Norepinephrine protects against apoptosis of mesenchymal stem cells induced by high glucose
| Autor: | Liuhanghang Cheng, Li Ma, Haihong Li, Yanan Kong, Biao Cheng, Yu Zhao |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Sympathetic nervous system Time Factors Cell Survival Physiology medicine.medical_treatment Clinical Biochemistry Apoptosis Protective Agents Diabetes Mellitus Experimental Norepinephrine 03 medical and health sciences 0302 clinical medicine Diabetes mellitus Internal medicine medicine Animals Sympathectomy Protein kinase B chemistry.chemical_classification Reactive oxygen species Mesenchymal stem cell Mesenchymal Stem Cells Cell Biology medicine.disease Mice Inbred C57BL Glucose 030104 developmental biology Endocrinology medicine.anatomical_structure chemistry Cytoprotection 030220 oncology & carcinogenesis Reactive Oxygen Species Proto-Oncogene Proteins c-akt Signal Transduction medicine.drug |
| Zdroj: | Journal of Cellular Physiology. 234:20801-20815 |
| ISSN: | 1097-4652 0021-9541 |
| Popis: | In diabetes, the number of bone mesenchymal stem cells (MSCs) decreases and their differentiation is impaired. However, the exact mechanism is unclear. Patients with diabetes often experience sympathetic nerve injury. Norepinephrine (NE), a major mediator of the sympathetic nervous system, influences rat MSC migration in culture and in vivo. The present study aimed to investigate the effect of NE on MSCs under high glucose conditions; therefore MSCs were treated with high glucose and NE. High glucose-induced MSCs apoptosis, which was reversed by NE. To verify the effect of NE, mice underwent sympathectomy and were used to establish a diabetic model. Diabetic mice with sympathectomy had a higher apoptosis rate and higher levels of reactive oxygen species in their bone marrow-derived cells than diabetic mice without sympathectomy. High glucose inhibited p-AKT production and B-Cell CLL/Lymphoma 2 expression, and promoted BAX and caspase-3 expression. NE reversed these effects of high glucose. An AKT inhibitor enhanced the effects of high glucose. Thus, NE had a protective effect on MSC apoptosis induced by high glucose, possibly via the AKT/BCL-2 pathway. |
| Databáze: | OpenAIRE |
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