Tripartite motif containing protein 37 involves in thrombin stimulated BV-2 microglial cell apoptosis and interleukin 1β release.

Intracerebral hemorrhage (ICH) is the most common of stroke with high mortality and severe morbidity. Peroxisome proliferator-activated receptor gamma (PPARγ) plays a neuronprotective role in ICH. In the current study, TRIM37 mRNA expression in peripheral blood mononuclear cells (PBMCs) was found to be increased in ICH patients compared to that in healthy controls (n = 15). TRIM37 bound to PPARγ and enhanced its ubiquitination in mouse microglial BV-2 cell line. According to previous studies, thrombin is produced in the brain instantaneously after ICH and triggers the activation of microglia. Here, thrombin induced TRIM37 expression, cell apoptosis and interleukin-1β (IL-1β) release in BV-2 cells, while TRIM37 knockdown partially reversed the effects of thrombin on BV-2 cells. TRIM37 overexpression showed similar effects as thrombin on BV-2 cells, and PPARγ agonist rosiglitazone abolished the effects of TRIM37. In summary, TRIM37 involved in apoptosis and IL-1β release in BV-2 microglia by regulating PPARγ ubiquitination. The present data established a potential biological role of TRIM37 in ICH-induced brain damage and may provide insight into the development of therapy strategies for ICH.

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