Exosomes Derived from Bone Marrow-Derived Mesenchymal Stem Cells (BM-MSC) Protect Submandibular Glands in Diabetic Rats

2021 ◽  
Vol 11 (11) ◽  
pp. 2168-2173
Author(s):  
Cong Zhang ◽  
Xiaohong Zhang ◽  
Min Zhang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Salivary Gland ◽  
Salivary Glands ◽  
Serum Amylase ◽  
Diabetic Rats ◽  
Submandibular Salivary Gland ◽  
Amylase Level ◽  
Group I

Our study assess whether exosomes derived from bone marrow mesenchymal stem cells (BM-MSC) ameliorates diabetic salivary gland complications. 10 SD rats were assigned into diabetes group I and exosome treatment group II. Diabetic rats were induced by streptozotocin (STZ) and injected with DMSO or exosomes through tail vein followed by collection of submandibular salivary gland samples for histological analysis and TGFβ, Smad2 and Smad3 level by PCR, saliva IgA and serum amylase level. Compared with control mice, exosome treatment mice showed less fibrosis of the submandibular salivary glands and duct components with a more complete structure. Exosome treatment inhibited TGFβ, Smad2 and Smad3 level to reduce diabetic salivary gland complications, effectively decreased blood sugar level, improved salivary glands function with significantly reduced serum amylase and salivary IgA levels. In conclusion, BM-MSC-derived exosomes may be a new therapeutic strategy for treating diabetic salivary gland complications.

Bone Marrow Mesenchymal Stem Cells (BMSCs) Transplantation Alleviates Acute Pancreatitis Through Inhibiting Inflammation and Promoting Caspase-8 Apoptosis Pathway

2022 ◽  
Vol 12 (5) ◽  
pp. 1034-1039
Author(s):  
Xiaoxiang Wang ◽  
Lan Yu ◽  
Xing Xiong ◽  
Yao Chen ◽  
Bo Men
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Acute Pancreatitis ◽  
Mesenchymal Stem Cells ◽  
Serum Amylase ◽  
Inflammatory Factors ◽  
Control Group ◽  
Caspase 8 ◽  
Apoptosis Pathway ◽  
Marrow Mesenchymal Stem Cells

Bone marrow mesenchymal stem cells (BMSCs) are capable of multipolar differentiation and repairing injured tissues. Herein, we aimed to investigate the mechanism by how BMSCs modulate the apoptotic pathway in the acute pancreatitis (AP). In this study, primary BMSCs were cultured and administrated into 10 AP mice while 10 healthy mice were taken as a blank group and 10 AP mice as a control group. The mouse pancreatic tissues were assessed by HE staining and evaluated by pancreatitis score and serum amylase detection. Level of inflammatory factors CRP and TNF-α was measured by ELISA and PIPK1, PIPK3, MLKL and Caspase-8 expression was detected by RT-qPCR and Western blot. The pancreatitis score (7.29±1.36) and the serum amylase score of (453.66±103.67) mu/ml of BMSCs group was significantly higher than that of control group, indicating increased tissue repair after BMSCs treatment. BMSCs group exhibited a higher level of CRP (711.01±115.31) and TNF-α (132.81±22.13) in serum compared to control group (p < 0.05). PIPK1, PIPK3, and MLKL expression in BMSCs group decreased (p < 0.05) whereas Caspase-8 was increased (p < 0.05). On the other hand, BMSCs group presented upregulated PIPK1, PIPK3, and MLKL (p < 0.05) and downregulated Caspase-8 (p < 0.05). In conclusion, BMSCs regulate cell apoptosis by upregulating Caspase-8 expression, and downregulating PIPK1, PIPK3 and MLKL level, thereby alleviating the inflammation in AP.

HIGH GLUCOSE INDUCED BONE LOSS VIA ATTENUATING THE PROLIFERATION AND OSTEOBLASTOGENESIS AND ENHANCING ADIPOGENESIS OF BONE MARROW MESENCHYMAL STEM CELLS

2013 ◽  
Vol 25 (05) ◽  
pp. 1340010 ◽  
Author(s):  
Wen-Tyng Li ◽  
Wen-Kai Hu ◽  
Feng-Ming Ho
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Loss ◽  
High Glucose ◽  
Chromatin Condensation ◽  
Diabetic Rats ◽  
Peroxisome Proliferator ◽  
Bone Marrow Mscs

Diabetes mellitus (DM) is associated with bone loss and leads to osteopenia and osteoporosis. This study was undertaken to investigate whether the impaired functions of mesenchymal stem cells (MSCs) derived from bone marrow play a role in pathogenesis of DM-associated bone loss. Bone marrow MSCs were taken from the alloxan-induced diabetic rats and normal rats. Bone mineral densities of tibias and femurs in diabetic rats decreased compared to those of normal rats as shown by dual energy X-ray absorptiometry. MSCs from diabetic rats exhibited reduced colony formation activity. The in vitro effects of high glucose (HG) (20 or 33 mM) on the growth, oxidative stress, apoptosis, and differentiation MSCs were next assessed. The viability and proliferation of MSCs derived from diabetic rats decreased significantly compared with that from normal rats. HG further suppressed the proliferation and viability of MSCs from both diabetic and normal rats. HG was associated with 38–40% increase in reactive oxygen species level and had significantly downregulated the activities of superoxide dismutase (SOD) and catalase (CAT) which could be recovered by the addition of L-ascorbic acid. The phenomena of apoptosis such as chromatin condensation and DNA fragmentation were found in cells cultured under HG conditions. As compared with 5.5 mM glucose, exposure of MSCs to HG enhanced adipogenic induction of triacylglycerol accumulation and inhibited osteogenic induction of alkaline phosphatase activity. HG increased peroxisome proliferator-activated receptor gamma expression during adipogenesis and reduced RUNX2 expression during osteoblastogenesis. These results indicate that MSCs derived from diabetic rats exhibited the inhibitory effects on cell growth and osteogenic ability. The oxidative stress, apoptosis, and adipogenic capability of MSCs were increased by HG. Furthermore, it is suggested that HG induces bone loss via attenuating the proliferation and osteoblastogenesis and enhancing adipogenesis mediated by the oxidative stress in rat bone marrow MSCs.

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