Comparison of human adipose stromal vascular fraction and adipose-derived mesenchymal stem cells for the attenuation of acute renal ischemia/reperfusion injury

Zhou, Liuhua; Song, Qun; Shen, Junda; Xu, Luwei; Xu, Zheng; Wu, Rongqian; Ge, Yu‐Zheng; Zhu, Jun; Wu, Jianping; Dou, Qingyu; Jia, Ru

doi:10.1038/srep44058

Cited by 37 publications

(28 citation statements)

References 37 publications

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“…On the other hand, the level of anti-inflammatory IL-10 was increased after ADMSC treatment. These results were similar to the previous reports, 32,36…”

Section: Discussionsupporting

confidence: 93%

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Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Zhang

Wang

et al. 2017

Clin Exp Pharma Physio

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Acute kidney injury (AKI) represents a group of complicated syndromes with a high mortality rate. The administration of adipose-derived mesenchymal stem cells (ADMSCs) has been tested as a possible treatment method for AKI. The long-term evaluation of AKI induced by ischemia/reperfusion (IR) and the probable renal protection of ADMSCs are limited. In this study we have established a rat AKI model induced by IR and investigated the possible protective effects of ADMSCs. Adult Sprague-Dawley (SD) rats were divided into three groups (n = 6/each group). The MOCK group was as the normal control. Rats in the IR-AKI and IR-AKI+ADMSCs groups were subjected to IR injury by clamping both renal pedicles for 40 minutes. Rats in the MOCK and IR-AKI groups were injected with PBS via the tail vein as negative treatment controls. Rats in the IR-AKI+ADMSCs group received ADMSCs therapy (2 × 10 cells were injected into the rats via the tail vein). We found that ADMSC transplantation restored the pathologic morphology induced by IR-AKI to normal compared with the MOCK group, suggesting the reparative function of ADMSCs in kidney tissues. Compared with IR-induced AKI alone, ADMSC treatment significantly decreased the number of apoptotic cells, the level of total urinary protein and serum creatinine, the expression of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IFN-γ, TNF-α, IFN-γ, and TGF-β), and the inflammation-associated proteins (HGF and SDF1), but increased the expression of the anti-inflammatory cytokine, IL-10, and the anti-apoptotic regulator, Bcl-2. Our data have indicated that ADMSC transplantation may protect against IR-induced AKI by anti-apoptotic and anti-inflammatory effects.

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“…On the other hand, the level of anti-inflammatory IL-10 was increased after ADMSC treatment. These results were similar to the previous reports, 32,36…”

Section: Discussionsupporting

confidence: 93%

“…On the other hand, the level of anti‐inflammatory IL‐10 was increased after ADMSC treatment. These results were similar to the previous reports, although our detection was performed in a later stage. It is necessary to further study the roles of proliferation and pro‐proliferative growth factors in MSC treatment of AKI.…”

Section: Discussionsupporting

confidence: 93%

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Zhang

Wang

et al. 2017

Clin Exp Pharma Physio

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“…I/R injury, a metabolic disorder of cells, is caused by I/R and usually leads to renal dysfunction and destruction [7]. Currently, major therapeutic approaches used for treating AKI include renal transplantation, dialysis and stem cell transplantation [8]. Additionally, pharmacological agents with therapeutic effects, such as anti-inflammation, anti-oxidative and anti-coagulation agents, can be used to potentially prevent the development and progression of AKI [9].…”

Section: Introductionmentioning

confidence: 99%

Lentivirus-Mediated Silencing of Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase 2 Inhibits Release of Inflammatory Cytokines and Apoptosis in Renal Tubular Epithelial Cells Via Inhibition of the TLR4/NF-kB Pathway in Renal Ischemia-Reperfusion Injury

Teng

Wang

Jia

et al. 2018

Kidney Blood Press Res

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Background/Aims: Renal reperfusion injury occurs after the blood flow to the ischemic kidney is re-established under various clinical conditions, such as organ transplantation, renal artery stenosis, embolic disease, and the repair of descending aortic. The current study aims to explore the effects of src homology 2 domain-containing protein tyrosine phosphatase 2 (SHP-2) on the release of inflammatory cytokines and the apoptosis of renal tubular epithelial cells by regulating the TLR4/NF-κB signaling pathway in rats with renal ischemia-reperfusion (I/R) injury. Methods: A total of 60 normal clean Sprague Dawley (SD) (WT) rats were used in this study. The levels of creatinine (Cr) and blood urea nitrogen (BUN) were determined using an automatic biochemical analyzer. The apoptosis in renal tissue was detected by TUNEL assay. The renal tubular epithelial cells of rats were cultured, infected and treated with different lentivirus vectors. The serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), IL-1β and SHP27 were measured. Reverse transcription quantitative polymerases chain reaction and Western blot analysis were performed to measure the expression of relevant genes and proteins. Furthermore, the effect of SHP-2 on the proliferation, cell cycle and apoptosis of renal tubular epithelial cells was also investigated. Results: In the serum of rats with renal I/R injury and prolonged reperfusion time, the contents of Cr and BUN were increased, the positive expression of SHP-2 was higher, the level of apoptosis was promoted, IL-6, TNF-α, IL-1β and SHP27 expression in the serum was increased, the expression of SHP2, TLR4, NF-κB, IL-6, TNF-α and Bax was up-regulated, and the expression of Bcl-2 was down-regulated. Lentivirus-mediated silencing of SHP-2 promoted the proliferation of renal tubular epithelial cells, inhibited their apoptosis, and reduced the expression of inflammatory factors in these cells by functionally suppressing the TLR4/NF-κB signaling pathway. Conclusion: The results indicated that lentivirus-mediated silencing of SHP-2 inhibited the release of inflammatory cytokines and the apoptosis of renal tubular epithelial cells, and promoted the proliferation of these cells by inhibiting the TLR4/NF-κB signaling pathway in rats with renal I/R injury.

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“…(It is important to note that isolation of SVF, which requires centrifugation steps and usually enzymatic digestion makes these cells “more than minimally manipulated” by FDA guidance.) SVF‐mediated renoprotective effects are similar to those of cultured adipose MSCs in a rat model of I/R injury . MSCs from cord blood show similar effects to bone marrow MSCs in models of both AKI and CKD .…”

Section: Different Types Of Stem Cells and Preclinical Models Of Renamentioning

confidence: 68%

“…AdMSCs also may not emerge until after extensive culture of the SVF. In one study, the unsorted SVF had a similar therapeutic effect to AdMSCs in a renal I/R injury model , but further comparisons of all these cell types are warranted.…”

Section: Important Variables In the Preclinical Renal Regeneration LImentioning

confidence: 99%

Concise Reviews: Stem Cells and Kidney Regeneration: An Update

Marcheque

Bussolati

Csete

et al. 2018

Stem Cells Translational Medicine

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Significant progress has been made to advance stem cell products as potential therapies for kidney diseases: various kinds of stem cells can restore renal function in preclinical models of acute and chronic kidney injury. Nonetheless this literature contains contradictory results, and for this reason, we focus this review on reasons for apparent discrepancies in the literature, because they contribute to difficulty in translating renal regenerative therapies. Differences in methodologies used to derive and culture stem cells, even those from the same source, in addition to the lack of standardized renal disease animal models (both acute and chronic), are important considerations underlying contradictory results in the literature. We propose that harmonized rigorous protocols for characterization, handling, and delivery of stem cells in vivo could significantly advance the field, and present details of some suggested approaches to foster translation in the field of renal regeneration. Our goal is to encourage coordination of methodologies (standardization) and long‐lasting collaborations to improve protocols and models to lead to reproducible, interpretable, high‐quality preclinical data. This approach will certainly increase our chance to 1 day offer stem cell therapeutic options for patients with all‐too‐common renal diseases. Stem Cells Translational Medicine 2019;8:82–92

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Comparison of human adipose stromal vascular fraction and adipose-derived mesenchymal stem cells for the attenuation of acute renal ischemia/reperfusion injury

Cited by 37 publications

References 37 publications

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Adipose‐derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia‐reperfusion in a rat model

Lentivirus-Mediated Silencing of Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase 2 Inhibits Release of Inflammatory Cytokines and Apoptosis in Renal Tubular Epithelial Cells Via Inhibition of the TLR4/NF-kB Pathway in Renal Ischemia-Reperfusion Injury

Concise Reviews: Stem Cells and Kidney Regeneration: An Update

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