PMID- 10913015
OWN - NLM
STAT- MEDLINE
DCOM- 20000824
LR  - 20200930
IS  - 0363-6143 (Print)
IS  - 0363-6143 (Linking)
VI  - 279
IP  - 2
DP  - 2000 Aug
TI  - VCAM-1-induced inwardly rectifying K(+) current enhances Ca(2+) entry in human 
      THP-1 monocytes.
PG  - C488-94
AB  - Hyperpolarization in human leukemia THP-1 monocytes adherent to vascular cell 
      adhesion molecule (VCAM)-1 is due to an induction of inwardly rectifying K(+) 
      currents (I(ir)) (Colden-Stanfield M and Gallin EK, Am J Physiol Cell Physiol 
      275: C267-C277, 1998). We determined whether the VCAM-1-induced hyperpolarization 
      is sufficient to augment the increase in intracellular free calcium ([Ca(2+)](i)) 
      produced by Ca(2+) store depletion with thapsigargin (TG) and readdition of 
      external CaCl(2) in fura 2-loaded THP-1 monocytes. Whereas there was a 2.1-fold 
      increase in [Ca(2+)](i) in monocytes bound to glass for 5 h in response to TG and 
      CaCl(2) addition, adherence to VCAM-1 produced a 5-fold increase in [Ca(2+)](i). 
      Depolarization of monocytes adherent to VCAM-1 by I(ir) blockade or exposure to 
      high [K(+)] abolished the enhancement of the peak [Ca(2+)](i) response. In 
      monocytes bound to glass, hyperpolarization of the membrane potential with 
      valinomycin, a K(+) ionophore, to the level of hyperpolarization seen in cells 
      adherent to VCAM-1 produced similar changes in peak [Ca(2+)](i). Adherence of 
      monocytes to E-selectin produced a similar peak [Ca(2+)](i) to cells bound to 
      glass. Thus monocyte adherence to the physiological substrate VCAM-1 produces a 
      hyperpolarization that is sufficient to enhance Ca(2+) entry and may impact 
      Ca(2+)-dependent monocyte function.
FAU - Colden-Stanfield, M
AU  - Colden-Stanfield M
AD  - Department of Physiology, Morehouse School of Medicine, Atlanta, Georgia 30310, 
      USA. stanfiel@msm.edu
FAU - Scanlon, M
AU  - Scanlon M
LA  - eng
GR  - G13-RR-03034/RR/NCRR 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  - Am J Physiol Cell Physiol
JT  - American journal of physiology. Cell physiology
JID - 100901225
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Integrin alpha4beta1)
RN  - 0 (Integrins)
RN  - 0 (Potassium Channels)
RN  - 0 (Receptors, Lymphocyte Homing)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 67526-95-8 (Thapsigargin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Calcium/*metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Humans
MH  - Integrin alpha4beta1
MH  - Integrins/drug effects/*metabolism
MH  - Membrane Potentials/drug effects/physiology
MH  - Monocytes/drug effects/*metabolism
MH  - Potassium Channels/drug effects/*metabolism
MH  - Receptors, Lymphocyte Homing/drug effects/*metabolism
MH  - Thapsigargin/pharmacology
MH  - Vascular Cell Adhesion Molecule-1/drug effects/*metabolism
EDAT- 2000/07/27 11:00
MHDA- 2000/08/29 11:01
CRDT- 2000/07/27 11:00
PHST- 2000/07/27 11:00 [pubmed]
PHST- 2000/08/29 11:01 [medline]
PHST- 2000/07/27 11:00 [entrez]
AID - 10.1152/ajpcell.2000.279.2.C488 [doi]
PST - ppublish
SO  - Am J Physiol Cell Physiol. 2000 Aug;279(2):C488-94. doi: 
      10.1152/ajpcell.2000.279.2.C488.