GDF11 Antagonizes Psoriasis-like Skin Inflammation via Suppression of NF-κB Signaling Pathway.

Abstract

Growth differentiation factor-11 (GDF11) is a key member of the transforming growth factor β (TGF-β) superfamily, which plays a momentous role in both normal physiological processes and pathophysiology processes. Recently, it was reported that GDF11 was closely associated with several inflammatory conditions and protected against development of inflammation. Psoriasis-like skin inflammation is a common skin inflammatory disease, yet much is unknown about the underlying mechanisms. In this study, we investigated the expression pattern of GDF11 in two psoriasis-like skin inflammation mice models and tumor necrosis factor-α (TNF-α)-induced RAW264.7 macrophages. Furthermore, RAW264.7 cell was cultured, and GDF11 antagonized the inflammatory function of TNF-α in vitro. Moreover, imiquimod-induced mice model and IL-23-induced mice model were established to investigate the anti-inflammatory role of GDF11 in vivo. As a result, the administration of GDF11 remarkably attenuated the severity of skin inflammation in both two mice models. Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation.