1,25-Dihydroxyvitamin D3 enhances neural stem cell proliferation and oligodendrocyte differentiation

Shirazi, Hasti Atashi; Rasouli, Javad; Ćirić, Bogoljub; Rostami, Abdolmohamad; Zhang, Guang-xian

doi:10.1016/j.yexmp.2015.02.004

Cited by 125 publications

(83 citation statements)

References 37 publications

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“…It was also demonstrated that vitamin D 3 plays a positive effect on the remyelination process by endogenous progenitor cells and support its possible therapeutic effects in the context of demyelinating disease like MS [16]. Vitamin D has been shown to have a direct effect on neural stem cell proliferation, survival and neuron/ oligodendrocyte differentiation, thus representing a novel mechanism underlying its remyelinating and neuroprotective effect in MS/EAE therapy [30]. A deficiency in vitamin D resulted in an increased susceptibility to EAE and vitamin D 3 or its analogs might potentially be important for treatment of MS [3].…”

Section: Discussionmentioning

confidence: 82%

Administration of vitamin D 3 induces CNPase and myelin oligodendrocyte glycoprotein expression in the cerebral cortex of the murine model of cuprizone-induced demyelination

Mashayekhi

Salehi²

2016

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A b s t r a c t In the central nervous system (CNS) the main proteins of myelin are proteolipid protein (PLP), myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG) and CNPase. Myelin oligodendrocyte glycoprotein is a minor component of the myelin sheath, but is an important autoantigen linked to the pathogenesis of multiple sclerosis (MS). CNPase is expressed exclusively by oligodendrocytes in the CNS, and the appearance of CNPase seems to be one of the earliest events of oligodendrocyte differentiation and myelination. In this study the effects of vitamin D on total protein concentration, CNPase and MOG expression in the cerebral cortex of the murine model of cuprizone-induced demyelination was investigated. The mice were treated by cuprizone for five weeks in order to induce demyelination. The mice were then divided into 3 groups. The first group was injected intraperitoneally (IP) with vitamin D diluted in olive oil in the amount of 5 µg/kg/daily body weight. The second group (SHAM) was injected IP with olive oil and the third group was left without any injection as the control group (n = 11 for each group). After five weeks the mice were killed and the cerebral cortex was collected and the expression of CNPase and MOG was studied by Western blot. Total protein concentration in the vitamin D injected, SHAM and control groups were 0.918 ± 0.003, 0917 ± 0.004 and 0.916 ± 0.004 g/l, respectively (p > 0.05

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Section: Discussionmentioning

confidence: 82%

Administration of vitamin D 3 induces CNPase and myelin oligodendrocyte glycoprotein expression in the cerebral cortex of the murine model of cuprizone-induced demyelination

Mashayekhi

Salehi²

2016

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“…In addition to the large contribution of VitD immunomodulatory activity in EAE, this treatment can also directly act on neural cells promoting CNS remyelination and other neuroprotective effects ( Figure 1B). In vitro assays indicated that this vitamin significantly enhanced proliferation of neural stem cells and their differentiation into neurons and oligodendrocytes [110]. In addition, VitD treatment modulated autophagic activity and neuroapoptosis in EAE mice.…”

Section: Therapeutic Effect Of Vitd In Eaementioning

confidence: 95%

Therapeutic and Prophylactic Potential of Vitamin D for Multiple Sclerosis

Zorzella-Pezavento¹,

Ishikawa²,

Fraga-Silva³

et al. 2017

A Critical Evaluation of Vitamin D - Clinical Overview

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A plethora of investigations demonstrated that vitamin D (VitD) has a broad immunomodulatory potential. It induces tolerogenic dendritic cells in vitro leading to the development of regulatory T cells that have a key role in immunomodulation of autoimmune diseases including multiple sclerosis (MS). Studies showed that many MS patients present lower serum levels of VitD than healthy subjects. In addition, VitD supplementation has been associated with a reduced relative risk of developing MS. Considering the alterations in VitD levels in patients and also the immunomodulatory properties of VitD, it would be interesting to evaluate VitD potential as a tolerogenic adjuvant in experimental models of MS. In this context, our research team has been investigating strategies employing VitD to establish an in vivo tolerance state toward central nervous system antigens in experimental autoimmune encephalomyelitis (EAE). We observed that the association between a myelin peptide and VitD determined both therapeutic and prophylactic effects on EAE development.

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“…[14][15][16] However, recent reports have focused on the novel direct action of vitamin D to several types of central nervous system cells, including neurons, glial cells and brain endothelial cells. [17][18][19][20][21] Breakdown of the blood-brain barrier (BBB), which subsequently induces inflammation in the central nervous system, is an important step in MS onset or relapse. Notably, a recent study reported that vitamin D has protective effects on mouse brain endothelial cells in an ischemic model through the modulation of tight junction protein and nuclear factor kappa B (NFjB) activation.…”

Section: Introductionmentioning

confidence: 99%

Active form of vitamin D directly protects the blood–brain barrier in multiple sclerosis

Takahashi

Maeda

Sano

et al. 2017

Clinical & Exp Neuroim

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Objectives The active form of vitamin D, 1a, 2 D 3 ), is reported to have protective effects for multiple sclerosis (MS), but the precise mechanisms of this effect on MS remain unclear. We hypothesized that 1a,25-(OH) 2 D 3 has protective effects on the blood-brain barrier (BBB) in MS. Methods The expression of vitamin D receptor in a human brain microvascular endothelial cell line (HBMEC) was examined. The effects of 1a,25-(OH) 2 D 3 on HBMEC after stimulation with tumor necrosis factor-a were observed. In addition, we assessed the effects of sera from MS patients, including those in the acute and stable phase of relapse-remitting MS or secondary progressive MS, on the BBB property in the presence or absence of 1a,25-(OH) 2 D 3 . Results HBMEC were found to express the vitamin D receptor at both the mRNA and protein level. Pretreatment of HBMEC with 1a,25-(OH) 2 D 3 attenuated the decrease of zonula occludens-1 and claudin-5, and the increase of intercellular adhesion molecule-1 (ICAM-1) induced by tumor necrosis factor-a. In addition, nuclear factor kappa B activation mediated by tumor necrosis factor-a was decreased after incubation with the activated vitamin D. Furthermore, incubation with 1a,25-(OH) 2 D 3 attenuated the increase of vascular cell adhesion molecule-1 and anti-phospho-nuclear factor kappa B in HBMEC after exposure to sera from patients with relapse-remitting MS and secondary progressive MS, and restored the decrease of zonula occludens-1 and claudin-5 in HBMEC after incubation with sera from the acute phase of relapse-remitting MS patients. Conclusions Treatment with 1a,25-(OH) 2 D 3 prevents BBB disruption caused by both relapse-remitting MS and secondary progressive MS sera through upregulation of tight junction proteins and downregulation of cell adhesion molecules in HBMEC, suggesting that 1a,25-(OH) 2 D 3 might have the direct protective effects on the fragile BBB in MS patients.

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1,25-Dihydroxyvitamin D3 enhances neural stem cell proliferation and oligodendrocyte differentiation

Cited by 125 publications

References 37 publications

Administration of vitamin D 3 induces CNPase and myelin oligodendrocyte glycoprotein expression in the cerebral cortex of the murine model of cuprizone-induced demyelination

Administration of vitamin D 3 induces CNPase and myelin oligodendrocyte glycoprotein expression in the cerebral cortex of the murine model of cuprizone-induced demyelination

Therapeutic and Prophylactic Potential of Vitamin D for Multiple Sclerosis

Active form of vitamin D directly protects the blood–brain barrier in multiple sclerosis

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