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Immunological evidence for hypochlorite-modified proteins in human kidney
E Malle1, C Woenckhaus, G Waeg
1Karl-Franzens University Graz, Germany.
The American Journal of Pathology
|February 1, 1997
Summary
Myeloperoxidase (MPO) and hypochlorite (HOCl)-modified proteins are present in diseased kidneys, suggesting a role in kidney injury and fibrosis. Mononuclear cells may drive these processes.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Oxidative stress and modified proteins are implicated in vascular and inflammatory diseases like atherosclerosis.
- The myeloperoxidase (MPO)-H2O2-halide system is a potential source of in vivo oxidants modifying proteins.
- MPO is found in atherosclerotic lesions and inflammatory conditions.
Purpose of the Study:
- To investigate the presence and role of MPO and hypochlorite (HOCl)-modified proteins in diseased human kidney tissues.
- To determine if MPO-derived oxidants contribute to glomerular and tubulointerstitial injury.
Main Methods:
- Western blot analysis and immunohistochemistry to detect MPO in kidney tissues.
- Immunohistochemistry using a monoclonal antibody specific for HOCl-modified proteins (clone 2D10G9).
- Competitive binding assays using in vitro HOCl-oxidized proteins (LDL, albumin) and diseased kidney tissue.
Main Results:
- MPO and HOCl-modified proteins were detected in diseased human kidney lesions (sclerotic, inflammatory).
- The antibody recognized HOCl-modified proteins in glomerular and tubulointerstitial lesions, particularly in mononuclear cells.
- Expression of HOCl-modified proteins correlated with MPO expression in the same tissue samples.
Conclusions:
- HOCl-mediated oxidation of proteins is proposed as a key event in glomerular and tubulointerstitial kidney injury.
- Mononuclear cells, as a source of MPO, may play a critical role in the pathogenesis of nephrosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis.