BACKGROUND:Mesenchymal stem cells (MSCs) may serve as immunoregulators by producing various anti-inflammatory molecules. Under sufficient level of TNF-α, MSCs become activated and adopt immune-suppressive phenotype (MSCs type-2) by releasing various anti-inflammatory molecule including TGF-β and IL-10. However, the ability of MSC itself to produce IL-10 under TNF-α stimulation and the correlation of TGF-β production of MSCs to IL-10 level remains to be elucidated.AIM:In this study, MSCs were activated with various TNF-α doses to determine the increase of IL-10 and TGF-β level as well as its correlation.MATERIAL AND METHODS:This study used post-test only control group design, by using 3 study groups, consist of 1 control (C) and 2 treatments (T) (TNF-α = 5 and 10 ng/mL) with triplicate induced in MSC for 24 hours, then the levels of IL-10 and TGF-β were measured by using ELISA assay.RESULTS:The results of this study showed a significant increase of TGF-β and IL-10 levels (p < 0.05) at TNF-α 5 and 10 ng/mL dose of TNF-α. Moreover, there was a significant negative correlation between TGF-β and IL-10 level on 5 and 10 ng/mL dose TNF-α treatment.CONCLUSION:Based on our study, we conclude that the 5 ng/mL dose of TNF-α is a sufficient dose for MSCs to suppress the inflammatory milieu. The higher increase of TGF beta is due to the controlled inflammation by IL-10.
Background: The mechanisms underlying peripheral disorders during systemic lupus erythematosus (SLE) were found to be shared with tolerance disorders and mediated by T-regulator (T-reg) cells. Mesenchymal stem cells (MSCs) may inhibit T-cell subset differentiation and induce the T-reg cell phenotype. However, the capacity of MSCs to promote functional T-reg cells in SLE patients remains unclear. Objectives: This study aimed to analyze the capacity of MSCs to induce the production of functional CD4+ CD25+ Foxp3+ T-reg cells, in vitro, under co-culture conditions with human SLE cells. Methods: This study used a pre- and post-test control group design. Peripheral blood mononuclear cells (PBMCs) were extracted from SLE patients at the Kariadi Hospital, and MSCs were derived from human umbilical cords (hUCs) The PBMC control group was treated with standard medium, and the treatment group was co-cultured with hUC-MSCs. After 24 hours of co-culture incubation, T-reg cells were removed from the PBMC pool, using magnetic-activated cell sorting (MACS), and the population was assessed using the trypan blue exclusion assay. Results: A significant increase in the population of T-reg cells was observed (P < 0.001) after 24 hours of co-culture incubation with hUC-MSCs. Conclusion: This study concluded that MSCs have the capacity to enhance the T-reg population in human SLE PBMCs. Bangladesh Journal of Medical Science Vol.19(4) 2020 p.743-748
Introduction: The massive hepatic necrosis of acute liver failure (ALF) results in a sudden loss of hepatic cells. Although most hepatocyte cells of ALF are completely lost, stem cell-derived circulating cells and endogenous progenitor cells rapidly regenerate them. Mesenchymal stem cells (MSCs) have a critical role in the regeneration of liver injury through regulating platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) levels. However, their fluctuating levels in the healing process and correlation to the decrease of liver function markers remain unclear. The aim of this study was to analyze the effects of MSCs in accelerating liver regeneration of ALF by measuring VEGF and PDGF levels on day 2 and 7, as well as SGPT and SGOT levels, and assessing histopathology appearance. Methods: Using an ALF rat model, 12 animals were randomly assigned into two groups: umbilical cord (UC)-MSC injection (T1) and vehicle control (Veh). ELISA assay was employed to measure PDGF and VEGF levels, an automatic analyzer was used to assess serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT), and hematoxylin and eosin (H&E) staining was used to evaluate morphological appearance. Results: The study showed an significant (P<0.001) increase of PDGF and VEGF levels on the 2nd day, followed by a decrease on the 7th day, along with a decrease of SGPT and SGOT levels as well as the normality of histology appearance. Conclusion: In conclusion, administration of MSCs may accelerate liver regeneration of ALF through PDGF and VEGF regulation.
<p>Background<br />Peritoneal adhesions (PAs) are generally described as fibrous bands between intra-abdominal organs following an abdominal surgical operation. The definitive treatments of PAs are currently ineffective yet. Hypoxia-mesenchymal stem cells (H-MSCs) have a higher capability to survive at the site of injury than normoxia-MSCs (N-MSCs) to repair injured tissue without fibrosis. This study aimed to analyze the effect of H-MSCs in controlling formation of PAs by reducing TGF-β level in a rat model. <br /><br />Methods <br />A study of post-test only control group design was conducted, involving eighteen PA rat models weighing 250 ± 25 g that were randomly assigned into 3 groups, comprising control group (C), and groups T1 and T2 receiving H-MSC treatment at doses of 3 x 106 and 1.5 x 106, respectively. To induce H-MSCs, MSCs were incubated in hypoxic conditions at 5% O2 and 37oC for 24 hours. Expression level of TGF-β was analyzed by enzyme-linked immunosorbent assay (ELISA) at 450 nm and adhesion formation was described macroscopically. The Kruskal-Wallis variance analysis was used to analyze significant differences among the groups.<br /><br />Results<br />The results of this study showed that H-MSCs in group T1 inhibited TGF-β expression significantly on day 8 (p<0.001) and day 14 (p<0.05). Moreover, there was almost no adhesion apparent following H-MSC administration in group T1. <br /><br />Conclusions<br />Based on this study, we conclude that H-MSCs may attenuate PA formation following inhibition of TGF-β expression in the PA rat model.</p>
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