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Int. J. Mol. Sci. 2016, 17(6), 916; doi:10.3390/ijms17060916

Prolonged Morphine Exposure Induces Increased Firm Adhesion in an in Vitro Model of the Blood–Brain Barrier

1
Department of Microbiology and Immunology, and Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Philadelphia, PA 19102, USA
2
Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA
3
School of Mathematical Sciences and Center for Statistical Science, Peking University, Beijing 100871, China
4
Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
5
Department of Medicine, Division of Hematology and Oncology, Weill Cornell Medical College, New York, NY 10065, USA
6
Department of Biological Sciences, Open University, Walton Hall, Milton Keynes MK7 6AA, UK
7
Institut Cochin, INSERM (Institut National de la Santé et de la Recherche Médicale), U1016, CNRS UMR8104, Université Paris Descartes, Sorbonne Paris Cité, Paris 75014, France
*
Author to whom correspondence should be addressed.
Academic Editor: Kurt A. Jellinger
Received: 30 March 2016 / Revised: 25 May 2016 / Accepted: 31 May 2016 / Published: 9 June 2016
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Abstract

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. View Full-Text
Keywords: blood–brain barrier; brain microvascular endothelial cells (BMEC); morphine; (peripheral blood mononuclear cell) PBMC; cellular adhesion molecules (CAM) blood–brain barrier; brain microvascular endothelial cells (BMEC); morphine; (peripheral blood mononuclear cell) PBMC; cellular adhesion molecules (CAM)
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MDPI and ACS Style

Strazza, M.; Pirrone, V.; Wigdahl, B.; Dampier, W.; Lin, W.; Feng, R.; Maubert, M.E.; Weksler, B.; Romero, I.A.; Couraud, P.-O.; Nonnemacher, M.R. Prolonged Morphine Exposure Induces Increased Firm Adhesion in an in Vitro Model of the Blood–Brain Barrier. Int. J. Mol. Sci. 2016, 17, 916.

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