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Metabolic Modulation of Cytokine‐Induced Brain Endothelial Adhesion Molecule Expression
Author(s) -
CHAITANYA GANTA VIJAY,
CROMER WALTER,
WELLS SHAN,
JENNINGS MERILYN,
MATHIS JAMES M,
MINAGAR ALIREZA,
ALEXANDER JONATHAN STEVEN
Publication year - 2012
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2011.00141.x
Subject(s) - hypoxia (environmental) , cytokine , inflammation , microcirculation , cell adhesion molecule , immune system , microbiology and biotechnology , vcam 1 , biology , immunology , chemistry , medicine , icam 1 , oxygen , organic chemistry
Please cite this paper as: Chaitanya GV, Cromer W, Wells S, Jennings M, Mathis JM, Minagar A and Alexander JS. Metabolic Modulation of Cytokine‐Induced Brain Endothelial Adhesion Molecule Expression. Microcirculation 19: 155–165, 2012. Abstract Objective: Cytokines contribute to cerebro‐vascular inflammatory and immune responses by inducing ECAMs’ expression. Ischemic insults can be separated into aglycemic and hypoxic components. However, whether aglycemia, hypoxia or OGD plays a major role in dysregulating BBB or promotes immune cell infiltration via ECAMs’ expression is not clear. We investigated how expression of ICAM‐1, VCAM‐1, MAdCAM‐1, PECAM‐1, E‐ and P‐selectin in response to TNF‐α, IL‐1β and IFN‐γ was altered by aglycemia (A), hypoxia (H) or combined oxygen glucose deprivation (OGD). Methods: A cell surface enzyme linked immunoabsorbent assay (cell surface ELISA) was used to analyze ECAM expression. Results: We observed that ICAM‐1 and PECAM‐1 expressions were insensitive to hypoxia, aglycemia or OGD. Conversely, VCAM‐1 and E‐selectin were increased by hypoxia, but not by aglycemia. MAdCAM‐1 and P‐selectin were induced by hypoxia, and decreased by aglycemia. Patterns of cytokine‐regulated ECAMs’ expression were also modified by metabolic conditions. Conclusions: Our results indicate that patterns of inflammation‐associated ECAMs represent cumulative influences from metabolic stressors, as well as cytokine activation. The expression of ECAMs following tissue injury reflects mechanistic interactions between metabolic disturbances, and alterations in tissue cytokines. Normalization of tissue metabolism, as well as cytokine profiles, may provide important targets for therapeutic treatment of inflammation.