Tamoxifen favoured the rat sensorial cortex regeneration after a penetrating brain injury

Rodríguez, Nancy Elizabeth Franco; Jiménez, Judith Marcela Dueñas; Valdovinos, Braniff De la Torre; Ruiz, J.R. López; Hernandez, Leonardo; Jiménez, S.H. Dueñas

doi:10.1016/j.brainresbull.2013.07.007

Cited by 27 publications

(17 citation statements)

References 32 publications

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“…14 Another possibility is that TAM may induce differentiation of progenitor cells into oligodendrocytes in the spinal cord, which may initiate a chronic remyelination process contributing to an increase in white matter after SCI. 16,42,43 Both mechanisms were observed by Franco-Rodriguez and colleagues 16 in brain injury, suggesting a similar mechanism may be activated by TAM after SCI.…”

Section: Discussionmentioning

confidence: 58%

“…Among the expected effects of TAM are reduction of inflammatory cytokines, microglial activation, and reduction in astrogliosis, as has been shown by others in models of SCI 12,14,17,18 and brain ischemia or trauma. 8,13,16,[44][45][46][47][48] Administration of TAM, 30 min after spinal cord contusion, attenuates neuronal apoptosis within the first few days, 12 possibly through the inactivation of caspase-3. 18 The effect of the drug to reduce cell death is not only observed in SCI conditions; in a model of irradiation-induced brain injury, reversible focal cerebral ischemia, and MCAo, the investigators observed that TAM administration reduced neuronal cell death.…”

Section: Discussionmentioning

confidence: 99%

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Tamoxifen Administration Immediately or 24 Hours after Spinal Cord Injury Improves Locomotor Recovery and Reduces Secondary Damage in Female Rats

Colón

Torrado

Cajigas

et al. 2016

Journal of Neurotrauma

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Spinal cord injury (SCI) is a condition with no available cure. The initial physical impact triggers a cascade of molecular and cellular events that generate a nonpermissive environment for cell survival and axonal regeneration. Spinal cord injured patients often arrive at the clinic hours after the initial insult. This indicates the need to study and develop treatments with a long therapeutic window of action and multiactive properties, which target the complex set of events that arise after the initial trauma. We provide evidence that tamoxifen (TAM), a drug approved by the Food and Drug Administration, exerts neuroprotective effects in an animal model when applied up-to 24 h after SCI. We hypothesized that continuous TAM administration will improve functional locomotor recovery by favoring myelin preservation and reducing secondary damage after SCI. Adult female Sprague-Dawley rats (*230 g) received a moderate contusion to the thoracic (T9-T10) spinal cord, using the MASCIS impactor device. To determine the therapeutic window available for TAM treatment, rats were implanted with TAM pellets (15 mg) immediately or 24 h after SCI. Locomotor function (Basso, Beattie, Bresnahan open field test, grid walk, and beam crossing tests) was assessed weekly for 35 days post-injury. TAMtreated rats showed significant functional locomotor recovery and improved fine movements when treated immediately or 24 h after SCI. Further, TAM increased white matter preservation and reduced secondary damage caused by astrogliosis, axonal degeneration, and cell death after trauma. These results provide evidence for TAM as a potential therapeutic agent to treat SCI up to 24 h after the trauma.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Tamoxifen Administration Immediately or 24 Hours after Spinal Cord Injury Improves Locomotor Recovery and Reduces Secondary Damage in Female Rats

Colón

Torrado

Cajigas

et al. 2016

Journal of Neurotrauma

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“…This reduction might be accounted by the overexpression of endogenous rCDNF due to the conversion of NG2 cells to astrocytes and expression of hCDNF. The conversion of NG2 cells to astrocytes was reported in the spinal cord [ 39 , 59 ], in the cerebellum [ 41 ] and in the cerebral cortex following a penetrating brain injury [ 60 ], but not in other regions of the brain. Supporting this feature, our work showed an apparent conversion of NG2 cells to astrocytes in the SNr of rats induced by the intrastriatal 6-OHDA lesion.…”

Section: Discussionmentioning

confidence: 99%

Transient transfection of human CDNF gene reduces the 6-hydroxydopamine-induced neuroinflammation in the rat substantia nigra

Nadella

Voutilainen

Saarma

et al. 2014

J Neuroinflammation

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BackgroundThe anti-inflammatory effect of the cerebral dopamine neurotrophic factor (CDNF) was shown recently in primary glial cell cultures, yet such effect remains unknown both in vivo and in 6-hydroxydopamine (6-OHDA) models of Parkinson’s disease (PD). We addressed this issue by performing an intranigral transfection of the human CDNF (hCDNF) gene in the critical period of inflammation after a single intrastriatal 6-OHDA injection in the rat.MethodsAt day 15 after lesion, the plasmids p3xNBRE-hCDNF or p3xNBRE-EGFP, coding for enhanced green florescent protein (EGFP), were transfected into the rat substantia nigra (SN) using neurotensin (NTS)-polyplex. At day 15 post-transfection, we measured nitrite and lipoperoxide levels in the SN. We used ELISA to quantify the levels of TNF-α, IL-1β, IL-6, endogenous rat CDNF (rCDNF) and hCDNF. We also used qRT-PCR to measure rCDNF and hCDNF transcripts, and immunofluorescence assays to evaluate iNOS, CDNF and glial cells (microglia, astrocytes and Neuron/Glial type 2 (NG2) cells). Intact SNs were additional controls.ResultsIn the SN, 6-OHDA triggered nitrosative stress, increased inflammatory cytokines levels, and activated the multipotent progenitor NG2 cells, which convert into astrocytes to produce rCDNF. In comparison with the hemiparkinsonian rats that were transfected with the EGFP gene or without transfection, 6-OHDA treatment and p3xNBRE-hCDNF transfection increased the conversion of NG2 cells into astrocytes resulting in 4-fold increase in the rCDNF protein levels. The overexpressed CDNF reduced nitrosative stress, glial markers and IL-6 levels in the SN, but not TNF-α and IL-1β levels.ConclusionOur results show the anti-inflammatory effect of CDNF in a 6-OHDA rat of Parkinson’s disease. Our results also suggest the possible participation of TNF-α, IL-1β and IL-6 in rCDNF production by astrocytes, supporting their anti-inflammatory role.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-014-0209-0) contains supplementary material, which is available to authorized users.

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“…and several types of traumatic injuries(Franco Rodriguez et al, 2013;Guptarak et al, 2014;Ismailoglu et al, 2010;Mosquera et al, 2014;Tian et al, 2009).Interestingly, SERMs also reduce gliosis and neuroinflammation. Tamoxifen and raloxifene decrease microglia activation in the cerebellum after systemic LPS administration(Tapia- Gonzalez et al, 2008) and in the hippocampus after a penetrating brain injury(Barreto et al, 2014); they also decrease the expression of proinflammatory molecules by microglia cell lines and primary cultures of microglia(Ishihara et al, 2015;Suuronen et al, 2005).…”

mentioning

confidence: 95%

Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions

Acaz‐Fonseca

Ávila-Rodriguez

Garcia-Segura

et al. 2016

Progress in Neurobiology

104

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Tamoxifen favoured the rat sensorial cortex regeneration after a penetrating brain injury

Cited by 27 publications

References 32 publications

Tamoxifen Administration Immediately or 24 Hours after Spinal Cord Injury Improves Locomotor Recovery and Reduces Secondary Damage in Female Rats

Tamoxifen Administration Immediately or 24 Hours after Spinal Cord Injury Improves Locomotor Recovery and Reduces Secondary Damage in Female Rats

Transient transfection of human CDNF gene reduces the 6-hydroxydopamine-induced neuroinflammation in the rat substantia nigra

Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions

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