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CD55 expression patterns on intestinal neuronal tissue are divergent from the brain.

ABSTRACT: BACKGROUND:and objectives: In this study, we investigated how enteric plexuses protect themselves from complement mediated attack. For this purpose, the expression patterns of membrane bound complement regulatory proteins (mCRP) and their association with C3 deposition was determined. In addition, mCRP expression patterns of enteric plexuses were compared with those in the central nervous system (CNS). METHODS:Immunohistochemical stainings were performed to discriminate neuronal cells from glial cells and to detect the presence of CD46, CD55, CD59, and C3d. RNA in situ hybridisation (RISH) was used to determine the cell types that produce CD55 mRNA. RESULTS:Enteric plexuses minimally expressed CD46 whereas CD55 and CD59 were highly expressed. CD55 expression was also observed in a ring around Auerbach's plexuses which was not observed for CD46 and CD59. C3d was deposited around the plexuses but plexus cells themselves did not stain for C3d. In contrast with CNS neurones, enteric neurones were shown to express CD55 whereas enteric glial cells did not. This was confirmed with CD55 RISH. Phospholipase C mediated cleavage of CD55 demonstrated that CD55 was most likely attached to elastic fibres surrounding the plexus. Attached CD55 might protect CD55 negative glial cells from complement mediated injury during inflammatory reactions. CD55 on elastic fibres surrounding the plexuses most likely originated from enteric neuronal cells. CONCLUSION:In contrast with the CNS, enteric neurones express CD55 and enteric glial cells lack CD55 expression. CD55, produced by neuronal cells, attached to elastic fibres surrounding the plexuses is proposed to protect the CD55 negative glial cells within plexuses.

SUBMITTER: Gelderman KA

PROVIDER: S-EPMC1773999 | biostudies-literature | 2004 Apr

REPOSITORIES: biostudies-literature

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CD55 expression patterns on intestinal neuronal tissue are divergent from the brain.

Gelderman K A KA Zijlmans H J M A A HJ Vonk M J MJ Gorter A A

Gut 20040401 4

<h4>Background</h4>and objectives: In this study, we investigated how enteric plexuses protect themselves from complement mediated attack. For this purpose, the expression patterns of membrane bound complement regulatory proteins (mCRP) and their association with C3 deposition was determined. In addition, mCRP expression patterns of enteric plexuses were compared with those in the central nervous system (CNS).<h4>Methods</h4>Immunohistochemical stainings were performed to discriminate neuronal c ...[more]

PMID: 15016744

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Project description:BackgroundSpinal muscular atrophy (SMA) is a form of motor neuron disease affecting primarily children characterised by the loss of lower motor neurons (MNs). Breakdown of the neuromuscular junctions (NMJs) is an early pathological event in SMA. However, not all motor neurons are equally vulnerable, with some populations being lost early in the disease while others remain intact at the disease end-stage. A thorough understanding of the basis of this selective vulnerability will give critical insight into the factors which prohibit pathology in certain motor neuron populations and consequently help identify novel neuroprotective strategies.MethodsTo retrieve a comprehensive understanding of motor neuron susceptibility in SMA, we mapped NMJ pathology in 20 muscles from the Smn2B/- SMA mouse model and cross-compared these data with published data from three other commonly used mouse models. To gain insight into the molecular mechanisms regulating selective resilience and vulnerability, we analysed published RNA sequencing data acquired from differentially vulnerable motor neurons from two different SMA mouse models.ResultsIn the Smn2B/- mouse model of SMA, we identified substantial NMJ loss in the muscles from the core, neck, proximal hind limbs and proximal forelimbs, with a marked reduction in denervation in the distal limbs and head. Motor neuron cell body loss was greater at T5 and T11 compared with L5. We subsequently show that although widespread denervation is observed in each SMA mouse model (with the notable exception of the Taiwanese model), all models have a distinct pattern of selective vulnerability. A comparison of previously published data sets reveals novel transcripts upregulated with a disease in selectively resistant motor neurons, including genes involved in axonal transport, RNA processing and mitochondrial bioenergetics.ConclusionsOur work demonstrates that the Smn2B/- mouse model shows a pattern of selective vulnerability which bears resemblance to the regional pathology observed in SMA patients. We found drastic differences in patterns of selective vulnerability across the four SMA mouse models, which is critical to consider during experimental design. We also identified transcript groups that potentially contribute to the protection of certain motor neurons in SMA mouse models.

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CD55 expression patterns on intestinal neuronal tissue are divergent from the brain.

Publications

CD55 expression patterns on intestinal neuronal tissue are divergent from the brain.

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