Abstract
In this study the role of CXCL6 in diabetic nephropathy (DN) was investigated. It was found to be overexpression in DN patients and DN rat model. And the expression of fibrosis-related cytokines was consistent with the expression of CXCL6. High glucose significantly increased the proliferation of rat renal fibroblasts NRK-49F cell and the expression of CXCL6. Knockdown of CXCL6 ameliorated the pro-proliferation effect of high glucose and decreased the expression of fibrosis-related cytokines, while CXCL6 overexpression exhibited the opposite phenomenon. Gene set enrichment analysis, Western blot and ELISA showed that Janus kinase-signal transducer and activator of transcription (JAK-STAT) and CYTOKINE_CYTOKINE_RECEPTOR_INTERACTION signaling pathways were correlative with CXCL6. This data indicates that CXCL6 may promote fibrosis-related factors to accelerate the development of DN renal interstitial fibrosis by activating JAK/STAT3 signaling pathway. CXCL6 is promising to be a potential novel therapeutic target and candidate biomarker for JAK/STAT3 signaling for the treatment of DN.
Highlights
Diabetic nephropathy (DN) is a well-known micro-vascular complication of diabetes, and the leading cause of End-stage renal disease (ESRD) (Gin et al, 2000)
It was found that C-X-C chemokine ligand 6 (CXCL6) (3.08 fold, P < 0.001) was significantly higher in diabetic nephropathy (DN) human kidney than in control (Figure 1B)
enzyme linked immunosorbent assay (Elisa) and qRTPCR were used to confirm the transcript of CXCL6 and it was found that CXCL6 was higher in plasma (Figure 1C) and kidney tissue (Figure 1D) of DN than in the control samples (P < 0.001)
Summary
Diabetic nephropathy (DN) is a well-known micro-vascular complication of diabetes, and the leading cause of ESRD (Gin et al, 2000). CXCL6 Promotes Renal Fibrosis the major cells that produce ECM in the renal interstitium and play an important role in the process of renal interstitial fibrosis (Grande and López-Novoa, 2009). Chemokines are a class of chemotactic and inducible small molecule peptides that are ubiquitous and play an important role in acute and chronic inflammation (Wasmuth et al, 2009). Microparticles, a small vesicle that accumulates in the synovial fluid of patients with rheumatoid arthritis, promotes the secretion of inflammatory cytokines by synovial fibroblasts and significantly induces the secretion of the chemokine CXCL6, thereby increasing the number of vascular endothelial cell migration and promoting angiogenesis and aggravation of joint inflammation (Reich et al, 2011). It has been reported that CXCL6 can promote lung fibrosis (Besnard et al, 2013) and it is significantly increased in patients with idiopathic pulmonary fibrosis
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