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Published on: September 9, 2021
Amelioration of diabetic tubulointerstitial damage in liver-type fatty acid-binding protein transgenic mice
Atsuko Kamijo-Ikemori1, Takeshi Sugaya, Ayako Sekizuka
1Department of Anatomy, Division of Medicine, Internal Medicine, St Marianna University School of Medicine, Tokyo, Japan.
Background:
Renoprotection of liver-type fatty acid binding protein (L-FABP) was demonstrated in a streptozotocin (STZ)-induced diabetic mouse model.
Methods:
Established human L-FABP (hL-FABP) transgenic (Tg) mice and wild-type (WT) mice were divided into two groups: diabetic mice were uninephrectomized and injected with STZ; control mice were uninephrectomized and injected with a citrate buffer alone. Although mouse L-FABP was not expressed in WT mice, hL-FABP was expressed in the proximal tubules of the diabetic Tg mice and in the control Tg mice at 8 and 14 weeks after these injections.
Results:
The expression of renal hL-FABP increased significantly in diabetic Tg mice compared to control Tg mice. A number of macrophages (F4/80) infiltrating the interstitium, the gene expressions of MCP-1, MCP-3, TGF-beta, Fas, Bax and RAGE were significantly lower in diabetic Tg kidneys compared with diabetic WT kidneys. In the diabetic Tg kidneys, the degree of the tubulointerstitial injury and the deposition of type IV collagen were significantly lower than that of diabetic WT kidneys. The expressions of catalase and glutathione peroxidase-1 were significantly lower in diabetic Tg kidneys compared with diabetic WT kidneys.
Conclusions:
Renal L-FABP ameliorated the tubulointerstitial damage of type 1 diabetic mice.
Insights
Liver-type fatty acid binding protein (L-FABP) protects kidneys in diabetic mice. This study shows renal L-FABP reduces tubulointerstitial damage in type 1 diabetes, offering potential therapeutic insights.
Area of Science:
- Nephrology
- Diabetology
- Molecular Biology
Background:
- Liver-type fatty acid binding protein (L-FABP) has shown renoprotective effects in diabetic mouse models.
- Understanding L-FABP's role in diabetic nephropathy is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the renoprotective effects of human L-FABP (hL-FABP) in a streptozotocin (STZ)-induced type 1 diabetic mouse model.
- To evaluate the impact of hL-FABP expression on kidney injury markers and inflammatory responses.
Main Methods:
- Human L-FABP transgenic (Tg) mice and wild-type (WT) mice were used, divided into diabetic (STZ-injected) and control groups.
- Renal hL-FABP expression was confirmed in diabetic Tg mice.
- Kidney tissues were analyzed for macrophage infiltration, gene expression of inflammatory and fibrotic markers, tubulointerstitial injury, and collagen deposition.
Main Results:
- Renal hL-FABP expression was significantly higher in diabetic Tg mice compared to controls.
- Diabetic Tg kidneys showed significantly lower macrophage infiltration (F4/80), and reduced expression of MCP-1, MCP-3, TGF-beta, Fas, Bax, and RAGE compared to diabetic WT kidneys.
- Tubulointerstitial injury and type IV collagen deposition were significantly reduced in diabetic Tg kidneys.
Conclusions:
- Renal L-FABP effectively ameliorates tubulointerstitial damage in type 1 diabetic mice.
- These findings highlight the potential of L-FABP as a therapeutic target for diabetic kidney disease.
