Sciatic nerve regeneration is accelerated in galectin-3 knockout mice.
The success of peripheral nerve regeneration depends on intrinsic properties of neurons and a favorable environment, although the mechanisms underlying the molecular events during degeneration and regeneration are still not elucidated. Schwann cells are considered one of the best candidates to be closely involved in the success of peripheral nerve regeneration. These cells and invading macrophages are responsible for clearing myelin and axon debris, creating an appropriate route for a successful regeneration. After injury, Schwann cells express galectin-3, and this has been correlated with phagocytosis; also, in the presence of galectin-3, there is inhibition of Schwann-cell proliferation in vitro. In the present study we explored, in vivo, the effects of the absence of galectin-3 on Wallerian degeneration and nerve-fiber regeneration. We crushed the sciatic nerves of galectin-3 knockout and wild-type mice, and followed the pattern of degeneration and regeneration from 24 h up to 3 weeks. We analyzed the number of myelinated fibers, axon area, fiber area, myelin area, G-ratio and immunofluorescence for beta-catenin, macrophages and Schwann cells in DAPI counterstained sections. Galectin-3 knockout mice showed earlier functional recovery and faster regeneration than the wild-type animals. We concluded that the absence of galectin-3 allowed faster regeneration, which may be associated with increased growth of Schwann cells and expression of beta-catenin. This would favor neuron survival, followed by faster myelination, culminating in a better morphological and functional outcome.
Narciso
Marcelo Sampaio
MS
Instituto de Ciências Biomédicas, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Brazil.
Mietto
Bruno de Siqueira
Bde S
Marques
Suelen Adriani
SA
Soares
Carolina Pontes
CP
Mermelstein
Claudia dos Santos
Cdos S
El-Cheikh
Márcia Cury
MC
Martinez
Ana Maria Blanco
AM
D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D001369:Axons / Q000473:pathology / Q000502:physiology; D004195:Disease Models, Animal; D037502:Galectin 3 / Q000172:deficiency*; D007211:Indoles; D008124:Locomotion / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009413:Nerve Fibers, Myelinated / Q000502:physiology; D009416:Nerve Regeneration / Q000235:genetics*; D020127:Recovery of Function / Q000235:genetics*; D009418:S100 Proteins / Q000378:metabolism; D012583:Schwann Cells / Q000473:pathology / Q000502:physiology; D020426:Sciatic Neuropathy / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors; D051176:beta Catenin / Q000378:metabolism
D000943:Antigens, Differentiation; D037502:Galectin 3; D007211:Indoles; D009418:S100 Proteins; D051176:beta Catenin; C036763:monocyte-macrophage differentiation antigen; C007293:DAPI