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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3592-3600
PHAGOCYTES
Down-regulation of L-selectin expression in neutrophils by
nonsteroidal anti-inflammatory drugs: role of intracellular ATP
concentration
Maria Victoria Gómez-Gaviro,
Carmen Domínguez-Jiménez,
Jorge Moreno Carretero,
Pedro Sabando,
Isidoro González-Alvaro,
Francisco Sánchez-Madrid, and
Federico Díaz-González
From Servicio de Reumatología e
Inmunología, Hospital de la Princesa, Universidad
Autónoma de Madrid, Servicio de Reumatología, Hospital
Universitario de Canarias, Universidad de La Laguna, Santa Cruz de
Tenerife, Spain.
L-selectin is an adhesion molecule that plays an essential role in
the early events of the inflammatory response. Our group has recently
described that several nonsteroidal anti-inflammatory drugs
(NSAIDs) are able to induce both in vivo and in vitro the shedding of L-selectin in neutrophils through an unknown mechanism. In
this work, we have studied potential mechanisms involved in the
shedding of L-selectin induced by NSAIDs. This effect of NSAIDs did
not involve any detectable intracellular calcium flux. Pretreatment of
neutrophils either with Ro 31-8220 and H7, 2 specific inhibitors of
protein kinase C (PKC), or with inhibitors of protein tyrosine kinases
such as tyrphostin A25 or herbimycin A did not prevent the
NSAID-mediated L-selectin shedding. However, the KD-IX-73-4, an
inhibitor of L-selectin proteolysis was able to block the effect of
NSAIDs on L-selectin expression. Remarkably, NSAIDs caused a variable
reduction in the neutrophil intracellular ATP concentration that highly
correlated with the differential ability of NSAIDs to trigger
L-selectin shedding (r = 0.8, P < .01). In
agreement with this finding, azide plus 2-deoxy-D-glucose, 2 metabolic
blockers, also induced a rapid L-selectin shedding (65% ± 8%)
without affecting the neutrophil viability, activation, or expression
level of other surface molecules with soluble isoforms such as CD16 and
CD59. These data indicate that the maintenance of L-selectin on the neutrophil surface requires energy consumption, which suggests that
L-selectin is shed in neutrophils by default. Interestingly, NSAIDs
seem to cause the shedding of L-selectin, at least in part, through the
reduction of the intracellular ATP concentration.
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