Claudin 14/15 play important roles in early wallerian degeneration after rat sciatic nerve injury / 中华创伤杂志(英文版)

PURPOSE@#Wallerian degeneration (WD) is an antegrade degenerative process distal to peripheral nerve injury. Numerous genes are differentially regulated in response to the process. However, the underlying mechanism is unclear, especially the early response. We aimed at investigating the effects of sciatic nerve injury on WD via CLDN 14/15 interactions in vivo and in vitro.@*METHODS@#Using the methods of molecular biology and bioinformatics analysis, we investigated the molecular mechanism by which claudin 14/15 participate in WD. Our previous study showed that claudins 14 and 15 trigger the early signal flow and pathway in damaged sciatic nerves. Here, we report the effects of the interaction between claudin 14 and claudin 15 on nerve degeneration and regeneration during early WD.@*RESULTS@#It was found that claudin 14/15 were upregulated in the sciatic nerve in WD. Claudin 14/15 promoted Schwann cell proliferation, migration and anti-apoptosis in vitro. PKCα, NT3, NF2, and bFGF were significantly upregulated in transfected Schwann cells. Moreover, the expression levels of the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK signaling pathways were also significantly altered.@*CONCLUSION@#Claudin 14/15 affect Schwann cell proliferation, migration, and anti-apoptosis via the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK pathways in vitro and in vivo. The results of this study may help elucidate the molecular mechanisms of the tight junction signaling pathway underlying peripheral nerve degeneration.

Degeneração Walleriana de origem vascular em ressonância magnética de paciente com paralisia supranuclear progressiva provável: fator etiológico ou associação fortuita? / Vascular Wallerian degeneration on magnetic resonance in a patient with probable progressive supranuclear palsy: aetiology or casual link?

Progressive supranuclear palsy (PSP) is one of the most important causes of parkinsonism non responsive to therapy. Vascular parkinsonism is not uncommon. However, the cause-effect relationship between them is uncertain. We report on a 65 year old man with probable PSP who developed the clinical features of the disease after a ischaemic stroke. Magnetic resonance imaging disclosed a corticospinal tract Wallerian degeneration. There is not such an observation in the literature about this possible correlation.

Paralisia supranuclear progressiva (PSP) é uma das principais causas de parkinsonismo-plus não responsivo a terapia. A ocorrência de doença cerebrovascular associada a parkinsonismo não é infreqüente, no entanto é difícil estabelecer a relação causa-efeito entre ambas. Relatamos o caso de um paciente de 65 anos com PSP provável iniciada após infarto cerebral, em que a imagem por ressonância magnética evidenciou sinais de degeneração walleriana do trato córtico-espinhal. Não há relato na literatura pesquisada sobre esta possível correlação.

Watery and dark axons in Wallerian degeneration of the opossum's optic nerve: different patterns of cytoskeletal breakdown?

In this paper we report a qualitative morphological analysis of Wallerian degeneration in a marsupial. Right optic nerves of opossums Didelphis marsupialis were crushed with a fine forceps and after 24, 48, 72, 96 and 168 hours the animals were anaesthetized and perfused with fixative. The optic nerves were immersed in fixative and processed for routine transmission electron microscopy. Among the early alterations typical of axonal degeneration, we observed nerve fibers with focal degeneration of the axoplasmic cytoskeleton, watery degeneration and dark degeneration, the latter being prevalent at 168 hours after crush. Our results point to a gradual disintegration of the axoplasmic cytoskeleton, opposed to the previous view of an "all-or-nothing'' process (Griffin et al 1995). We also report that, due to an unknown mechanism, fibers show either a dark or watery pattern of axonal degeneration, as observed in axon profiles. We also observed fibers undergoing early myelin breakdown in the absence of axonal alterations