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-beta1 and fibronectin. These data suggest that SOCS-1 inhibits HG-induced overexpression of TGF-beta1 and synthesis of fibronectin in HMC, which may be via JAK/STAT pathway.
No takes yet. Share an insight, caveat, or question.
Shi et al. (2008) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: