PMID- 10468049
OWN - NLM
STAT- MEDLINE
DCOM- 19990921
LR  - 20190915
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 12
IP  - 1
DP  - 1999 Jul
TI  - Neutrophil heat shock protein expression and activation correlate with increased 
      apoptosis following transmigration through the endothelial barrier.
PG  - 32-8
AB  - Polymorphonuclear leukocytes (PMN) undergo endothelial transmigration upon 
      activation or in response to a chemoattractant. Such cells are stressed and have 
      an increased capacity to incite tissue injury. Little is known about the effect 
      of transmigration on PMN stress gene responses, PMN activation, and ultimately 
      programmed cell death (apoptosis). Human endothelial cells (ECV-304) were plated 
      onto transwell membranes to form an endothelial monolayer and PMN 
      transendothelial migration through this endothelial barrier was examined. 
      Chemotaxis was induced by formyl-methionyl-leucyl-phenylalanine (fMLP). Flow 
      cytometry was used to determine PMN receptor expression (CD11b, CD14, CD16, CD18, 
      CD54), phagocytosis, and apoptosis. Heat shock protein (Hsp) expression was 
      evaluated by Western blotting. fMLP-induced PMN transendothelial migration 
      resulted in increased adhesion receptor expression and phagocytosis. Migrated PMN 
      also had an increased rate of apoptosis as evaluated by uptake of propidium 
      iodide and decreased FcgammaR III (CD16) expression. Increased PMN apoptosis 
      coincided with induction of Hsp72 following transmigration. Thus, naive PMN that 
      migrate through endothelium in response to a chemoattractant undergo activation 
      as represented by increased phagocytosis and expression of adhesion receptors.
FAU - Hennigan, S M
AU  - Hennigan SM
AD  - Department of Surgery, The Royal College of Surgeons in Ireland, Beaumont 
      Hospital, Dublin.
FAU - Wang, J H
AU  - Wang JH
FAU - Redmond, H P
AU  - Redmond HP
FAU - Bouchier-Hayes, D
AU  - Bouchier-Hayes D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Antigens, CD)
RN  - 0 (Heat-Shock Proteins)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
SB  - IM
MH  - Antigens, CD/biosynthesis
MH  - *Apoptosis
MH  - Cells, Cultured
MH  - Chemotaxis, Leukocyte/drug effects/*physiology
MH  - Endothelium, Vascular/*pathology/physiology
MH  - Heat-Shock Proteins/*physiology
MH  - Humans
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - *Neutrophil Activation
MH  - Neutrophils/*pathology/*physiology
EDAT- 1999/09/01 00:00
MHDA- 1999/09/01 00:01
CRDT- 1999/09/01 00:00
PHST- 1999/09/01 00:00 [pubmed]
PHST- 1999/09/01 00:01 [medline]
PHST- 1999/09/01 00:00 [entrez]
AID - 10.1097/00024382-199907000-00005 [doi]
PST - ppublish
SO  - Shock. 1999 Jul;12(1):32-8. doi: 10.1097/00024382-199907000-00005.