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 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.