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Articles in PresS, published online ahead of print May 29, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00608.2001
Submitted on December 20, 2001
Accepted on May 24, 2002
1 Research, Bonfils Blood Center, Denver, CO, USA; Pediatrics, University of Colorado School of Medicine, Denver, CO, USA; Surgery, University of Colorado School of Medicine, Denver, CO, USA
2 Surgery, Denver Health Medical Center, Denver, CO, USA; Surgery, University of Colorado School of Medicine, Denver, CO, USA
3 Surgery, Denver Health Medical Center, Denver, CO, USA
4 Research, Bonfils Blood Center, Denver, CO, USA
5 Surgery, University of Colorado School of Medicine, Denver, CO, USA
6 Shionogi Research Laboratories, Shionogi & Co., Osaka, Japan
7 Pediatrics, University of Colorado School of Medicine, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: ernest{at}.moore@dhha.org.
Secretory phospholipase A2 (sPLA2) produces lipids that stimulate PMNs. With the discovery of sPLA2 receptors (sPLA2-R) we hypothesize that sPLA2 stimulates PMNs through a receptor. Scatchard analysis was used to determine the presence of a sPLA2 ligand. Lysates were probed with an antibody to the M-type sPLA2-R, and the immunoreactivity was localized. PMNs were treated with active and inactive (+EGTA) sPLA2 (1-100 u/ml, IA, IB, and IIA), and elastase release and PMN adhesion were measured. PMNs incubated with inactive, FITC-linked sPLA2-IB, but not IA, demonstrated the presence of a sPLA2-R with saturation at 2.77 fM and a Kd of 167 pM. SPLA2-R immunoreactivity was present at 185kD and localized to the membrane. Inactive sPLA2-IB activated p38 MAP kinase (MAPk), and p38 MAPk inhibition attenuated elastase release. Active sPLA2-IA caused elastase release, but inactive type IA did not. SPLA2-IB stimulated elastase release independent of activity; inactive sPLA2-IIA partially stimulated PMNs. SPLA2-IB and sPLA2-IIA caused PMN adhesion. We conclude that PMNs contain a membrane M-type sPLA2-R that activates p38 MAPk.
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