Korean J Physiol Pharmacol.
1999 Apr;3(2):199-205.
Increase of intracellular Ca2+ concentration by Vibrio vulnificus cytolysin in rat platelets; triggering mechanism of platelet cytolysis
- Affiliations
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- 1Department of Pharmacology, Chonbuk National University Medical School, Chonju, 560-182 South Korea.
- 2Institute of Cardiovascular Research, Chonbuk National University Medical School, Chonju, 560-182 South Korea.
Abstract
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Vibrio vulnificus cytolysin caused platelet cytolysis and increased
intracellular calcium concentration ((Ca2+))i) of rat platelets in a
concentration-dependent manner. In the presence of V. vulnificus
cytolysin (3 HU/ml), lactate dehydrogenase (LDH) activity was increased
from 1.3+/-0.4% of control to 64.3+/-3.4% in platelet suspension buffer.
In Ca2+-free platelet suspension buffer, however, V. vulnificus
cytolysin did not induce (Ca2+)i increase and LDH release. Addition of
EGTA (2 mM) to suspension buffer after the initial Ca2+ influx reversed
(Ca2+)i to the control level. However, a Ca2+ channel blocker verapamil
(20 muM) or mefenamic acid (20 muM) did not inhibit V. vulnificus
cytolysin-induced (Ca2+)i increase and LDH release. Divalent cations
such as Co2+, Cd2+ or Mn2+ (2 mM each) also did not alter V. vulnificus
cytolysin-induced (Ca2+)i increase and LDH release. V. vulnificus
cytolysin (3 HU/ml)-induced calcium influx was completely blocked by
lanthanum (2 mM). Lanthanum (2 mM) also completely blocked V.
vulnificus cytolysin (3 HU/ml)-induced LDH release. Osmotic protectants
such as, raffinose, sucrose or PEG600 (50 mM each) did not inhibit the
lytic activity of V. vulnificus cytolysin. In conclusion, lanthanum
sensitive Ca2+ influx plays a significant role in Vibrio vulnificus
cytolysin-induced platelet cytolysis and thrombocytopenia in V.
vulnificus infection.