Behaviour of oligodendrocytes and Schwann cells in an experimental model of toxic demyelination of the central nervous system

Graça, Dominguita Lühers; Bondan, Eduardo Fernandes; Fernandes, Cristina Gevehr; Maiorka, Paulo César

doi:10.1590/s0004-282x2001000300009

Cited by 25 publications

(26 citation statements)

References 16 publications

(36 reference statements)

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“…The EB-induced lesions were similar to those previously described in the brainstem of diabetic (13)(14)(15) and non-diabetic rats (1)(2)(3)(4)(5)(6). In general terms, they were characterized by demyelinated areas in the ventral surface of the pons and mesencephalon, con-taining in the central region phagocytic cells, variable amounts of myelin-derived membranes in a distended extracellular space as well as naked axons.…”

Section: General Aspects From Eb-induced Lesionssupporting

confidence: 81%

“…t is widely described that focal injection of the gliotoxic agent ethidium bromide (EB) in the white matter of the central nervous system (CNS) causes local oligodendroglial and astrocytic death, with consequent primary demyelination, blood-brain barrier disruption and Schwann cell invasion due to the glia limitans breakdown (1)(2)(3)(4)(5)(6). Hyperglycemia found in diabetes mellitus is known to cause well described morphological and functional changes in peripheral neurons and Schwann cells (7).…”

mentioning

confidence: 99%

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Propentofylline reverses delayed remyelination in streptozotocin-induced diabetic rats

Bondan

Martins

Bernardi

2015

Arch. Endocrinol. Metab.

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Objective: The diabetic state induced by streptozotocin injection is known to impair oligodendroglial remyelination in the rat brainstem following intracisternal injection with the gliotoxic agent ethidium bromide (EB). In such experimental model, propentofylline (PPF) recently showed to improve myelin repair, probably due to its neuroprotective, antiinflammatory and antioxidant effects. The aim of this study was to evaluate the effect of PPF administration in diabetic rats submitted to the EB-demyelinating model. Materials and methods: Adult male rats, diabetic or not, received a single injection of 10 microlitres of 0.1% EB solution into the cisterna pontis. For induction of diabetes mellitus the streptozotocin-diabetogenic model was used (50 mg/kg, intraperitoneal route -IP). Some diabetic rats were treated with PPF (12.5 mg/kg/day, IP route) during the experimental period. The animals were anesthetized and perfused from 7 to 31 days after EB injection and brainstem sections were collected for analysis of the lesions by light and transmission electron microscopy. Results: Diabetic rats injected with EB showed larger amounts of myelin-derived membranes in the central areas of the lesions and considerable delay in the remyelinating process played by surviving oligodendrocytes and invading Schwann cells after the 15 th day. On the other hand, diabetic rats that received PPF presented lesions similar to those of non-diabetic animals, with rapid remyelination at the edges of the lesion site and fast clearance of myelin debris from the central area. Conclusion: The administration of PPF apparently reversed the impairment in remyelination induced by the diabetic state. Arch Endocrinol Metab. 2015;59(1):47-53

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Section: General Aspects From Eb-induced Lesionssupporting

confidence: 81%

mentioning

confidence: 99%

Propentofylline reverses delayed remyelination in streptozotocin-induced diabetic rats

Bondan

Martins

Bernardi

2015

Arch. Endocrinol. Metab.

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“…Ethidium bromide (EB) injections in the white matter of the central nervous system (CNS) are known to act like a gliotoxin, causing local oligodendroglial and astrocytic death, leading to primary demyelination, neuroinflammation, blood-brain barrier disruption and Schwann cell invasion due to the glia limitans breakdown 1,2,3,4 . Surviving astrocytes present a vigorous reaction around the injury site with increased immunoreactivity to the specific cell marker glial fibrillary acidic protein (GFAP), as well as re-expression of vimentin 3 .…”

mentioning

confidence: 99%

Curcumin decreases astrocytic reaction after gliotoxic injury in the rat brainstem

Bondan

Cardoso

Martins

2017

Arq. Neuro-Psiquiatr.

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Recent studies have demonstrated that curcumin (Cur) has antioxidant, anti-inflammatory and anti-fibrotic effects. Ethidium bromide (EB) injections into the central nervous system (CNS) are known to induce local oligodendroglial and astrocytic loss, resulting in primary demyelination and neuroinflammation. Peripheral astrogliosis is seen around the injury site with increased immunoreactivity to glial fibrillary acidic protein (GFAP). This investigation aimed to evaluate the effect of Cur administration on astrocytic response following gliotoxic injury. Wistar rats were injected with EB into the cisterna pontis and treated, or not, with Cur (100 mg/kg/day, intraperitoneal route) during the experimental period. Brainstem sections were collected at 15, 21 and 31 days after EB injection and processed for GFAP immunohistochemical staining. Astrocytic reactivity was measured in a computerized system for image analysis. In Cur-treated rats, the GFAP-stained area around the lesion was significantly smaller in all periods after EB injection compared to untreated animals, showing that Cur reduces glial scar development following injury.Keywords: astrocytes; curcumin; ethidium; gliosis; gliotoxin. RESUMOEstudos recentes têm demonstrado que a curcumina (Cur) possui efeitos antioxidantes, anti-inflamatórios e antifibróticos. Sabe-se que a injeção de brometo de etídio (EB) no sistema nervoso central induz a perda oligodendroglial e astrocitária, resultando em desmielinização primária e neuroinflamação. Astrogliose periférica é observada ao redor da lesão com aumento da imunorreatividade à proteína glial fibrilar ácida (GFAP). A presente investigação objetivou avaliar o efeito da Cur sobre a resposta astrocitária após injúria gliotóxica. Ratos Wistar foram injetados com EB na cisterna basal e tratados ou não com Cur (100 mg/kg/dia, via intraperitoneal) durante o período experimental. Amostras do tronco encefálico foram coletadas aos 15, 21 e 31 dias pós-injeção de EB e processadas para estudo imuno-histoquímico para a GFAP. A reatividade astrocitária foi medida em um sistema computadorizado para análise de imagem. Nos ratos tratados com Cur, a área marcada para GFAP foi significantemente menor em todos os períodos pós-injeção de EB, indicando que a Cur reduz o desenvolvimento da cicatriz glial após injúria.

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“…Our group studied NTPDase and 5'-nucleotidase activities in synaptosomes and platelets of rats submitted to demyelination by ethidium bromide (EB). We observed that EB selectively destroyed glial cells (oligodendrocytes and astrocytes), which control the processes of demyelination and remyelination [55,87,88]. The results demonstrated that NTPDase and 5'nucleotidase activities were increased in synaptosomes [120] and reduced in platelets [87,119,120], indicating that there is an interaction between these enzymes and demyelinating events.…”

Section: Ectonucleotidases and Demyelinationmentioning

confidence: 85%

NTPDase and 5'‐nucleotidase activities in physiological and disease conditions: New perspectives for human health

et al. 2007

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Abstract. Extracellular nucleotides and nucleosides act as signaling molecules involved in a wide spectrum of biological effects. Their levels are controlled by a complex cell surface-located group of enzymes called ectonucleotidases. There are four major families of ectonucleotidases, nucleoside triphosphate diphosphohydrolases (NTPDases/CD39), ectonucleotide pyrophosphatase/phosphodiesterases (E-NPPs), alkaline phosphatases and ecto-5'-nucleotidase. In the last few years, substantial progress has been made toward the molecular identification of members of the ectonucleotidase families and their enzyme structures and functions. In this review, there is an emphasis on the involvement of NTPDase and 5'-nucleotidase activities in disease processes in several tissues and cell types. Brief background information is given about the general characteristics of these enzymes, followed by a discussion of their roles in thromboregulatory events in diabetes, hypertension, hypercholesterolemia and cancer, as well as in pathological conditions where platelets are less responsive, such as in chronic renal failure. In addition, immunomodulation and cell-cell interactions involving these enzymes are considered, as well as ATP and ADP hydrolysis under different clinical conditions related with alterations in the immune system, such as acute lymphoblastic leukemia (ALL), Bchronic lymphocytic leukemia (B-CLL) and infections associated with human immunodeficiency virus (HIV). Finally, changes in ATP, ADP and AMP hydrolysis induced by inborn errors of metabolism, seizures and epilepsy are discussed in order to highlight the importance of these enzymes in the control of neuronal activity in pathological conditions. Despite advances made toward understanding the molecular structure of ectonucleotidases, much more investigation will be necessary to entirely grasp their role in physiological and pathological conditions.

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Behaviour of oligodendrocytes and Schwann cells in an experimental model of toxic demyelination of the central nervous system

Cited by 25 publications

References 16 publications

Propentofylline reverses delayed remyelination in streptozotocin-induced diabetic rats

Propentofylline reverses delayed remyelination in streptozotocin-induced diabetic rats

Curcumin decreases astrocytic reaction after gliotoxic injury in the rat brainstem

NTPDase and 5'‐nucleotidase activities in physiological and disease conditions: New perspectives for human health

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