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Abstract

Intercellular adhesion molecule 1 (ICAM-1, CD54) is a widely expressed glycoprotein, which plays an important role in leukocyte extravasation and in the interaction of lymphocytes with antigen-presenting cells. In the current study we examined the regulation of ICAM-1 in the mouse facial motor nucleus after facial nerve transection, using immunohistochemistry, confocal laser microscopy and electron microscopy. In the normal facial nucleus ICAM-1 immunoreactivity was restricted to vascular endothelium. Transection of the facial nerve led to a strong and selective upregulation of ICAM-1 on activated microglia. Quantitation of microglial ICAM-1 immunoreactivity revealed a biphasic increase. The first peak 1-2 days post operation paralleling the early stage of microglial activation was followed by a decline at 4-7 days. The second induction of ICAM-1 occurred at day 14 accompanying the period of neuronal cell death and microglial phagocytosis of neuronal debris. Immunoelectron microscopy showed strong ICAM-1 reactivity on the cell membrane of activated microglia at day 2. During the second peak (day 14), ICAM-1 was also observed on lymphocytes adhering to phagocytotic microglia forming aggregates around neuronal debris. No immunolabelling was observed on neurons, astrocytes or oligodendroglia. These data suggest the involvement of ICAM-1 in the adhesion of activated microglia, in their phagocytosis of neuronal debris, and also in the interaction with infiltrating lymphocytes following this injury.

A physiologically realistic in vitro model of microvascular networks

“…Endothelial cell adhesion molecules (ECAMs) of endothelial cells lining the SMN, upregulated by either 4 or 24 hours of incubation with TNF-α, demonstrated an adhesion molecule profile consistent with other studies both in vitro and in vivo (Mulligan et al 1993; Gaehtgens 1992). In addition, the increase in the number of anti-ICAM-1 microsphere adhesion 24 hours after activation of endothelial cells is in general agreement with previous finding from our group and others (Kiani et al 2002; Werner et al 1998). …”

Local Over-Expression of VEGF-DΔNΔC in the Uterine Arteries of Pregnant Sheep Results in Long-Term Changes in Uterine Artery Contractility and Angiogenesis

“…Following one wash with PBS supplemented with 0.1% bovine serum albumin and two washes with PBS, the sections were incubated with ABC solution (PK4000, Vector Laboratories, Peterborough, UK) for one hour. The deposited ABC complex was detected via covalent conjugation of biotinylated tyramide (1∶1000, Dupont, UK), reacted in the presence of 0.01% Hydrogen peroxide in PBS for 10 minutes at room temperature [20]. This treatment with biotinylated tyramide allowed us to transform an initially noncovalent form of biotin labeling into a covalent one, to allow the label to withstand the post-treatment with 2N Hydrochloric acid (HCl) for 45 minutes at room temperature needed to expose the BrdU antigen.…”

Role of Facial Nerve Reconstruction With Anastomosis and Polyglycolic Acid Tube in Accelerating Functional Recovery After Axotomy in the Rat Facial Nucleus

“…Moreover, local glial cells (microglia and astrocytes) are activated as a result of a remote injury to the peripheral nerve axons [3][4][5]. Metabolic and trophic factors are involved in nerve protection in response to the stimulation of various nerve cleavages [6][7][8]. These cellular responses are speculated to be mediated by specific signaling pathways following facial nerve transection.…”