Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Class A scavenger receptors (SR-A) mediate microglial interaction with fibrillar beta-amyloid (fAbeta). We report here that neonatal microglia from SR-A knockout mice (SR-A-/-) adhere to surface-bound fAbeta, and produce reactive oxygen species (ROS) as efficiently as wildtype microglia; that both wildtype and SR-A-/- microglia express SR-BI; that antibodies against SR-BI do not affect adhesion or ROS production by wildtype microglia, but inhibit adhesion and ROS production of SR-A-/- microglia to immobilized fAbeta by approximately 40%. Adhesion to fAbeta-coated surfaces, and uptake of fAbeta by both wildtype and SR-A-/- microglia was almost completely inhibited by incubation with fucoidan. Thus SR-BI and SR-A mediate similar effector functions in neonatal microglia, which suggests that SR-BI plays as important a role as SR-A, and can maintain the wildtype phenotype in SR-A-/- microglia.
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PMID:Scavenger receptor class B type I (SR-BI) mediates adhesion of neonatal murine microglia to fibrillar beta-amyloid. 1124 25

A role of oxidative stress in atherosclerosis lies on experimental results carried out in vitro and in animal models. In humans, the supplementation with the antioxidant vitamin E has given in some cases supportive results and in others no effects. From in vitro studies, a large amount of data has shown that alpha-tocopherol (the major component of vitamin E) regulates key events in the cellular pathogenesis of atherosclerosis. We first described the inhibition of protein kinase C (PKC) activity by alpha-tocopherol to be at the basis of the vascular smooth muscle cell growth inhibition by this compound. Subsequently, PKC was recognized to be the target of alpha-tocopherol in different cell types, including monocytes, macrophages, neutrophils, fibroblasts and mesangial cells. Inhibiting the activity of protein kinase C by alpha-tocopherol results in different events in different cell types: inhibition of platelet aggregation, of nitric oxide production in endothelial cells, of superoxide production in neutrophils and macrophages as well as impairment of smooth muscle cell proliferation. Adhesion molecule expression and inflammatory cell cytokine production are also influenced by alpha-tocopherol. Scavenger receptors, particularly important in the formation of atherosclerotic foam cells, are also modulated by alpha-tocopherol. The oxidized LDL scavenger receptors SR-A and CD36 are down regulated at the transcriptional level by alpha-tocopherol. The relevance of CD36 expression in the onset of atherosclerosis has been indicated by the protection against atherosclerosis by CD36 knockout mice. In conclusion, the effect of alpha-tocopherol against atherosclerosis is not due only to the prevention of LDL oxidation but also to the down regulation of the scavenger receptor CD36 and to the inhibition of PKC activity.
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PMID:The role of alpha-tocopherol in preventing disease. 1505 95

Astrocytes and microglia associate to amyloid plaques, a pathological hallmark of Alzheimer disease. Microglia are activated by and can phagocytose beta-amyloid (Abeta). Scavenger receptors (SRs) are among the receptors mediating the uptake of fibrillar Abeta in vitro. However, little is known about the function of the astrocytes surrounding the plaques or the nature of their interaction with Abeta. It is unknown whether glial cells bind to nonfibrillar Abeta and if binding of astrocytes to Abeta depends on the same Scavenger receptors described for microglia. We determined the binding of glia to Abeta by an adhesion assay and evaluated the presence of scavenger receptors in glial cells by immunocytochemistry, immunohistochemistry of brain sections, and immunoblot. We found that astrocytes and microglia from neonatal rats adhered in a concentration-dependent manner to surfaces coated with fibrillar Abeta or nonfibrillar Abeta. Fucoidan and poly(I), known ligands for SR-type A, inhibited adhesion of microglia and astrocytes to Abeta and also inhibited Abeta phagocytosis. In contrast, a ligand for SR-type B like low density lipoprotein, did not compete glial adhesion to Abeta. Microglia presented immunodetectable SR-BI, SR-AI/AII, RAGE, and SR-MARCO (macrophage receptor with collagenous structure, a member of the SR-A family). Astrocytes presented SR-BI and SR-MARCO. To our knowledge, this is the first description of the presence of SR-MARCO in astrocytes. Our results indicate that both microglia and astrocytes adhere to fibrillar and nonfibrillar Abeta. Adhesion was mediated by a fucoidan-sensitive receptor. We propose that SR-MARCO could be the Scavenger receptor responsible for the adhesion of astrocytes and microglia to Abeta.
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PMID:Expression of scavenger receptors in glial cells. Comparing the adhesion of astrocytes and microglia from neonatal rats to surface-bound beta-amyloid. 1598 91