scholarly journals Combination of Nonwoven Filters and Mesenchymal Stem Cells Reduced Glomerulosclerotic Lesions in Rat Chronic Kidney Disease Models

2019 ◽  
Vol 10 (03) ◽  
pp. 135-149
Author(s):  
Hideo Hori ◽  
Masanori Shinzato ◽  
Yoshiyuki Hiki ◽  
Shigeru Nakai ◽  
Gen Niimi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Kidney Disease ◽  
Disease Models

scholarly journals P0026METFORMIIN IMPROVES DYSFUNCTION OF MESENCHYMAL STEM CELLS ASSOCIATED WITH CHRONIC KIDNEY DISEASE VIA SENESCENCE INHIBITION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Hyunjin Noh ◽  
Mi Ra Yu ◽  
Kyoungin Choi ◽  
Dohui Hwang
Keyword(s):  
Chronic Kidney Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Kidney Disease ◽  
Cellular Senescence ◽  
Critical Factor ◽  
Protective Role ◽  
Metformin Treatment ◽  
Promising Source

Abstract Background and Aims Mesenchymal stem cells (MSC) are promising source of cell-based regenerative therapy; however, adequate cell functionality is a critical factor for the success of autotransplantation. Method We investigated the effects of metformin on chronic kidney disease (CKD)-associated cellular senescence using MSC isolated from sham operated and subtotal nephrectomized mice and further explored the protective role of metformin-treated CKD MSC in renal progression. Results When compared to normal MSC, MSC isolated from CKD mice displayed reduced proliferation and early senescence as determined by enlarged cell morphology, increased oxidative stress, accumulation of DNA damage response marker p53 binding protein 1 (53BP1), phospho p53, p16INK4a, and β-gal expression, and decreased cyclin-dependent kinase 4 (CDK4) and cyclin D. CKD MSC exhibited activation of NFκB resulting in expression of senescence-associated secretory phenotype (SASP) factors compared to normal MSC. All of these changes were significantly prevented by metformin treatment. In vivo, metformin-treated CKD MSC attenuated inflammation and fibrosis in UUO kidney as compared to CKD MSC. Co-culture of LPS or TGF-β1-treated HK2 cells with metformin-treated CKD MSC markedly decreased LPS or TGF-β-induced tubular expression of proinflammatory markers and fibrogenesis when compared to CKD MSC suggesting paracrine action of CKD MSC enhanced by metformin treatment. Conclusion Our data suggest that metformin inhibits cellular senescence of CKD MSC and improves their renoprotective effects.

scholarly journals Potential and Therapeutic Efficacy of Cell-based Therapy Using Mesenchymal Stem Cells for Acute/chronic Kidney Disease

2019 ◽  
Vol 20 (7) ◽  
pp. 1619 ◽  
Author(s):  
Chul Yun ◽  
Sang Lee
Keyword(s):  
Chronic Kidney Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Kidney Disease ◽  
Therapeutic Efficacy ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Kidney Diseases ◽  
Diverse Range ◽  
Cell Based Therapy

Kidney disease can be either acute kidney injury (AKI) or chronic kidney disease (CKD) and it can lead to the development of functional organ failure. Mesenchymal stem cells (MSCs) are derived from a diverse range of human tissues. They are multipotent and have immunomodulatory effects to assist in the recovery from tissue injury and the inhibition of inflammation. Numerous studies have investigated the feasibility, safety, and efficacy of MSC-based therapies for kidney disease. Although the exact mechanism of MSC-based therapy remains uncertain, their therapeutic value in the treatment of a diverse range of kidney diseases has been studied in clinical trials. The use of MSCs is a promising therapeutic strategy for both acute and chronic kidney disease. The mechanism underlying the effects of MSCs on survival rate after transplantation and functional repair of damaged tissue is still ambiguous. The paracrine effects of MSCs on renal recovery, optimization of the microenvironment for cell survival, and control of inflammatory responses are thought to be related to their interaction with the damaged kidney environment. This review discusses recent experimental and clinical findings related to kidney disease, with a focus on the role of MSCs in kidney disease recovery, differentiation, and microenvironment. The therapeutic efficacy and current applications of MSC-based kidney disease therapies are also discussed.

Terapia Celular com células tronco mesenquimais em gatos com doença renal crônica / Cell therapy with mesenchymal stem cells in cats with chronic kidney disease

2021 ◽  
Vol 7 (7) ◽  
pp. 70741-70760
Author(s):  
Pedro Henrique Martins De Melo ◽  
Hilana dos Santos Sena Brunel ◽  
Patrícia Furtado Malard ◽  
Carlos Alberto Da Cruz Júnior
Keyword(s):  
Chronic Kidney Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Kidney Disease ◽  
Cell Therapy

scholarly journals Pioglitazone Improves the Function of Human Mesenchymal Stem Cells in Chronic Kidney Disease Patients

2019 ◽  
Vol 20 (9) ◽  
pp. 2314 ◽  
Author(s):  
Yeo Min Yoon ◽  
Jun Hee Lee ◽  
Chul Won Yun ◽  
Sang Hun Lee
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Kidney Disease ◽  
Er Stress ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Cellular Prion Protein ◽  
Oxygen Species

Mesenchymal stem cells (MSCs) are optimal sources of autologous stem cells for cell-based therapy in chronic kidney disease (CKD). However, CKD-associated pathophysiological conditions, such as endoplasmic reticulum (ER) stress and oxidative stress, decrease MSC function. In this work, we study the protective effect of pioglitazone on MSCs isolated from CKD patients (CKD-MSCs) against CKD-induced ER stress. In CKD-MSCs, ER stress is found to induce mitochondrial reactive oxygen species generation and mitochondrial dysfunction. Treatment with pioglitazone reduces the expression of ER stress markers and mitochondrial fusion proteins. Pioglitazone increases the expression of cellular prion protein (PrPC) in CKD-MSCs, which is dependent on the expression levels of proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). Treatment with pioglitazone is found to protect CKD-MSCs against reactive oxygen species generation, aberrant mitochondrial oxidative phosphorylation of complexes I and IV, and aberrant proliferation capacity through the PGC-1α-PrPC axis. These results indicate that pioglitazone protects the mitochondria of MSCs from CKD-induced ER stress. Pioglitazone treatment of CKD-MSCs may be a potential therapeutic strategy for CKD patients.

Sign in / Sign up

Export Citation Format

Share Document