Leptin reverses corticosterone-induced inhibition of neural stem cell proliferation through activating the NR2B subunits of NMDA receptors |
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Authors: | Wen-Zhu Shi Yu-Liang Miao Wen-Zhi Guo Wei Wu Bao-Wei Li Li-Na An Wei-Wu Fang Wei-Dong Mi |
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Institution: | 1. Anesthesia and Operation Center, Hainan Branch of Chinese PLA General Hospital, Hainan 572013, China;2. Department of Anesthesiology, PLA No. 306 Hospital, Beijing 100101, China;3. Department of Anesthesiology, Beijing Military General Hospital of Chinese People’s Liberation Army, Beijing 100700, China;4. Department of Head and Neck Surgery of Otolaryngology, PLA No. 306 Hospital, Beijing 100101, China;5. Department of Anesthesiology, Armed Police General Hospital, Beijing 100039, China;6. Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing 100853, China |
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Abstract: | Corticosterone inhibits the proliferation of hippocampal neural stem cells (NSCs). The removal of corticosterone-induced inhibition of NSCs proliferation has been reported to contribute to neural regeneration. Leptin has been shown to regulate brain development, improve angiogenesis, and promote neural regeneration; however, its effects on corticosterone-induced inhibition of NSCs proliferation remain unclear. Here we reported that leptin significantly promoted the proliferation of hippocampal NSCs in a concentration-dependent pattern. Also, leptin efficiently reversed the inhibition of NSCs proliferation induced by corticosterone. Interestingly, pre-treatment with non-specific NMDA antagonist MK-801, specific NR2B antagonist Ro 25-6981, or small interfering RNA (siRNA) targeting NR2B, significantly blocked the effect of leptin on corticosterone-induced inhibition of NSCs proliferation. Furthermore, corticosterone significantly reduced the protein expression of NR2B, whereas pre-treatment with leptin greatly reversed the attenuation of NR2B expression caused by corticosterone in cultured hippocampal NSCs. Our findings demonstrate that leptin reverses the corticosterone-induced inhibition of NSCs proliferation. This process is, at least partially mediated by increased expression of NR2B subunits of NMDA receptors. |
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Keywords: | Leptin Corticosterone NSCs Proliferation NR2B subunit N-methyl-d-aspartate receptor siRNA |
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