High Glucose Condition Suppresses Neurosphere Formation by Human Periodontal Ligament-Derived Mesenchymal Stem Cells

2014 ◽  
Vol 115 (5) ◽  
pp. 928-939 ◽  
Author(s):  
Chenphop Sawangmake ◽  
Prasit Pavasant ◽  
Piyarat Chansiripornchai ◽  
Thanaphum Osathanon
2017 ◽  
Vol 35 (7) ◽  
pp. 407-413 ◽  
Author(s):  
Elaheh Zafarvahedian ◽  
Azam Roohi ◽  
Mohammad Reza Sepand ◽  
Seyed Nasser Ostad ◽  
Mohammad Hossein Ghahremani

2020 ◽  
Vol 47 (10) ◽  
pp. 7505-7516 ◽  
Author(s):  
Kuneerat Aswamenakul ◽  
Parin Klabklai ◽  
Supitcha Pannengpetch ◽  
Tulyapruek Tawonsawatruk ◽  
Chartchalerm Isarankura-Na-Ayudhya ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Wenjun Zhu ◽  
Qihong Qiu ◽  
Haoyuan Luo ◽  
Fuping Zhang ◽  
Juan Wu ◽  
...  

Objective. This research is aimed at investigating how high glucose affects the proliferation and apoptosis in periodontal ligament stem cells (PDLSCs) in the presence of TNF-α. Methods. PDLSCs obtained from periodontal healthy permanent teeth were treated under either high-glucose condition (30 mmol/L, G30 group) or normal glucose condition (5.6 mmol/L, G5.6 group) in the presence or absence of TNF-α (10 ng/ml) for 2 to 6 days. Cell proliferation and cell cycle were evaluated by CCK-8, EdU incorporation assay, and flow cytometry. Cell apoptosis was assessed by annexin V/PI staining. Protein expression was detected by western blotting. Cellular ROS expression was evaluated by CellROX labeling and flow cytometry. Specific antibodies targeting TNFR1 and TNFR2 were used to block TNF-α signaling. Vitamin C was also used to verify if the blockage of ROS can rescue PDLSCs in the presence of high glucose and TNF-α. Results. CCK-8 assay showed that high glucose exacerbated TNF-α-induced cell viability inhibition (57.0%, 85.2%, and 100% for the G30+TNF-α group, G5.6+TNF-α group, and control group, respectively) on day 6. High glucose increased protein expression of TNFR1 compared with the control group on day 2 (1.24-fold) and day 6 (1.26-fold). Blocking TNFR1 totally reversed the proliferative inhibition in G30+TNF-α group. The addition of vitamin C or TNFR1 antibody totally reversed the elevation of intracellular ROS expression caused by high glucose and TNF-α. Vitamin C partially restored cell proliferation in the presence of high glucose and TNF-α. Conclusion. High glucose exacerbates TNF-α-induced proliferative inhibition in human periodontal ligament stem cells through the upregulation and activation of TNF receptor 1. Inhibition of intracellular ROS expression by vitamin C partially rescues PDLSCs in terms of cell proliferation.


2019 ◽  
Vol 19 (9) ◽  
pp. 688-698 ◽  
Author(s):  
Azam Roohi ◽  
Mahin Nikougoftar ◽  
Hamed Montazeri ◽  
Shadisadat Navabi ◽  
Fazel Shokri ◽  
...  

Background: Oxidative stress and chronic hyperglycemia are two major side effects of type 2 diabetes affecting all cell types including mesenchymal stem cells (MSCs). As a cell therapy choice, understanding the behavior of MSCs will provide crucial information for efficient treatment. Methods: Placental mesenchymal stem cells were treated with various concentrations of glucose, metformin, rapamycin, and hydrogen peroxide to monitor their viability and cell cycle distribution. Cellular viability was examined via the MTT assay. Cell cycle distribution was studied by propidium iodide staining and apoptosis was determined using Annexin Vpropidium iodide staining and flow cytometry. Involvement of potential signaling pathways was evaluated by Western blotting for activation of Akt, P70S6K, and AMPK. Results: The results indicated that high glucose augmented cell viability and reduced metformin toxic potential. However, the hydrogen peroxide and rapamycin toxicities were exacerbated. Conclusion: Our findings suggest that high glucose concentration has a major effect on placental mesenchymal stem cell viability in the presence of rapamycin, metformin and hydrogen peroxide in culture.


Author(s):  
Sema S. Hakki ◽  
Buket S. Bozkurt ◽  
Erdogan E. Hakki ◽  
Erdal Karaoz ◽  
Ali Unlu ◽  
...  

2021 ◽  
Vol 22 (9) ◽  
pp. 4604
Author(s):  
Giuliana Mannino ◽  
Anna Longo ◽  
Florinda Gennuso ◽  
Carmelina Daniela Anfuso ◽  
Gabriella Lupo ◽  
...  

A pericyte-like differentiation of human adipose-derived mesenchymal stem cells (ASCs) was tested in in vitro experiments for possible therapeutic applications in cases of diabetic retinopathy (DR) to replace irreversibly lost pericytes. For this purpose, pericyte-like ASCs were obtained after their growth in a specific pericyte medium. They were then cultured in high glucose conditions to mimic the altered microenvironment of a diabetic eye. Several parameters were monitored, especially those particularly affected by disease progression: cell proliferation, viability and migration ability; reactive oxygen species (ROS) production; inflammation-related cytokines and angiogenic factors. Overall, encouraging results were obtained. In fact, even after glucose addition, ASCs pre-cultured in the pericyte medium (pmASCs) showed high proliferation rate, viability and migration ability. A considerable increase in mRNA expression levels of the anti-inflammatory cytokines transforming growth factor-β1 (TGF-β1) and interleukin-10 (IL-10) was observed, associated with reduction in ROS production, and mRNA expression of pro-inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), and angiogenic factors. Finally, a pmASC-induced better organization of tube-like formation by retinal endothelial cells was observed in three-dimensional co-culture. The pericyte-like ASCs obtained in these experiments represent a valuable tool for the treatment of retinal damages occurring in diabetic patients.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Fangzi Gong ◽  
Le Gao ◽  
Luyao Ma ◽  
Guangxin Li ◽  
Jianhong Yang

Abstract Background Progressive population aging has contributed to the increased global prevalence of diabetes and osteoporosis. Inhibition of osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) by hyperglycemia is a potential pathogenetic mechanism of osteoporosis in diabetic patients. Uncarboxylated osteocalcin (GluOC), a protein secreted by mature osteoblasts, regulates bone development as well as glucose and lipid metabolism. In our previous studies, GluOC was shown to promote osteoblastic differentiation of BMSCs; however, the underlying mechanisms are not well characterized. Tumor protein 63 (TP63), as a  transcription factor, is closely related to bone development and glucose metabolism. Results In this study, we verified that high glucose suppressed osteogenesis and upregulated adipogenesis in BMSCs, while GluOC alleviated this phenomenon. In addition, high glucose enhanced TP63 expression while GluOC diminished it. Knock-down of TP63 by siRNA transfection restored the inhibitory effect of high glucose on osteogenic differentiation. Furthermore, we detected the downstream signaling pathway PTEN/Akt/GSK3β. We found that diminishing TP63 decreased PTEN expression and promoted the phosphorylation of Akt and GSK3β. We then applied the activator and inhibitor of Akt, and concluded that PTEN/Akt/GSK3β participated in regulating the differentiation of BMSCs. Conclusions Our results indicate that GluOC reduces the inhibitory effect of high glucose on osteoblast differentiation by regulating the TP63/PTEN/Akt/GSK3β pathway. TP63 is a potential novel target for the prevention and treatment of diabetic osteoporosis.


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