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Norepinephrine protects against apoptosis of mesenchymal stem cells induced by high glucose
Author(s) -
Kong Yanan,
Cheng Liuhanghang,
Ma Li,
Li Haihong,
Cheng Biao,
Zhao Yu
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28686
Subject(s) - mesenchymal stem cell , apoptosis , bone marrow , protein kinase b , sympathectomy , endocrinology , medicine , diabetes mellitus , stem cell , biology , microbiology and biotechnology , biochemistry
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.