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Heparanase mediates renal dysfunction during early sepsis in mice
Melissa I Lygizos1, Yimu Yang1, Christopher J Altmann2
1Program in Translational Lung Research, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado School of Medicine Aurora, Colorado.
Physiological Reports
|January 9, 2014
Summary
Heparanase activation in the kidneys contributes to acute kidney injury during sepsis. Inhibiting heparanase protected kidney function in a mouse model, suggesting a new therapeutic target for septic kidney damage.
Area of Science:
- Biochemistry
- Nephrology
- Immunology
Background:
- Heparanase enzyme is implicated in lung injury during sepsis.
- Its role in septic acute kidney injury (AKI) is not well understood.
Purpose of the Study:
- To investigate the role of glomerular heparanase activation in septic AKI.
- To determine if heparanase inhibitors can prevent kidney dysfunction during sepsis.
Main Methods:
- Polymicrobial sepsis was induced in mice via cecal ligation and puncture (CLP).
- Mice received heparanase inhibitors (heparin or NAH) or vehicle.
- Renal function, glomerular filtration, systemic inflammation, and kidney histology were assessed.
Main Results:
- CLP induced glomerular heparanase activation, leading to decreased glomerular filtration and increased blood urea nitrogen.
- Heparanase inhibitors attenuated the loss of kidney function.
- Glomerular heparanase activation did not increase renal neutrophil infiltration but reduced inflammatory gene expression in the kidneys.
Conclusions:
- Glomerular heparanase is activated during sepsis and contributes to AKI.
- Heparanase inhibition may be a therapeutic strategy for septic AKI.
- The mechanisms differ from those in sepsis-induced lung injury.
