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Phosphatidylcholine-specific phospholipase C, but not phospholipase D, is involved in pemphigus IgG-induced signal

M Seishima1, Y Iwasaki-Bessho, Y Itoh

  • 1Department of Dermatology, Ogaki Municipal Hospital, Japan.

Archives of Dermatological Research
|January 19, 2000
PubMed

Insights

Pemphigus IgG binding to desmogleins triggers a signaling cascade involving phosphatidylcholine-specific phospholipase C (PC-PLC). This pathway prolongs diacylglycerol generation, potentially activating protein kinase C and contributing to pemphigus pathogenesis.

Area of Science:

  • Molecular biology
  • Cell signaling
  • Dermatology

Background:

  • The exact mechanism of acantholysis in pemphigus, following pemphigus IgG binding to desmogleins (Dsg) 3 and/or Dsg 1, remains unclear.
  • Previous studies indicated that pemphigus IgG (P-IgG) transiently increases intracellular calcium and inositol 1,4,5-trisphosphate, activating protein kinase C (PKC) in DJM-1 cells.

Purpose of the Study:

  • To investigate the involvement of phosphatidylcholine (PC)-specific phospholipase C (PLC) and phospholipase D (PLD) in P-IgG-induced signaling.
  • To determine the role of diacylglycerol (DAG) and phosphatidylbutanol (PBut) production in P-IgG-mediated cellular responses.

Main Methods:

  • DJM-1 cells were treated with P-IgG to assess DAG and PBut production.
  • The effects of D609 (PC-PLC inhibitor) and propranolol (phosphatidate phosphohydrolase inhibitor) on DAG accumulation were evaluated.
  • Pemphigus serum, pre-adsorbed against Dsg 3 and Dsg 1, was used to assess Dsg-specific effects.
  • Levels of [3H]phosphocholine, a PC-PLC metabolite, were measured.

Main Results:

  • A biphasic accumulation of DAG was observed, with a sustained second phase.
  • The second phase of DAG accumulation was significantly inhibited by D609, but not propranolol.
  • P-IgG did not induce DAG formation after pemphigus antibodies were adsorbed to Dsg 3 and Dsg 1.
  • PBut was not generated, and [3H]phosphocholine levels were elevated following P-IgG addition.

Conclusions:

  • The PC-PLC pathway plays a significant role in P-IgG-induced transmembrane signaling.
  • Prolonged DAG generation via PC-PLC may lead to sustained PKC activation, contributing to pemphigus pathology.
  • These findings elucidate a key signaling mechanism in P-IgG-induced cellular responses.

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