 |
MR Vol.11 No.1 indexに戻る
 |
MODERN RHEUMATOLOGY
Vol.11 No.1 |
 |
|
|
 |
|
|
Pentoxifylline induces the shedding of
L-selectin on polymorphonuclear cells by stimulation via adenosine
receptor
as well as by the inhibition of phosphodiesterase |
|
|
| M. Tajima1, K. Haruta1, S. Kobayashi1,
N. Tamura1, H. Hashimoto1 |
| (1)Department of Rheumatology and Internal Medicine,
Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo
113-8421, Japan |
| |
| Abstract |
| Abstract We investigated the effects of pentoxifylline
(PTX) on the expression of L-selectin on polymorphonuclear leukocytes
(PMN). PTX induced the down-regulation of L-selectin expression
in dose- and time-dependent manner. The measurement of soluble
L-selectin in the culture medium by ELISA indicated that the down-regulation
of L-selectin expression by PTX was due to the shedding of L-selectin
from PMN. The mechanism by which PTX induced the shedding of L-selectin
was investigated. The concentration of intracellular cyclic AMP
(cAMP) was increased after treatment of PMN with PTX. However,
an elevation of cAMP induced by dibutyryl cAMP (dbcAMP) as well
as other methylxanthine derivatives (caffeine, aminophylline, and
theophylline) did not induce the shedding of L-selectin. Although
stimulation of the adenosine receptor with 5'-N-ethylcarboxamidoadenosine
(NECA) or 5'-(N-cyclopropyl)-carboxamido-adenosine (CPCA) adenosine
receptor agonists did not induce the shedding of L-selectin, shedding
of L-selectin was demonstrated when PMN was incubated simultaneously
with rolipram, a phosphodiesterase (PDE) inhibitor, and CPCA. Moreover,
shedding of L-selectin induced by PTX was attenuated by aminophylline,
an adenosine receptor antagonist. These results indicated that
PTX induces the shedding of L-selectin on PMN by stimulation via
the adenosine receptor as well as inhibition of PDE. |
| |
| Key words |
| Key words cAMP ・ Cell adhesion molecule ・
Methylxanthine ・ Neutrophil ・ Shedding |
|
|
 |
|
|
