PMID- 8449983
OWN - NLM
STAT- MEDLINE
DCOM- 19930413
LR  - 20190508
IS  - 0021-9525 (Print)
IS  - 1540-8140 (Electronic)
IS  - 0021-9525 (Linking)
VI  - 120
IP  - 6
DP  - 1993 Mar
TI  - Endothelial cell cytosolic free calcium regulates neutrophil migration across 
      monolayers of endothelial cells.
PG  - 1371-80
AB  - Polymorphonuclear leukocytes (PMN) traverse an endothelial cell (EC) barrier by 
      crawling between neighboring EC. Whether EC regulate the integrity of their 
      intercellular adhesive and junctional contacts in response to chemotaxing PMN is 
      unresolved. EC respond to the binding of soluble mediators such as histamine by 
      increasing their cytosolic free calcium concentration ([Ca++]i) (Rotrosen, D., 
      and J.I. Gallin. 1986. J. Cell Biol. 103:2379-2387) and undergoing shape changes 
      (Majno, G., S. M. Shea, and M. Leventhal. 1969. J. Cell Biol. 42:617-672). 
      Substances such as leukotriene C4 (LTC4) and thrombin, which increased the 
      permeability of EC monolayers to ions, as measured by the electrical resistance 
      of the monolayers, transiently increased EC [Ca++]i. To determine whether 
      chemotaxing PMN cause similar changes in EC [Ca++]i, human umbilical vein 
      endothelial cells (HUVEC) maintained as monolayers were loaded with fura-2. 
      [Ca++]i was measured in single EC during PMN adhesion to and migration across 
      these monolayers. PMN-EC adhesion and transendothelial PMN migration in response 
      to formyl-methionyl-leucyl-phenylalanine (fMLP) as well as to interleukin 1 
      (IL-1) treated EC induced a transient increase in EC [Ca++]i which temporally 
      corresponded with the time course of PMN-EC interactions. When EC [Ca++]i was 
      clamped at resting levels with a cell permeant calcium buffer, PMN migration 
      across EC monolayers and PMN induced changes in EC monolayer permeability were 
      inhibited. However, clamping of EC [Ca++]i did not inhibit PMN-EC adhesion. These 
      studies provide evidence that EC respond to stimulated PMN by increasing their 
      [Ca++]i and that this increase in [Ca++]i causes an increase in EC monolayer 
      permeability. Such [Ca++]i increases are required for PMN transit across an EC 
      barrier. We suggest EC [Ca++]i regulates transendothelial migration of PMN by 
      participating in a signal cascade which stimulates EC to open their intercellular 
      junctions to allow transendothelial passage of leukocytes.
FAU - Huang, A J
AU  - Huang AJ
AD  - Department of Medicine, College of Physicians and Surgeons, Columbia University, 
      New York, New York 10032.
FAU - Manning, J E
AU  - Manning JE
FAU - Bandak, T M
AU  - Bandak TM
FAU - Ratau, M C
AU  - Ratau MC
FAU - Hanser, K R
AU  - Hanser KR
FAU - Silverstein, S C
AU  - Silverstein SC
LA  - eng
GR  - HL02202/HL/NHLBI NIH HHS/United States
GR  - HL32210/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Biol
JT  - The Journal of cell biology
JID - 0375356
RN  - 0 (Chelating Agents)
RN  - 0 (SRS-A)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 820484N8I3 (Histamine)
RN  - 91416-19-2 (5,5'-dimethyl-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate)
RN  - EC 3.4.21.5 (Thrombin)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - Amnion/physiology
MH  - Calcium/*metabolism
MH  - Cell Communication
MH  - Cell Membrane Permeability
MH  - Cells, Cultured
MH  - Chelating Agents/pharmacology
MH  - *Chemotaxis, Leukocyte/drug effects
MH  - Cytosol/metabolism
MH  - Egtazic Acid/analogs & derivatives/pharmacology
MH  - Endothelium, Vascular/cytology/*physiology
MH  - Fura-2
MH  - Histamine/pharmacology
MH  - Humans
MH  - Kinetics
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Neutrophils/drug effects/*physiology
MH  - SRS-A/pharmacology
MH  - Thrombin/pharmacology
MH  - Umbilical Veins
PMC - PMC2119745
EDAT- 1993/03/01 00:00
MHDA- 1993/03/01 00:01
PMCR- 1993/09/02
CRDT- 1993/03/01 00:00
PHST- 1993/03/01 00:00 [pubmed]
PHST- 1993/03/01 00:01 [medline]
PHST- 1993/03/01 00:00 [entrez]
PHST- 1993/09/02 00:00 [pmc-release]
AID - 93194943 [pii]
AID - 10.1083/jcb.120.6.1371 [doi]
PST - ppublish
SO  - J Cell Biol. 1993 Mar;120(6):1371-80. doi: 10.1083/jcb.120.6.1371.