scholarly journals Investigate the therapeutic effect of autologous adipose-derived stem cells (ADSCs) on ischemic renal failure in dogs.

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Masaaki Ii ◽  
Ayumi Yokoyama ◽  
Miki Horii ◽  
Hiroshi Akimaru ◽  
Takayuki Asahara

Background: Recently, human multipotent adipose-derived stem cells (hMADSs) have been isolated featuring extensive expansion capacity ex vivo. However, little is known about the therapeutic efficacy of hMADS in ischemic heart diseases. We tested the hypothesis that hMADS transplantation may contribute to cardiac functional recovery following myocardial infarction (MI). Methods and Results: Nude rats were either transplanted with hMADSs (5x10 5 /rat, n=10) or PBS (control, n=9) in ischemic myocardium immediately following MI induction. The cardiac function, infarct size and capillary density in the peri-infarct area were evaluated by echocardiography and immunostaining 28 days after surgery. The cardiac function was significantly greater with increased capillary density and reduced fibrosis area in the hMADS group than that in the control group. Next, we examined tissue regeneration in the infarct heart by the transplanted hMADSs. However, remarkable differentiation of hMADSs into any cardiac cell lineages was not detected. To explore another mechanism for the favorable effect of hMADSs, we further examined mRNA expression of cytokines in hMADSs under hypoxic conditions. Although hypoxia decreased the expressions, robust VEGF, bFGF, and SDF-1α expressions were detected in hMADSs. Notably, the stem/progenitor chemokine SDF-1α expression in hMADSs was significantly greater than that in human mesenchymal stem cells that are well known to have a therapeutic effect on ischemic heart diseases. We then focused on SDF-1α /CXCR4 axis and examined the contribution of bone marrow (BM)-derived endothelial progenitor cells (EPCs), that have CXCR4 receptor for SDF-1v, to ischemic myocardium using a Tie2/LacZ BM transplantation nude mouse model. β-gal positive EPCs are frequently observed in ischemic myocardium in the hMADS group compared to the control group. Conclusion: hMADSs exhibit a therapeutic effect on cardiac function following MI with the production of VEGF, bFGF, and SDF-1α demonstrating paracrine effects rather than direct contribution to cardiac regeneration. These findings suggest that transplanted hMADSs and recruited EPCs may synergistically promote angiogenesis playing a role in ischemic myocardium.


2016 ◽  
Vol 25 (5) ◽  
pp. 899-912 ◽  
Author(s):  
Kang Chi ◽  
Ru-Huei Fu ◽  
Yu-Chuen Huang ◽  
Shih-Yin Chen ◽  
Shinn-Zong Lin ◽  
...  

2021 ◽  
Author(s):  
Ziqiang Zhang ◽  
Yingying Sun ◽  
Haojie Wang ◽  
Yuxiang Yang ◽  
Ruiqi Dong ◽  
...  

Abstract Background and PurposeIn this study, the therapeutic effect of Mel-incubated ADSCs on CCl4-induced hepatic fibrosis was investigated. MethodsThe experiment was arranged into ADSCS group, ADSCS + Mel group, Model group and Control group with 10 mice in each group. The other three groups of mice were intraperitoneally injected with 8% CCl4, and the control group was injected with the same dose of PBS twice a week for 4 weeks. From the fifth week, ADSCs group and ADSCs + Mel group mice were injected with 1×106 cells/1 ml PBS dose of ADSCs and 50 μM Mel pretreated ADSCs into tail vein, respectively, twice a week for 2 weeks, and mice in the control and model groups were injected with the same dose of PBS. Samples were tested after six weeks. ResultsIn model group, severe histomathological changes were observed in liver, including severe vacuolation, nuclear fragmentation and liver fibrosis, and these changes were ameliorated by Mel pretreated ADSCs. At the same time, RT-qPCR results showed that Mel-induced ADSCs significantly inhibited the expression of pro-apoptotic genes (Caspase-8, Bax and Caspase-3), and promoted the expression of anti-apoptotic gene (Bcl-2). Immunohistochemical results showed that a large number of MMP-9, TGF-β, MMP-2 yellow-stained positive cells were found in the liver tissues of the model group, while the expression of positive cells was blocked by Mel-induced ADSCs. Conclusion and ImplicationsADSCs pretreated with Mel significantly improved CCl4-induced liver fibrosis, which provides a reference for clinical treatment of liver injury with mesenchymal stem cells.


2012 ◽  
Vol 9 (8) ◽  
pp. 1968-1979 ◽  
Author(s):  
Shuyu Piao ◽  
In Gul Kim ◽  
Ji Young Lee ◽  
Sung Hoo Hong ◽  
Sae Woong Kim ◽  
...  

2015 ◽  
Vol 8 (2) ◽  
pp. 170-180 ◽  
Author(s):  
Gihan Ibrahim Aboul-Fotouh ◽  
Maha Baligh Zickri ◽  
Hala Gabr Metwally ◽  
Ihab Refaat Ibrahim ◽  
Samaa Samir Kamar ◽  
...  

2021 ◽  
Author(s):  
Jingyan Guan ◽  
Yibao Li ◽  
Feng Lu ◽  
Jingwei Feng

Abstract Background: Mesenchymal stem cells (MSCs) has therapeutic potential for Atopic dermatitis (AD) due to their immunoregulatory effects. However, the underlying mechanisms for therapeutic efficacy of ADSCs on AD is still unclear. Objectives: We sought to investigate the therapeutic effect and mechanisms of adipose-derived stem cells (ADSCs) on AD using an ovalbumin-induced AD mouse model. Methods: AD mice were treated with mice-derived ADSCs, cortisone, or PBS. The therapeutic effect was determined via gross examination and additional in vitro assays using skin samples and blood. To further explore the underlying mechanisms, RNA sequencing analyses and co-culture assays were conducted.Results: ADSCs treatment attenuated the symptoms associated with AD, decreased the serum IgE level and mast cells infiltration. Tissue levels of T-cell relevant pro-inflammatory cytokine production, including IL-4R and IL-17A, were suppressed in both ADSCs and cortisone treatment groups. Genomics and bioinformatics analyses demonstrated a significant enrichment of certain of inflammation related pathway in the down regulated genes after the application of ADSCs and cortisone, specifically the IL-17 signaling pathway. Co-culture experiments revealed that ADSCs significantly suppressed the expression of pro-inflammation cytokines IL-17A and RORγT, as well as the proliferation of Th17 cells. Moreover, the expression of PD-L1, TGF-β, PGE2 was significantly upregulated in the co-cultured ADSCs compare to monocultured ADSCs. Conclusion: Taken together, our data may demonstrate that ADSCs ameliorate OVA- induced AD in mice by down-regulating IL-17 secretion of Th17 cells.


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