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Department of Cell Biology, University of Alabama, Birmingham, AL 35294
ICAM-1 is a transmembrane glycoprotein of the Ig superfamily
involved in cell adhesion. ICAM-1 is aberrantly expressed by astrocytes
in CNS pathologies such as multiple sclerosis, experimental allergic
encephalomyelitis, and Alzheimer’s disease, suggesting a possible role
for ICAM-1 in these disorders. ICAM-1 has been shown to be important
for leukocyte diapedesis through brain microvessels and subsequent
binding to astrocytes. However, other functional roles for ICAM-1
expression on astrocytes have not been well elucidated. Therefore, we
investigated the intracellular signals generated upon ICAM-1 engagement
on astrocytes. ICAM-1 ligation by a mAb to rat ICAM-1 induced mRNA
expression of proinflammatory cytokines such as IL-1
, IL-1ß, IL-6,
and TNF-. Examination of cytokine protein production revealed that
ICAM-1 ligation results in IL-6 secretion by astrocytes, whereas
IL-1ß and IL-1 protein is expressed intracellularly in astrocytes.
The involvement of mitogen-activated protein kinases (MAPKs) in
ICAM-1-mediated cytokine expression in astrocytes was tested, as the
MAPK extracellular signal-regulated kinase (ERK) was previously shown
to be activated upon ICAM-1 engagement. Our results indicate that
ERK1/ERK2, as well as p38 MAPK, are activated upon ligation of ICAM-1.
Studies using pharmacological inhibitors demonstrate that both p38 MAPK
and ERK1/2 are involved in ICAM-1-induced IL-6 expression, whereas only
ERK1/2 is important for IL-1 and IL-1ß expression. Our data
support the role of ICAM-1 on astrocytes as an inflammatory mediator in
the CNS and also uncover a novel signal transduction pathway through
p38 MAPK upon ICAM-1 ligation.
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