PAF-mediated Ca2+ influx in human neutrophils occurs via store-operated mechanisms.
Many inflammatory mediators activate neutrophils (PMN) partly by increasing cytosolic calcium concentration ([Ca2+]i). Modulation of PMN [Ca2+]i might therefore be useful in regulating inflammation after shock or sepsis. The hemodynamic effects of traditional Ca2+ channel blockade, however, could endanger unstable patients. Store-operated calcium influx (SOCI) is known now to contribute to Ca2+ flux in "nonexcitable" cells. Therefore, we studied the role of SOCI in human PMN responses to the proinflammatory ligand PAF. PMN [Ca2+]i was studied by spectrofluorometry with and without external calcium. We studied the effects o
Hauser
C J
CJ
Department of Surgery, University of Medicine and Dentistry of New Jersey/New Jersey Medical School, Newark 07103, USA. hausercj@UMDNJ.edu
Fekete
Z
Z
Adams
J M
JM
Garced
M
M
Livingston
D H
DH
Deitch
E A
EA
D002118:Calcium / Q000502:physiology*; D002478:Cells, Cultured; D006801:Humans; D017136:Ion Transport / Q000187:drug effects / Q000502:physiology; D009504:Neutrophils / Q000502:physiology*; D010972:Platelet Activating Factor / Q000494:pharmacology*; D015398:Signal Transduction
D010972:Platelet Activating Factor; D002118:Calcium