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B-Dependent Adhesion Molecule Gene Expression in Microvascular Endothelial Cells Through Intracellular Calcium Mobilization1
*
Department of Dermatology and the Emory Skin Diseases Research Core Center, Emory University School of Medicine, Atlanta, GA 30322;
Veterans Administration Medical Center, Atlanta, GA 30322; and
Departments of Physiology and Surgery, University of California, San Francisco, CA 94143-0660
Upon stimulation, cutaneous sensory nerves release neuropeptides
such as substance P (SP), which modulate responses in the skin by
activating a number of target cells via neurokinin receptors. We have
demonstrated that SP preferentially binds to the NK-1R on human dermal
microvascular cells, resulting in increased intracellular
Ca2+ and induction of ICAM-1 and VCAM-1 expression. In the
current studies, we identify specific elements in the regulatory
regions of ICAM-1 and VCAM-1 genes as necessary and sufficient for
SP-dependent transcriptional activation. SP treatment of human dermal
microvascular endothelial cells leads to coincident activation and
binding of the transcription factor NF-AT to the -191/-170 region of
the ICAM-1 gene (a region bound by activated p65/p65 homodimers in
response to TNF-
), and NF-
B (p65/p50) to tandem NF-B binding
sites at -76/-52 of the VCAM-1 gene. The SP-elicited intracellular
Ca2+ signal was required for activation and subsequent
binding of both NF-AT and NF-B. The transacting factor induction by
SP was specific, since a selective NK-1R antagonist blocked SP
activation and subsequent NF-AT and NF-B activation and binding.
These data demonstrate coincident activation of NF-AT and NF-B via
SP-induced intracellular Ca2+ mobilization and indicate a
crucial role for neuropeptides in modulating localized cutaneous
inflammatory responses.
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