Suppressor of cytokine signaling-1 reduces high glucose-induced TGF-β1 and fibronectin synthesis in human mesangial cells

Janus kinase (JAK) signal transducers, and activators of transcription (STAT), contribute to diabetic nephropathy. Here we show that one of the suppressors of cytokine signaling (SOCS) proteins, SOCS-1, was upregulated in human mesangial cells (HMCs) under high glucose conditions, along with the activation of JAK2, STAT1, and STAT3. Overexpression of SOCS-1 in HMCs inhibited HG-induced JAK2/STAT activation, c-Fos/c-Jun expression, and increased synthesis of TGF-β1 and fibronectin. These data suggest that SOCS-1 inhibits HG-induced overexpression of TGF-β1 and synthesis of fibronectin in HMC, which may be via JAK/STAT pathway.