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TNF‐α induced variability of ICAM‐1 expression in skeletal muscle microvasculature
Author(s) -
Sumagin Ronen,
Sarelius Ingrid H
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a702-d
Subject(s) - cremaster muscle , icam 1 , intravital microscopy , microcirculation , endothelium , venule , inflammation , chemistry , tumor necrosis factor alpha , arteriole , intercellular adhesion molecule 1 , pathology , cell adhesion molecule , microbiology and biotechnology , medicine , biology
The observation that leukocyte‐endothelial cell (EC) interactions are localized to specific regions on the vessel wall suggests that adhesion molecule distribution on the endothelium is not uniform. We used intravital confocal microscopy to compare the expression of ICAM‐1 in arterioles vs venules in control and TNF‐α (500 ng, intrascrotally) induced inflammation. ICAM‐1 expression levels were indicated by normalized intensity of fluorescently labeled surface ICAM‐1 in blood perfused cremaster muscle microvessels of anesthetized mice (Nembutal, 74 mg/ml) and were found to be not uniform. Under normal conditions venular ICAM‐1 expression was approximately two fold higher than the expression in arterioles. Following TNF‐α treatment ICAM‐1 expression was significantly increased, 2.8±0.2 fold in arterioles and 1.7±0.2 in venules (n=4, p‐value <0.05). However, ICAM‐1 expression on activated arteriolar ECs only reached the level of venular ICAM‐1 expression observed under control conditions. Additionally, arteriolar but not venular ECs underwent redistribution of ICAM‐1 among cells, where some cells increased and some decreased the ICAM‐1 expression, magnifying the variability of ICAM‐1. Also, TNF‐α treatment resulted in longer bright regions per unit length of the vessel (42% in control, 70% in TNF‐α) along the arteriolar wall, but no significant change was observed in venules. The fact that arteriolar ECs respond to TNF‐α by upregulation of ICAM‐1 expression, although in a different way compared to venules, suggests an explicit role for arterioles in inflammation. (Supported by NIH HL18208 and HL75186)