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Activation of liver X receptor inhibits osteopontin and ameliorates diabetic nephropathy
Hiromi Tachibana1, Daisuke Ogawa, Yuichi Matsushita
1Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan.
Abstract:
Osteopontin is a proinflammatory cytokine and monocyte chemoattractant implicated in the pathogenesis of diabetic nephropathy. Synthetic agonists for liver X receptors (LXRs) suppress the expression of proinflammatory genes, including osteopontin, but whether LXR activation modulates diabetic nephropathy is unknown. We administered the LXR agonist T0901317 to mice with streptozotocin-induced diabetes and evaluated its effects on diabetic nephropathy. The LXR agonist decreased urinary albumin excretion without altering blood glucose levels and substantially attenuated macrophage infiltration, mesangial matrix accumulation, and interstitial fibrosis. LXR activation suppressed the gene expression of inflammatory mediators, including osteopontin, in the kidney cortex. In vitro, LXR activation suppressed osteopontin expression in proximal tubular epithelial cells by inhibiting AP-1-dependent transcriptional activation of the osteopontin promoter. Taken together, these results suggest that inhibition of renal osteopontin by LXR agonists may have therapeutic potential for diabetic nephropathy.
Insights
Liver X receptor (LXR) activation reduced kidney damage in diabetic nephropathy by suppressing osteopontin. This suggests LXR agonists may offer a novel therapeutic strategy for this condition.
Area of Science:
- Nephrology
- Immunology
- Endocrinology
Background:
- Diabetic nephropathy is linked to inflammation and osteopontin.
- Liver X receptors (LXRs) regulate inflammatory genes, but their role in diabetic nephropathy is unclear.
Purpose of the Study:
- To investigate the therapeutic potential of LXR activation in a mouse model of diabetic nephropathy.
Main Methods:
- Administration of an LXR agonist (T0901317) to mice with streptozotocin-induced diabetes.
- Evaluation of kidney function, histological changes, and gene expression.
- In vitro studies on proximal tubular epithelial cells.
Main Results:
- LXR activation decreased albuminuria and attenuated kidney inflammation, mesangial expansion, and fibrosis.
- Osteopontin expression was suppressed in the kidney cortex.
- In vitro, LXR activation inhibited osteopontin promoter activity.
Conclusions:
- LXR activation ameliorates diabetic nephropathy in mice.
- Inhibition of renal osteopontin by LXR agonists shows therapeutic promise for diabetic nephropathy.
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