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Increased expression of toll-like receptor 2 in rat diabetic nephropathy
Fanglin Li1, Niansheng Yang, Lili Zhang
1Department of Nephrology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Background/Aims:
Inflammation is implicated in the pathogenesis of diabetic nephropathy (DN). This study examined the role of Toll-like receptor 2 (TLR2) in the progression of renal injury in a model of rat DN.
Methods:
DN was induced by intravenous injection of streptozotocin and rats were sacrificed at week 2, 4 and 8. Functional and pathologic markers, inflammatory infiltration, expression of TLR2, MCP-1, MyD88, HSP70, HMGB1 and activation of NF-kappaB were assessed. The effects of glucose on the expression of TLR2 by renal tubular epithelial cells were also examined in vitro.
Results:
The expression of TLR2 mRNA and protein level was significantly upregulated in the kidneys of diabetic rats (p < 0.01), which was associated with increased renal expression of MyD88 and MCP-1, activation of NF-kappaB and infiltration of macrophages. The expression of HSP70 and HMGB1, endogenous ligands of TLRs, was also significantly upregulated in the kidneys of diabetic rats. In human renal biopsy of DN, there was prominent expression of TLR2 in both the glomeruli and tubulointerstitium. In vitro study showed that high glucose induced the expression of TLR2 mRNA by NRK-52E cells (p < 0.01).
Conclusions:
Enhanced renal expression of TLR2 is associated with inflammatory infiltration in DN.
Insights
Toll-like receptor 2 (TLR2) is upregulated in diabetic nephropathy (DN) kidneys, correlating with inflammation and injury. High glucose also increases TLR2 expression in kidney cells, suggesting a key role in DN pathogenesis.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Diabetic nephropathy (DN) pathogenesis involves inflammation.
- Toll-like receptor 2 (TLR2) is a potential mediator in kidney disease.
Purpose of the Study:
- To investigate the role of TLR2 in a rat model of diabetic nephropathy.
- To assess the relationship between TLR2 expression and renal injury markers.
Main Methods:
- Diabetic nephropathy induced by streptozotocin in rats.
- Assessed functional, pathological, and inflammatory markers, including TLR2, MCP-1, MyD88, NF-kappaB activation, and macrophage infiltration.
- In vitro study on high glucose effects on TLR2 expression in renal tubular epithelial cells.
Main Results:
- Significantly upregulated TLR2 mRNA and protein in diabetic rat kidneys.
- Associated with increased MyD88, MCP-1, NF-kappaB activation, and macrophage infiltration.
- High glucose induced TLR2 mRNA expression in vitro; prominent TLR2 expression observed in human DN renal biopsies.
Conclusions:
- Enhanced renal TLR2 expression is linked to inflammatory infiltration in diabetic nephropathy.
- TLR2 may play a significant role in the progression of DN.
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