Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injection of Fluoro-Gold (FG) into the whisker pad of rats yields a stable retrograde labeling of facial motoneurons. After removal of 10 mm from the facial nerve the microglia phagocytose the FG-prelabeled dead neurons and assume the label. A subsequent brightfield immunostaining of the sections with HRP-DAB as end-product fully quenches the fluorescence of FG from all specifically stained structures (immunoquenching). Combining FG-labeling of neuronophages with immunoquenching, we recently described a population of enigmatic fluorescent cells, found in immediate vicinity to the motoneurons after the general neuronofugal migration of microglia. As the fluorescence of these cells was not quenched after a triple immunostaining with anti neuron-specific enolase, anti-GFAP, and OX-42 (quenching all fluorescence from neurons and glia), they seemed to represent a new, immunologically not identified neuronophage. Now we have further characterized this cell type. Following triple immunostaining, we tested a broad panel of mabs (OX-33, OX-19, OX-18, OX-6, R73, ED1, and ED2) to stain, quench fluorescence, and thus immunotype the unknown phagocytes. Only the mab ED2, the classical marker for perivascular cells, specifically stained the small round neuronophages. This surprising migration of perivascular cells toward decaying neurons was additionally tested and confirmed by intracerebroventricular application of FG prior to resection of the facial nerve Providing evidence for neuronophagia by ED2-positive cells, our results strongly support the hypothesis that the latter are the APC (antigen presenting cells) of the CNS.
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PMID:ED2-positive perivascular cells act as neuronophages during delayed neuronal loss in the facial nucleus of the rat. 892

The HED (hidrotic ectodermal dysplasia) or Clouston syndrome gene (named ED2) has been mapped to the pericentromeric region of chromosome 13 (13q11) to a 2.4-cM interval flanked by markers D13S1828 and D13S1830. We have developed a BAC/PAC-based contig map of this region. This contig, comprising 23 clones and spanning 1.5 Mb, was established by mapping of 27 BAC/PAC end-derived STSs, 11 known polymorphic markers, 2 previously mapped genes, and 14 ESTs. The genomic clone overlaps were confirmed by restriction fragment fingerprint analysis. This contig provides the basis for genomic sequencing and gene identification in the ED2 critical region. Of the 14 ESTs mapped to the contig, 6 show homology to human genes and 8 appear to be novel. Expression patterns of the genes/ESTs were tested by Northern blot and RT-PCR. Full characterization of some of these genes, as well as the novel ESTs, will be useful in assessing their involvement in the HED/Clouston syndrome.
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PMID:A 1.5-Mb physical map of the hidrotic ectodermal dysplasia (Clouston syndrome) gene region on human chromosome 13q11. 1090 49

Methods that facilitate the accurate counting of specific neural cell types would be of substantial value in evaluating the efficacy of treatments applied to spinal cord injury. This report describes reliable procedures for identification of neurons, oligodendrocytes, astrocytes, endothelial cells and inflammatory cells (neutrophils and activated macrophage/microglial cells) in paraformaldehyde-fixed, paraffin-embedded injured adult rat spinal cord. Antigen retrieval techniques (enzymatic and thermal) were used to improve antibody access to masked epitopes. To decrease background immunofluorescence and autofluorescence of hemoglobin, the tissue sections were pretreated with 0.1% sodium borohydride in PBS (30min), followed by 1-5min incubation in 0.5% Sudan black in 70% ethanol. Commercially available techniques to amplify the primary signal such as tyramide signal amplification (TSA) and avidin/biotin/peroxidase/DAB/nickel/cobalt amplification (ABP/DABA) were also tested. Hoechst 33342 nuclear staining was used to indicate cell location, number, and integrity, thereby avoiding misidentification of cells. The best antibodies were: anti-NeuN antibody for neurons, anti-S100 for astrocytes, and anti-S100 and APC-7 antibodies in combination for oligodendrocytes, anti-laminin (LN) for endothelial cells, and ED1 antibody for activated macrophages and microglia. Amplification of the primary signal with TSA or ABP/DABA was also found to be beneficial.
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PMID:Improved immunocytochemical identification of neural, endothelial, and inflammatory cell types in paraffin-embedded injured adult rat spinal cord. 1535 16