Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Search research articles

Related Experiment Videos

Phosphatidylcholine-directed phospholipase C: activation by complement C5b-9

A V Cybulsky¹, M D Cyr

¹Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.

The American Journal of Physiology

|October 1, 1993

Summary

This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Complement C5b-9 induces cyclooxygenase-2 gene transcription in glomerular epithelial cells.

American journal of physiology. Renal physiology·2001

Same author

Cytosolic phospholipase A2-alpha associates with plasma membrane, endoplasmic reticulum and nuclear membrane in glomerular epithelial cells.

The Biochemical journal·2000

Same author

Complement C5b-9-mediated arachidonic acid metabolism in glomerular epithelial cells : role of cyclooxygenase-1 and -2.

The American journal of pathology·2000

Same author

Growth factor pathways in proliferative glomerulonephritis.

Current opinion in nephrology and hypertension·2000

Same author

Complement-induced phospholipase A2 activation in experimental membranous nephropathy.

Kidney international·2000

Same author

Cyclooxygenases-1 and 2 couple to cytosolic but not group IIA phospholipase A2 in COS-1 cells.

Prostaglandins & other lipid mediators·2000

Same journal

Blood coagulation in fish.

The American journal of physiology·2011

Same journal

Renal tubular reabsorption, metabolic utilization and isomeric fractionation of lactic acid in the dog.

The American journal of physiology·2010

Same journal

The inactivation of placental toxin by human serum.

The American journal of physiology·2010

Same journal

Adrenal function following ovariectomy in the rat.

The American journal of physiology·2010

Same journal

Capillary permeability; perfusion of frog and guinea pig hind limbs.

The American journal of physiology·2010

Same journal

Evaluation of protective measures against sunburn.

The American journal of physiology·2010

See all related articles

Complement C5b-9 stimulates phosphatidylcholine-directed phospholipase C, generating diacylglycerol (DAG) in rat glomerular epithelial cells. This DAG production may limit complement-mediated cell injury.

Area of Science:

Cell Biology
Biochemistry
Nephrology

Background:

Complement C5b-9 causes glomerular epithelial cell (GEC) injury and proteinuria in rat membranous nephropathy.
In cultured rat GEC, C5b-9 activates phospholipase C (PLC), and its products reduce C5b-9-mediated GEC injury.

Purpose of the Study:

To investigate if C5b-9-induced hydrolysis of phosphatidylcholine (PC) provides an additional source of 1,2-diacylglycerol (DAG).
To determine the physiological regulation and characteristics of PC-directed PLC activity in GEC.

Main Methods:

Rat GEC were labeled with [3H]lyso-PC to trace PC-derived DAG.
Protein kinase C (PKC) depletion was achieved using phorbol 12-myristate 13-acetate (PMA).
PC-directed PLC activity was assessed in GEC homogenates using [14C]DAG release from exogenous PC.

Related Experiment Videos

Main Results:

C5b-9 assembly increased PC-derived [3H]DAG and [3H]phosphatidic acid (PA) in intact GEC.
PMA treatment reduced C5b-9-induced [3H]DAG increase, suggesting involvement of PKC.
PC-directed PLC activity was observed at physiological Ca2+ concentrations and stimulated by PMA in cell homogenates.

Conclusions:

GEC possess a physiologically regulated, PC-directed PLC active at nanomolar Ca2+ concentrations.
C5b-9 stimulates this PC-directed PLC, leading to DAG production.
The generated DAG may play a role in limiting GEC injury during complement attack.