PubMed · 6987531
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B B Boycott. 1980-03-20. David Scott Gilbert.. https://doi.org/10.1038/284290a0
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Cell adhesion molecules (CAMs) play a role in the normal development and regeneration of tissues as well as in the biological behaviour of tumors. We studied the immunohistochemical expression of various CAMs, such as neural cell adhesion molecule (NCAM), its polysialylated isoform (PSA-NCAM), epithelial (E-) cadherin, and beta1 integrins (alpha2beta1, alpha5beta1, alpha6beta1) in a series of frozen specimens of 10 normal nerves, 5 axonal neuropathies, 26 benign Schwannomas and 2 malignant peripheral nerve sheath tumors (MNST). NCAM was expressed by non-myelinating Schwann cells from normal nerves and overexpressed by Schwann cells from patients with chronic axonal neuropathies and Schwannomas. The expression was lower in MNST. Expression of PSA-NCAM was heterogeneously displayed by Schwann cells from the various tissues studied. Anti E-cadherin immunoreactivity was present in myelin sheath in normal nerves and axonopathies. It was expressed in some Schwannomas especially in vestibular Schwannomas. Integrins VLA alpha2 and VLA alpha6 were widely expressed by Schwann cells from normal nerves, axonal neuropathies and Schwannomas but their expression was low in MNST. VLA alpha5 was not expressed by Schwann cells from normal nerve and Schwannomas but present in chronic axonal neuropathies and MNST. In addition VLA alpha6 was strongly expressed by perineurial cells. These data show that CAMs have a characteristic pattern of expression in normal nerve. Also, some CAMs are always expressed by Schwann cells but the expression of others differs in normal nerves versus axonopathies or tumors, suggesting a role of the microcellular environment in the regulation of CAM expression. Schwannomas have different pattern of expression than MNST.
Paired helical filaments (PHFs) in the neurofibrillary tangles (NFTs) in Alzheimer's disease (AD) brains are composed of highly phosphorylated isoforms of tau (PHFtau) that fail to bind microtubules (MTs), and the levels of MT-binding competent tau are decreased in AD brains with abundant PHFtau. Because this loss of MT binding could compromise the viability of tangle-bearing AD neurons by destabilizing MTs, we asked whether these events could be initiated by inhibiting protein phosphatase 1 (PP1) and PP2A in cultured human neurons (NT2N cells) using okadaic acid (OK) and calyculin-A (CL-A). The treatment of NT2N cells with OK and CL-A increased tau phosphorylation, decreased the binding of tau to MTs, and selectively depolymerized the more stable detyrosinated MTs but not the more labile tyrosinated MTs. Significantly, this led to the rapid degeneration of axons, which are enriched in the more stable detyrosinated MTs, and PP2A was implicated in the initiation of this cascade of events because PP2A but not PP1 was closely associated with MTs in the NT2N cells. These studies imply that inactivation of PP2A in vulnerable neurons of the AD brain may play a mechanistic role in the conversion of normal tau into PHFtau, in the depolymerization of stable MTs, and in the degeneration of axons emanating from tangle-bearing neurons.
We have studied the expression pattern of two cell adhesion proteins of the immunoglobin (Ig) superfamily, BEN/SC1/DM-GRASP (BEN) and the transient axonal glycoprotein TAG-1, during the development of the human nervous system. This study was performed by immunocytochemistry on sections of human embryos ranging from 4 to 13 weeks postconception. The overall distribution of the two proteins during development is very similar to that reported in other vertebrate species, but several important differences have been observed. Both proteins exhibit a transient expression on selected neuronal populations, which include the motor and the sensory neurons. In addition, BEN was also detected on virtually all neurons derived from the neural crest as well as in nonneuronal tissues. A major difference of expression with the chick embryo is that, in the motor neurons, BEN expression was not observed at early stages of development, thus arguing against a role of this molecule in pathfinding and fasciculation. BEN was observed to be restricted to subsets of motor neurons, such as the medial column at the upper limb level. Expression was also detected in a laterodorsal population of the ventral horn cells, which are likely to correspond to migrating preganglionic neurons that originate from the motor pool at the thoracic level. TAG-1 was found on commissural neurons and weakly on the sympathetic neurons; it was also detected on restricted nonneuronal populations. In addition, we observed TAG-1 expression in fibers that could correspond either to subsets of dorsal root ganglia (DRGs) central afferences (including the Ia fibers) or to the axons of association interneurons and in scattered motoneurons likely to correspond either to preganglionic neurons, to gamma-motoneurons, or to late-born motoneurons. Therefore, our results indicate that the molecular strategies used to establish the axonal scaffolding of the nervous system in humans are extremely conserved among the different vertebrates.