Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 17, Issue 6, Pages -Publisher
MDPI AG
DOI: 10.3390/ijms17060916
Keywords
blood-brain barrier; brain microvascular endothelial cells (BMEC); morphine; (peripheral blood mononuclear cell) PBMC; cellular adhesion molecules (CAM)
Funding
- Public Health Service, National Institutes of Health through grants from the National Institute of Mental Health Comprehensive NeuroAIDS Core Center (CNAC) Developmental Grant [1P30 MH-092177-01A]
- National Institute of Neurological Disorders and Stroke [NS32092, NS46263]
- National Institute of Drug Abuse [DA19807]
- Ruth L. Kirschstein National Research Service Award [5T32MH079785]
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The blood-brain barrier (BBB) has been defined as a critically important protective barrier that is involved in providing essential biologic, physiologic, and immunologic separation between the central nervous system (CNS) and the periphery. Insults to the BBB can cause overall barrier damage or deregulation of the careful homeostasis maintained between the periphery and the CNS. These insults can, therefore, yield numerous phenotypes including increased overall permeability, interendothelial gap formation, alterations in cytokine and chemokine secretion, and accelerated cellular passage. The current studies expose the human brain microvascular endothelial cell line, hCMEC/D3, to prolonged morphine exposure and aim to uncover the mechanisms underlying alterations in barrier function in vitro. These studies show alterations in the mRNA and protein levels of the cellular adhesion molecules (CAMs) intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and activated leukocyte cell adhesion molecule that correlate with an increased firm adhesion of the CD3+ subpopulation of peripheral blood mononuclear cells (PBMCs). Overall, these studies suggest that prolonged morphine exposure may result in increased cell migration into the CNS, which may accelerate pathological processes in many diseases that involve the BBB.
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