ECTRIMS eLearning

Evaluation of vitamin D on the activation of neurogenesis and adult gliogenesis in a model of acute demyelination
ECTRIMS Learn. Pytel V. 10/27/17; 200613; P958
Vanesa Pytel
Vanesa Pytel
Contributions
Abstract

Abstract: P958

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models

Background: CNS demyelinating diseases constitute a broad spectrum of idiopathic inflammatory diseases where different processes and factors are characterized by damage to the myelin in CNS. The role of vitamin D on the activation of the neurogenesis, generation of oligodendrocyte progenitor cells (OPC) and remyelination is controversial.
Objectives: To evaluate if the administration of vitamin D promotes remyelination and the generation of OPC in a model of demyelinating injury by lysolecithin.
Methods: 24 adult male Wistar rats were used for the present study, 8 Sham (S), 8 lysolecithin (LLC) and 8 received lysolecithin and vitamin D (LLC+VD) during 30 days (500IU/kg/day) in a period of 15 days before and after injury. All the animals were evaluated clinically and sacrificed 30 days after injury, previous administration of BrdU. Immunohistochemistry techniques were used to analyze cell proliferation, generation of neuroblasts, OPCs, reactive gliosis, myelination and cell death.
Results: In LLC+VD animals, a rapid recovery in the inclined plane analysis was found, as well as a greater expression of myelin basic protein (MBP) in the area of ​​the lesion (P< 0.05). In the analysis of proliferation in the subventricular zone (SVZ), there was an increase in BrdU positive in LLC+VD, which were mainly DCX/BrdU (P< 0,05), in addition to a greater number of OPCs identified by Olig2 in the corpus callosum and in the lesion area (P< 0.05). There was a decrease in the number of neurons caspase 3 in the perilesional zone (P< 0,05) and a smaller number of amoeboid IBA1 cells in LLC+VD.
Conclusions: Vitamin D has effects on cell proliferation in the SVZ and the corpus callosum. Vitamin D stimulates the differentiation of DCX and Olig2 positive cells, and modulates the microglial response favoring regeneration. Vitamin D is neuroprotective by reducing the number of caspase-3 positive neurons in the neighborhood of the lesion.
Disclosure:
Jesus-Adriel Cuevas: nothing to disclose
Vanesa Pytel: nothing to disclose
Jordi A. Matias-Guiu: nothing to disclose
Maria Soledad Benito-Martin: nothing to disclose
Lidia Moreno-Jimenez: nothing to disclose
Laura Torre-Fuentes: nothing to disclose
Álvaro Gómez-Graña: nothing to disclose
Paloma Montero: nothing to disclose
Ulises Gómez-Pinedo: nothing to disclose
Jorge Matias-Guiu: nothing to disclose

Abstract: P958

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models

Background: CNS demyelinating diseases constitute a broad spectrum of idiopathic inflammatory diseases where different processes and factors are characterized by damage to the myelin in CNS. The role of vitamin D on the activation of the neurogenesis, generation of oligodendrocyte progenitor cells (OPC) and remyelination is controversial.
Objectives: To evaluate if the administration of vitamin D promotes remyelination and the generation of OPC in a model of demyelinating injury by lysolecithin.
Methods: 24 adult male Wistar rats were used for the present study, 8 Sham (S), 8 lysolecithin (LLC) and 8 received lysolecithin and vitamin D (LLC+VD) during 30 days (500IU/kg/day) in a period of 15 days before and after injury. All the animals were evaluated clinically and sacrificed 30 days after injury, previous administration of BrdU. Immunohistochemistry techniques were used to analyze cell proliferation, generation of neuroblasts, OPCs, reactive gliosis, myelination and cell death.
Results: In LLC+VD animals, a rapid recovery in the inclined plane analysis was found, as well as a greater expression of myelin basic protein (MBP) in the area of ​​the lesion (P< 0.05). In the analysis of proliferation in the subventricular zone (SVZ), there was an increase in BrdU positive in LLC+VD, which were mainly DCX/BrdU (P< 0,05), in addition to a greater number of OPCs identified by Olig2 in the corpus callosum and in the lesion area (P< 0.05). There was a decrease in the number of neurons caspase 3 in the perilesional zone (P< 0,05) and a smaller number of amoeboid IBA1 cells in LLC+VD.
Conclusions: Vitamin D has effects on cell proliferation in the SVZ and the corpus callosum. Vitamin D stimulates the differentiation of DCX and Olig2 positive cells, and modulates the microglial response favoring regeneration. Vitamin D is neuroprotective by reducing the number of caspase-3 positive neurons in the neighborhood of the lesion.
Disclosure:
Jesus-Adriel Cuevas: nothing to disclose
Vanesa Pytel: nothing to disclose
Jordi A. Matias-Guiu: nothing to disclose
Maria Soledad Benito-Martin: nothing to disclose
Lidia Moreno-Jimenez: nothing to disclose
Laura Torre-Fuentes: nothing to disclose
Álvaro Gómez-Graña: nothing to disclose
Paloma Montero: nothing to disclose
Ulises Gómez-Pinedo: nothing to disclose
Jorge Matias-Guiu: nothing to disclose

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