear separation between the AKI and AKI + JPYSF group. A total of 68 and 87 significantly differentially expressed metabolites were identified in the kidney of AKI mice responding to JPYSF treatment in negative and positive ion mode, respectively. The pivotal pathways affected by JPYSF included vitamin B6 metabolism, alanine, aspartate and glutamate metabolism, lysine biosynthesis, and butanoate metabolism. In conclusion, JPYSF can protect the kidney from cisplatin-induced AKI, which may be associated with regulating renal metabolic disorders.

Super-resolution ultrasound imaging for in vivo microvasculature assessment in acute kidney injury mouse model

2019 ◽  
Vol 145 (3) ◽  
pp. 1859-1859
Author(s):  
Qiyang Chen ◽  
Brittney M. Rush ◽  
Jaesok Yu ◽  
Roderick Tan ◽  
Kang Kim
Keyword(s):  
Acute Kidney Injury ◽  
Mouse Model ◽  
Ultrasound Imaging ◽  
Kidney Injury ◽  
Super Resolution

Ligustrazine suppresses renal NMDAR1 and caspase-3 expressions in a mouse model of sepsis-associated acute kidney injury

2019 ◽  
Vol 464 (1-2) ◽  
pp. 73-81 ◽  
Author(s):  
Jing Ying ◽  
Jin Wu ◽  
Yiwei Zhang ◽  
Yangyang Han ◽  
Xinger Qian ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Mouse Model ◽  
Caspase 3 ◽  
Kidney Injury

scholarly journals The prominent impairment of liver/intestinal cytochrome P450 and intestinal drug transporters in sepsis-induced acute kidney injury over acute and chronic renal ischemia, a mouse model comparison

Renal Failure ◽  
2019 ◽  
Vol 41 (1) ◽  
pp. 314-325 ◽  
Author(s):  
Warumphon Sukkummee ◽  
Patcharin Jittisak ◽  
Piyanuch Wonganan ◽  
Supeecha Wittayalertpanya ◽  
Pajaree Chariyavilaskul ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cytochrome P450 ◽  
Mouse Model ◽  
Model Comparison ◽  
Drug Transporters ◽  
Kidney Injury ◽  
Renal Ischemia

scholarly journals A mouse model of Townes-Brocks syndrome expressing a truncated mutant Sall1 protein is protected from acute kidney injury

2015 ◽  
Vol 309 (10) ◽  
pp. F852-F863 ◽  
Author(s):  
Sara Hirsch ◽  
Tarek El-Achkar ◽  
Lynn Robbins ◽  
Jeannine Basta ◽  
Monique Heitmeier ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Mouse Model ◽  
Congenital Anomalies ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Acute Injury ◽  
Null Alleles ◽  
Heme Oxygenase 1 ◽  
Adult Kidney

It has been postulated that developmental pathways are reutilized during repair and regeneration after injury, but functional analysis of many genes required for kidney formation has not been performed in the adult organ. Mutations in SALL1 cause Townes-Brocks syndrome (TBS) and nonsyndromic congenital anomalies of the kidney and urinary tract, both of which lead to childhood kidney failure. Sall1 is a transcriptional regulator that is expressed in renal progenitor cells and developing nephrons in the embryo. However, its role in the adult kidney has not been investigated. Using a mouse model of TBS ( Sall1 TBS), we investigated the role of Sall1 in response to acute kidney injury. Our studies revealed that Sall1 is expressed in terminally differentiated renal epithelia, including the S3 segment of the proximal tubule, in the mature kidney. Sall1 TBS mice exhibited significant protection from ischemia-reperfusion injury and aristolochic acid-induced nephrotoxicity. This protection from acute injury is seen despite the presence of slowly progressive chronic kidney disease in Sall1 TBS mice. Mice containing null alleles of Sall1 are not protected from acute kidney injury, indicating that expression of a truncated mutant protein from the Sall1 TBS allele, while causative of congenital anomalies, protects the adult kidney from injury. Our studies further revealed that basal levels of the preconditioning factor heme oxygenase-1 are elevated in Sall1 TBS kidneys, suggesting a mechanism for the relative resistance to injury in this model. Together, these studies establish a functional role for Sall1 in the response of the adult kidney to acute injury.

scholarly journals Human amniotic epithelial cells ameliorate kidney damage in ischemia-reperfusion mouse model of acute kidney injury

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yifei Ren ◽  
Ying Chen ◽  
Xizi Zheng ◽  
Hui Wang ◽  
Xin Kang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Mouse Model ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Mouse Bone Marrow ◽  
Tissue Integration

Abstract Background Acute kidney injury (AKI) is a common clinical disease with complex pathophysiology and limited therapeutic choices. This prompts the need for novel therapy targeting multiple aspects of this disease. Human amnion epithelial cell (hAEC) is an ideal stem cell source. Increasing evidence suggests that exosomes may act as critical cell–cell communicators. Accordingly, we assessed the therapeutic potential of hAECs and their derived exosomes (hAECs-EXO) in ischemia reperfusion mouse model of AKI and explored the underlying mechanisms. Methods The hAECs were primary cultured, and hAECs-EXO were isolated and characterized. An ischemic-reperfusion injury-induced AKI (IRI-AKI) mouse model was established to mimic clinical ischemic kidney injury with different disease severity. Mouse blood creatinine level was used to assess renal function, and kidney specimens were processed to detect cell proliferation, apoptosis, and capillary density. Macrophage infiltration was analyzed by flow cytometry. hAEC-derived exosomes (hAECs-EXO) were used to treat hypoxia-reoxygenation (H/R) injured HK-2 cells and mouse bone marrow-derived macrophages to evaluate their protective effect in vitro. Furthermore, hAECs-EXO were subjected to liquid chromatography-tandem mass spectrometry for proteomic profiling. Results We found that systematically administered hAECs could improve mortality and renal function in IRI-AKI mice, decrease the number of apoptotic cells, prevent peritubular capillary loss, and modulate kidney local immune response. However, hAECs showed very low kidney tissue integration. Exosomes isolated from hAECs recapitulated the renal protective effects of their source cells. In vitro, hAECs-EXO protected HK-2 cells from H/R injury-induced apoptosis and promoted bone marrow-derived macrophage polarization toward M2 phenotype. Proteomic analysis on hAECs-EXO revealed proteins involved in extracellular matrix organization, growth factor signaling pathways, cytokine production, and immunomodulation. These findings demonstrated that paracrine of exosomes might be the key mechanism of hAECs in alleviating renal ischemia reperfusion injury. Conclusions We reported hAECs could improve survival and ameliorate renal injury in mice with IRI-AKI. The anti-apoptotic, pro-angiogenetic, and immunomodulatory capabilities of hAECs are at least partially, through paracrine pathways. hAECs-EXO might be a promising clinical therapeutic tool, overcoming the weaknesses and risks associated with the use of native stem cells, for patients with AKI.

scholarly journals Concordant Changes of Plasma and Kidney MicroRNA in the Early Stages of Acute Kidney Injury: Time Course in a Mouse Model of Bilateral Renal Ischemia-Reperfusion

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e93297 ◽  
Author(s):  
Melissa A. Bellinger ◽  
James S. Bean ◽  
Melissa A. Rader ◽  
Kathleen M. Heinz-Taheny ◽  
Jairo S. Nunes ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Mouse Model ◽  
Time Course ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Early Stages

scholarly journals Panaxadiol Saponin and Dexamethasone Improve Renal Function in Lipopolysaccharide-Induced Mouse Model of Acute Kidney Injury

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0134653 ◽  
Author(s):  
Yan Chen ◽  
Yanwei Du ◽  
Yang Li ◽  
Xiaoqin Wang ◽  
Pin Gao ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Mouse Model ◽  
Kidney Injury
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