Effects of 1α,25 dihydroxyvitamin D3 on the expression of HO-1 and GFAP in glial cells of the photothrombotically lesioned cerebral cortex

Oermann, Evelyn; Bidmon, Hans‐Jürgen; Witte, Otto-W.; Zilles, Karl

doi:10.1016/j.jchemneu.2004.07.003

Cited by 43 publications

(30 citation statements)

References 80 publications

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“…Although Nissl staining suggested that the hippocampus was spared direct injury by cortical photothrombosis and FJB-positive somata were not detected in the hippocampus at any time following photothrombosis, reduced NeuN IR in the hippocampus suggested some degree of neuronal dysfunction and/or a changed phosphorylation state of the NeuN protein (Lind et al, 2005). The distribution of increased GFAP IR was similar to that previously reported for the photothrombosis model (Bidmon et al, 2001b;Kharlamov et al, 2000;Oermann et al, 2004;Schroeter et al, 1995).…”

Section: Discussionsupporting

confidence: 85%

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov

Kelly

2007

Brain Research

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This study characterized morphological changes in the cortex and hippocampus of Sprague-Dawley rats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neuropeptide Y (NPY) expression. Animals were lesioned in the left sensorimotor cortex and compared with age-matched naïve and sham-operated controls by immunohistochemical techniques at 1, 3, 7, and 180 days post-lesioning (DPL). NPY immunostaining was assessed by light microscopy and quantified by the optical fractionator technique using unbiased stereological methods. At 1, 3, and 7 DPL, the number of NPY-positive somata in the lesioned cortex was increased significantly compared to controls and the contralateral cortex. At 180 DPL, lesioned epileptic animals with frequent seizure activity demonstrated significant increases of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyrus. In addition to NPY immunostaining, neuronal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific markers. Nissl and NeuN staining showed reproducible infarctions at each investigated time point. FJB-positive somata were most abundant in the infarct core at 1 DPL, decreased markedly at 3 DPL, and virtually absent by 7 DPL. Activated astroglia were detected in the cortex and hippocampus following lesioning and the development of seizure activity. In summary, NPY protein expression and morphological changes following cortical photothrombosis were time-, region-and pathologic state-dependent. Alterations in NPY expression may reflect reactive or compensatory responses of the rat brain to acute infarction and to the development and expression of epileptic seizures.

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Section: Discussionsupporting

confidence: 85%

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov

Kelly

2007

Brain Research

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“…Quite unpredicted, calcitriol seems able to delay the effect of Heme oxygenase, reducing the glial fibrillary immunoreactivity [280]. Finally, vitamin D seems to interfere the activity of Poly (ADP-Ribose) Polymerase-1, also called PARP1.…”

Section: Vitamin D Deficiency and Neurodegenerative Diseasesmentioning

confidence: 99%

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact

Moretti

Morelli

Caruso

2018

Preprint

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It is widely known that vitamin D receptors have been found in neurons and glial cells and their highest expression is in the hippocampus, hypothalamus, thalamus and subcortical grey nuclei, and substantia nigra. The vitamin D helps the regulation of neurotrophin, neural differentiation and maturation, through the control operation of growing factors synthesis (ie NGF and GDNF), the trafficking of the septo-hyppocampal pathway, and the control of the synthesis process of different neuromodulators (such as Ach, DA, and GABA).Based on these assumptions, we have written this review in order to summarize the potential role of vitamin D in neurological pathologies. The work could be titanic, and might result very fuzzy and even incoherent, if we would not have conjectured to taper our first intentions and devoted our interests towards three mainstreams: demyelinating pathologies, vascular syndromes and neurodegeneration.Due to the lack of effective therapeutic options, a part from the disease modifying strategies, the role of different risk factors should be investigated in neurology, as far as their correction may lead to the improvement of the cerebral conditions.We have explored the relationships between the gene-environmental influence and long term vitamin D deficiency, as a risk factor for the development of different types of neurological disorders, along with the role and the rationale of therapeutic trials with vitamin D implementation. Peer-reviewed version available at Int. J. Mol. Sci. 2018, 19, 2245 doi:10.3390/ijms19082245 3 SEARCH STRATEGY AND SELECTION CRITERIAWe searched MEDLINE using the search terms: "vitamin D central nervous system" , both "vitamin D" and "central nervous system"; "vitamin D immune system/response", both "vitamin D" and "immune system" or "immune response"; "vitamin D multiple sclerosis risk", both "vitamin D" and "multiple sclerosis risk"; "vitamin D multiple sclerosis relapse", both "vitamin D" and "multiple sclerosis relapse"; "vitamin D multiple sclerosis magnetic resonance imaging", both "vitamin D" and "multiple sclerosis magnetic resonance imaging"; "vitamin D multiple sclerosis disability", both "vitamin D" and "multiple sclerosis disability"; "vitamin D supplementation/therapy/treatment multiple sclerosis", both "vitamin D supplementation" or "vitamin D therapy" or "vitamin D treatment" and "multiple sclerosis"; "vascular dementia", both as -vascular-and -dementia-, "subcortical vascular dementia", both assubcortical-and -dementia-, "Alzheimer's disease", "pathogenesis neurodegeneration" "amyloid", "cholinergic afferents", "arteriolosclerosis", "cerebral flow regulation", "stroke". Publications were selected mostly form the past 20years, but did not exclude frequently referenced and highly regarded older publications. . Congress abstracts and isolated case reports were not considered. We searched the reference lists of articles identified by this search strategy and selected those we judged relevant. Review articles and book chapters are cited to provide with ...

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“…1,25(OH) 2 D alters the rate of mitosis and cell death and alters gene expression in apoptotic and mitotic pathways [13] . In vitro experiments have clearly shown that vitamin D has neuroprotective qualities [14][15][16][17][18] . For example, pretreatment with 1,25(OH) 2 D reduces the impact of glucocorticoid-induced neuronal changes [19] .…”

Section: Introductionmentioning

confidence: 99%

No Association between Serum 25-Hydroxyvitamin D<sub>3</sub> Level and Performance on Psychometric Tests in NHANES III

et al. 2007

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Background: Animal studies and in vitro experiments indicate that vitamin D is involved in a diverse range of neurobiological functions. We had the opportunity to examine the relationship between serum 25-hydroxyvitamin D₃ [25(OH)D] levels and performance on various cognitive tasks, based on a large, representative community sample. Methods: Three age groups were available from the population-based NHANES III survey: adolescent group (n = 1,676, age range 12–17 years), adult group (n = 4,747, 20–60 years), elderly group (n = 4,809, 60–90 years). The associations between eight psychometric measures and serum 25(OH)D were assessed. Results: In the adolescent and adult groups, none of the psychometric measures were associated with 25(OH)D levels. In the elderly group there was a significant difference between 25(OH)D quintiles performance on a learning and memory task; however, those with the highest quintile of 25(OH)D were most impaired on the task, contrary to the hypotheses. Conclusion: Lower 25(OH)D levels were not associated with impaired performance on various psychometric measures. While it remains to be seen if chronic exposure to low 25(OH)D levels alters brain function in the long term, this cross-sectional study suggests that 25(OH)D levels do not influence neurocognitive performance.

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Effects of 1α,25 dihydroxyvitamin D3 on the expression of HO-1 and GFAP in glial cells of the photothrombotically lesioned cerebral cortex

Cited by 43 publications

References 80 publications

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Vitamin D in Neurological Diseases: A Rationale for a Pathogenic Impact

No Association between Serum 25-Hydroxyvitamin D<sub>3</sub> Level and Performance on Psychometric Tests in NHANES III

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