Bone marrow-derived mesenchymal stem cells ameliorate nephrosis through repair of impaired podocytes

Chen, Yi; Wan, Jianxin; Gao, Na; Cui, Jiong; You, Danyu; Zou, Zhenhuan

doi:10.25011/cim.v40i1.28050

Cited by 6 publications

(4 citation statements)

References 40 publications

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“…It is well known that proteinuria is a biomarker for kidney dysfunction and an important prognostic factor for the progression of kidney disease 4 . Our results are in agreement with previous reports that mSC administration results in decreased protein excretion in the 5/6 nephrectomy model 15 and in the anti-Thy glomerulonephritis 1.1 model 21 , as well as in mice receiving one single dose of PAN, demonstrating a protective role of CTm in the reduction of proteinuria 22 . On the other hand, mSC administration in the adriamycin-induced nephropathy model did not modify the proteinuria 16,17 .…”

Section: Discussionsupporting

confidence: 93%

“…While the induction of podocyte injury led to significant alterations in molecular composition, characterized by decreased WT1 expression and the downregulation of nephrin, podocin, synaptopodin, and podocalyxin expression, the administration of mSC in this disease model has shown a protective role by inducing a significant upregulation of WT1 and partial recovery of nephrin, synaptopodin, podocin, and podocalyxin expression. Our data confirm previous findings regarding the protective effect of mSC on podocytes 17,22,23 .…”

Section: Discussionsupporting

confidence: 93%

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Mesenchymal Stromal Cells Induce Podocyte Protection in the Puromycin Injury Model

Ornellas

Ramalho

Fanelli

et al. 2019

Sci Rep

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Podocytes are specialized cells with a limited capacity for cell division that do not regenerate in response to injury and loss. Insults that compromise the integrity of podocytes promote proteinuria and progressive renal disease. The aim of this study was to evaluate the potential renoprotective and regenerative effects of mesenchymal stromal cells (mSC) in a severe form of the podocyte injury model induced by intraperitoneal administration of puromycin, aggravated by unilateral nephrectomy. Bone derived mSC were isolated and characterized according to flow cytometry analyses and to their capacity to differentiate into mesenchymal lineages. Wistar rats were divided into three groups: Control, PAN, and PAN+ mSC, consisting of PAN rats treated with 2 × 105 mSC. PAN rats developed heavy proteinuria, hypertension, glomerulosclerosis and significant effacement of the foot process. After 60 days, PAN rats treated with mSC presented a significant amelioration of all these abnormalities. In addition, mSC treatment recovered WT1 expression, improved nephrin, podocin, synaptopodin, podocalyxin, and VEGF expression, and downregulated proinflammatory Th1 cytokines in the kidney with a shift towards regulatory Th2 cytokines. In conclusion, mSC administration induced protection of podocytes in this experimental PAN model, providing new perspectives for the treatment of renal diseases associated with podocyte damage.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Mesenchymal Stromal Cells Induce Podocyte Protection in the Puromycin Injury Model

Ornellas

Ramalho

Fanelli

et al. 2019

Sci Rep

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“…TRAF6 is specifically required for JNK and p38 signaling activation in a Smad-independent way. Other researchers found that the upregulation of TRAF6 in the peripheral blood of LN patients increased the possibility of ESRD progression and recurrence within 1 year ( Chen et al, 2017 ). In this study, the expression of p-Smad3 in the renal tissue was significantly increased in the LN model group but significantly inhibited in the UC-MSC + MP group.…”

Section: Discussionmentioning

confidence: 99%

Umbilical Cord Mesenchymal Stem Cells Ameliorate Kidney Injury in MRL/Ipr Mice Through the TGF-β1 Pathway

Huang

Meng

et al. 2022

Front. Cell Dev. Biol.

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The therapeutic effects and mechanism of umbilical cord mesenchymal stem cells (UC-MSC) on kidney injury in MRL/Ipr mice were studied. UC-MSC, methylprednisolone (MP), and their combination were used to treat MRL/Ipr mice. The therapeutic effects were evaluated by renal function assessment, and HE, PAS, and Masson staining were carried out on renal tissues and visualized by electron microscopy. Subsequently, podocyte injury was detected by the presence of podocin in renal tissues by immunofluorescence. To further explore the mechanism, serum TGF-β1 was measured, and TGF-β1, p-Smad3, and TRAF6 in the renal tissue were detected by Western blotting. In vitro, TGF-β1 was used to stimulate podocytes, and the podocyte activity and changes in synaptopodin were observed after UC-MSC treatment. Significant improvements in renal function and pathological injury were observed in the UC-MSC group compared to the lupus nephritis (LN) model group. UC-MSC and MP treatment improved podocyte injury in MRL/Ipr mice. Western blot examination showed a significant increase in TGF-β1, p-Smad3, and TRAF6 expression in renal tissues of the LN model group, while significant downregulation of those proteins was observed in the UC-MSC group. After TGF-β1 stimulation in vitro, podocyte activity decreased, and UC-MSC treatment improved podocyte activity and restored synaptopodin expression. UC-MSC therapy could improve the deterioration of renal function and the pathological changes of the renal tissues in MRL/Ipr mice. Our study suggested that UC-MSC may improve kidney injury and podocyte injury in LN mice by inhibiting the TGF-β1 pathway.

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“…After administration of BMSCs, the expression of nephrin, CD2AP, and synaptopodin was up-regulated, while TRPC6 was down-regulated. Administration of BMSCs reduced excretion of protein through urine and protected podocytes from deleterious effects of PAN 10 . In a novel study, BM-MSCs along with human umbilical cord extract were used to enhance the proliferative capability of BM-MSCs against DN.…”

Section: Mesenchymal Stem Cells For Diabetic Nephropathymentioning

confidence: 98%

Mesenchymal stem cells transplantation reduces diabetic nephropathy

Kazmi

Muhammad

et al. 2019

Prog. Stem Cell

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Diabetes mellitus is a metabolic disease in which the pancreas is unable to produce enough insulin due to the destruction of b -cells or the body does not utilize insulin properly. Continuous fluctuation of blood glucose levels is responsible for prolonged complications such as diabetic nephropathy (DN), diabetic retinopathy, or diabetic cardiomyopathy. Approximately, 20-30% of all diabetic patients face DN, which causes the formation of diabetic glomerular lesions and reduced glomerular filtration rate. In the case of renal failure, kidney transplantation is the only available therapy, however, it is expensive and almost unattainable due to unavailability of donors and host immune rejection. Stem cells are an alternative and attractive source of therapy because of their proliferative nature and the ability to produce distinct specialized cells. Mesenchymal stem cells (MSCs), which are derived from bone marrow, possess an anti-inflammatory property and the ability of selfrenewal and differentiation into a variety of specialized cells. MSCs are widely used to treat different diseases including DN and they have shown encouraging outcomes. This review provides details about the regenerative efficiency of using MSCs in treating diabetic nephropathy.

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Bone marrow-derived mesenchymal stem cells ameliorate nephrosis through repair of impaired podocytes

Cited by 6 publications

References 40 publications

Mesenchymal Stromal Cells Induce Podocyte Protection in the Puromycin Injury Model

Mesenchymal Stromal Cells Induce Podocyte Protection in the Puromycin Injury Model

Umbilical Cord Mesenchymal Stem Cells Ameliorate Kidney Injury in MRL/Ipr Mice Through the TGF-β1 Pathway

Mesenchymal stem cells transplantation reduces diabetic nephropathy

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