Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (26): 2441-2448.doi: 10.3969/j.issn.1673-5374.2013.26.005

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miR-137, a new target for post-stroke depression?

Lixia Zhao1, 2, Huazi Li3, Ruiyou Guo2, Teng Ma2, Rongyao Hou2, Xiaowei Ma2, Yifeng Du1   

  1. 1 Department of Neurology, Shandong Provincial Hospital, Jinan 250021, Shandong Province, China

    2 Department of Neurology, Haici Hospital Affiliated to Medical College of Qingdao University, Qingdao 266033, Shandong Province, China

    3 Department of Medical Imaging, Haici Hospital Affiliated to Medical College of Qingdao University, Qingdao 266033, Shandong Province, China
  • Received:2013-03-15 Revised:2013-07-11 Online:2013-09-15 Published:2013-09-15
  • Contact: Yifeng Du, M.D., Chief physician, Department of Neurology, Shandong Provincial Hospital, Jinan 250021, Shandong Province, China, zhaolixia1313@126.com.
  • About author:Lixia Zhao, M.D., Attending physician.

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Abstract:

Expression of miR-137 is downregulated in brain tissue from patients with depression and suicidal behavior, and is also downregulated in peripheral blood from stroke patients. However, it is not yet known if miR-137 acts as a bridge between stroke and depression. To test this, we used middle cerebral artery occlusion and chronic mild stress to establish a post-stroke depression model in rats. Compared with controls, we found significantly lower miR-137 levels in the brain and peripheral blood from post-stroke depression rats. Injection of a miR-137 antagonist into the brain ventricles upregulated miR-137 levels, and improved behavioral changes in post-stroke depression rats. Lu-ciferase assays showed miR-137 bound to the 3′UTR of Grin2A, regulating Grin2A expression in a neuronal cell line. Grin2A gene overexpression in the brain of post-stroke depression rats, noticea-bly suppressed the inhibitory effect of miR-137 on post-stroke depression. Overall, our results show that miR-137 suppresses Grin2A protein expression through binding to Grin2A mRNA, thereby ex-erting an inhibitory effect on post-stroke depression. Our results offer a new therapeutic direction for post-stroke depression.

Key words: neural regeneration, brain injury, post-stroke depression, microRNA, cerebrovascular disease, Grin2A, miR-137, neuroregeneration