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Neuropeptide regulation of human dermal microvascular endothelial cell ICAM-1 expression and function
K L Quinlan1, I S Song, N W Bunnett
1Department of Dermatology and Emory Skin Diseases Research Core Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
The American Journal of Physiology
|December 9, 1998
Summary
Substance P (SP) from sensory nerves directly activates human skin cells, increasing intercellular adhesion molecule 1 (ICAM-1) expression. This finding highlights the neurological system's role in skin inflammation.
Area of Science:
- Dermatology
- Neuroimmunology
- Cell Biology
Background:
- Sensory nerves release neuropeptides like substance P (SP), implicated in skin inflammation.
- The direct impact of SP on human dermal microvascular endothelial cells (HDMECs) and their inflammatory molecule expression requires further elucidation.
Purpose of the Study:
- To investigate the direct effect of substance P (SP) on intercellular adhesion molecule 1 (ICAM-1) expression and function in human dermal microvascular endothelial cells (HDMECs).
- To explore the role of the cutaneous neurological system in modulating skin inflammatory processes.
Main Methods:
- HDMECs were cultured and analyzed for neurokinin receptor (NK-R) mRNA and protein expression.
- SP was added to HDMECs to assess intracellular calcium levels, ICAM-1 mRNA, and cell surface expression.
- Cell adhesion assays were performed using labeled lymphoblastoid cells.
- In vivo studies involved capsaicin application to skin to evaluate microvascular ICAM-1 immunostaining.
Main Results:
- HDMECs expressed NK-1R, NK-2R, and NK-3R, with SP primarily activating NK-1R and increasing intracellular calcium.
- SP significantly upregulated ICAM-1 mRNA and cell surface expression in HDMECs.
- This led to a threefold increase in lymphoblastoid cell binding to HDMECs.
- In vivo, capsaicin application markedly increased microvascular ICAM-1 immunostaining in the skin.
Conclusions:
- Substance P directly activates HDMECs, leading to increased expression of functional ICAM-1.
- These findings support the role of the cutaneous neurological system in regulating inflammatory responses within the skin.