Tumor necrosis factor α (TNF-α) plays an important role in cell proliferation and apoptosis, and defects in TNF-α-induced apoptosis are associated with various diseases. TRIM27 is a tripartite motif (TRIM) protein containing RING finger, B-box, and coiled-coil domains. We recently reported that TRIM27 positively regulates TNF-α-induced apoptosis through deubiquitination of receptor-interacting protein 1 (RIP1). Multiple studies have suggested a link between TNF-α pathway and various diseases, such as diabetes and colitis. Here, we report that Trim27-deficient mice were susceptible to streptozotocin (STZ)-induced diabetes, a mouse model of diabetes. Infiltration of T cells and cleaved caspase-3 signals were enhanced, and β-cell mass was decreased in Trim27-deficient islets compared to wild-type islets. On the other hand, Trim27-mutation did not affect the dextran sodium sulphate (DSS)-induced colitis. These data support the idea that the TRIM27 mutation is responsible for the development of certain types of diseases.
Keywords: Apoptosis; DSS, dextran sodium sulphate; Diabetes; Disease; H&E, hematoxylin and eosin; RIP1, receptor-interacting protein 1; STZ, streptozotocin; TNF-α; TNF-α, tumor necrosis factor-α; TRIM, tripartite motif; TRIM27; Ub, ubiquitin.