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Complement-induced phospholipase A2 activation in experimental membranous nephropathy.

A V Cybulsky¹, T Takano, J Papillon

¹Department of Medicine, McGill University Health Center, Montreal, Quebec, Canada. acybul@po-box.mcgill.ca

Kidney International

|March 18, 2000

Summary

In membranous nephropathy, C5b-9 activates phospholipase A2 (PLA2) in kidney cells, leading to cell injury. This study shows cytosolic PLA2 (cPLA2) mediates arachidonic acid release, not secretory PLA2 (sPLA2).

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Area of Science:

Nephrology
Cell Biology
Molecular Biology

Background:

Passive Heymann nephritis (PHN) involves C5b-9-induced glomerular epithelial cell (GEC) injury and proteinuria, partly mediated by eicosanoids.
In cultured GEC, C5b-9 activates phospholipase A2 (PLA2), releasing arachidonic acid (AA) and eicosanoids.

Purpose of the Study:

To investigate the mechanisms of PLA2 activation by C5b-9 in GEC.
To determine the roles of cytosolic PLA2 (cPLA2) and secretory PLA2 (sPLA2) isoforms in this process.

Main Methods:

PLA2 expression analyzed via PCR and immunoblotting.
PLA2 activity assessed using in vitro assays and free AA measurement.
Overexpression studies of cPLA2 and group IIA sPLA2 in GEC.

Main Results:

C5b-9 increased free AA in GEC, indicating PLA2 activation.
cPLA2 overexpression amplified C5b-9-induced AA release; sPLA2 overexpression had no effect.
PHN model showed increased glomerular PLA2 activity, identified as cPLA2, without altered cPLA2 protein levels.

Conclusions:

C5b-9-induced AA release in GEC, both in vitro and in vivo, is mediated by cPLA2.
The mechanism involves post-translational regulation of cPLA2 activity.
C5b-9 does not induce expression or stimulate activity of sPLA2 isoforms in GEC.