miR-137 offers new therapeutic direction for post-stroke depression

MiRNAs likely play an important role in the occurrence and development of depression, and can be used as potential targets for treatment of depression. Studies have shown that miR-137 expression is downregulated in the brain from depression patients with suicidal behavior. Moreover, miR-137 expression is also downregulated in peripheral blood from stroke patients. However, it is not yet known if miRNAs are associated with post-stroke depression. To test this, Dr. Lixia Zhao and colleagues from Shandong Provincial Hospital, China used middle cerebral artery occlusion and chronic mild stress to establish a post-stroke depression model in rats. Compared with controls, the researchers 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. Luciferase 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, noticeably suppressed the inhibitory effect of miR-137 on post-stroke depression. Overall, these results, published in the Neural Regeneration Research (Vol. 8, No. 26, 2013), show that miR-137 suppresses Grin2A protein expression through binding to Grin2A mRNA, thereby exerting an inhibitory effect on post-stroke depression. Our results offer a new therapeutic direction for post-stroke depression.