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Hemopexin Modulates Expression of Complement Regulatory Proteins in Rat Glomeruli
Maria G Detsika1, Elias A Lianos2
11st Department of Critical Care Medicine and Pulmonary Services, G. P. Livanou and M. Simou Laboratories, School of Medicine, National and Kapodistrian University of Athens, Evangelismos Hospital, 10675 Athens, Greece.
Current Issues in Molecular Biology
|September 25, 2021
Summary
Hemopexin (HPX) depletion in kidney injury exposes glomeruli to heme, activating complement. HPX influences heme-induced complement regulators, potentially protecting against glomerular injury.
Area of Science:
- Nephrology
- Immunology
- Biochemistry
Background:
- Systemic hemolysis and hematuria deplete hemopexin (HPX), leading to unbound heme exposure in glomeruli.
- Unbound heme can cause oxidative injury and activate complement cascades, worsening kidney damage.
- The effect of unbound heme on complement regulatory proteins in glomeruli is unknown.
Purpose of the Study:
- To investigate whether unbound heme activates complement regulatory proteins in glomeruli.
- To determine if hemopexin (HPX) modulates the heme-mediated induction of these complement regulators.
Main Methods:
- Isolated rat glomeruli were incubated with HPX-deficient or HPX-containing sera.
- Expression of heme oxygenase (HO)-1, decay-accelerating factor (DAF), CD59, and complement receptor-related gene Y (Crry) was assessed via western blot.
Main Results:
- HPX-deficient sera increased the expression of HO-1, DAF, and CD59 in glomeruli.
- Crry expression was unaffected by HPX-deficient sera but increased with exogenous heme.
- HPX modulated the heme-induced expression of complement activation controllers.
Conclusions:
- Hemopexin (HPX) influences the heme-mediated induction of complement activation controllers in glomeruli.
- This modulation may offer a protective mechanism against glomerular injury in conditions involving heme exposure.
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