1,25(OH)2D3 Alleviates Aβ(25-35)-Induced Tau Hyperphosphorylation, Excessive Reactive Oxygen Species, and Apoptosis Through Interplay with Glial Cell Line-Derived Neurotrophic Factor Signaling in SH-SY5Y Cells

Lin, Chin-Kai; Chang, Yi; Kao, Ning Jo; Lee, Wei Ju; Cross, Tzu Wen L.; Lin, Shyh Hsiang

doi:10.3390/ijms21124215

Cited by 26 publications

(13 citation statements)

References 74 publications

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“…Our results support the relieving effect of calcitriol on parthanatos. Calcitriol increases the expression of GDNF and nuclear factor erythroid-2-related factor 2 to protect cells from damage caused by ROS, which is in accordance with our results (Pertile et al, 2018;Lin et al, 2020). Next, we verified the role of calcitriol in the MPTP mouse model.…”

Section: Discussionsupporting

confidence: 89%

Calcitriol Alleviates MPP+- and MPTP-Induced Parthanatos Through the VDR/PARP1 Pathway in the Model of Parkinson’s Disease

Wan

et al. 2021

Front. Aging Neurosci.

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The pathogenesis of Parkinson’s disease (PD) is currently unclear. Recent studies have suggested a correlation between vitamin D and PD. Vitamin D and its analogs have protective effects in animal models of PD, but these studies have not clarified the mechanism. Parthanatos is a distinct type of cell death caused by excessive activation of poly (ADP-ribose) polymerase-1 (PARP1), and the activation of PARP1 in PD models suggests that parthanatos may exist in PD pathophysiology. 1,25-Dihydroxyvitamin D3 (calcitriol) is a potential inhibitor of PARP1 in macrophages. This study aimed to investigate whether calcitriol treatment improves PD models and its effects on the parthanatos pathway. A 1-methyl-4-phenylpyridinium (MPP+)-induced cell model and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) subacute animal model were selected as the in vitro and in vivo PD models, and calcitriol was applied in these models. Results showed that parthanatos existed in the MPP+-induced cell model and pretreatment with calcitriol improved cell viability, reduced the excessive activation of PARP1, and relieved parthanatos. The application of calcitriol in the MPTP subacute animal model also improved behavioral tests, restored the damage to dopamine neurons, and reduced the activation of PARP1-related signaling pathways. To verify whether calcitriol interacts with PARP1 through its vitamin D receptor (VDR), siRNA, and overexpression plasmids were used to downregulate or overexpress VDR. Following the downregulation of VDR, the expression and activation of PARP1 increased and PARP1 was inhibited when VDR was overexpressed. Coimmunoprecipitation verified the combination of VDR and PARP1. In short, calcitriol can substantially improve parthanatos in the MPP+-induced cell model and MPTP model, and the protective effect might be partly through the VDR/PARP1 pathway, which provides a new possibility for the treatment of PD.

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Section: Discussionsupporting

confidence: 89%

Calcitriol Alleviates MPP+- and MPTP-Induced Parthanatos Through the VDR/PARP1 Pathway in the Model of Parkinson’s Disease

Wan

et al. 2021

Front. Aging Neurosci.

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“…Vitamin D supplementation in this model improves memory possibly via the suppression of collapsin response mediator protein-2 (CRMP2) phosphorylation [ 158 ]. An in vitro study has also shown 1,25(OH) 2 D 3 alleviates Tau hyperphosphorylation and reduces ROS in a neuronal cell model treated with Aβ possibly via vitamin D’s role in enhancing GDNF [ 159 ].…”

Section: Vitamin D Is Neuroprotective In Neurons and Adult Brainmentioning

confidence: 99%

Vitamin D and the Central Nervous System: Causative and Preventative Mechanisms in Brain Disorders

Cui

Eyles

2022

Nutrients

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Twenty of the last one hundred years of vitamin D research have involved investigations of the brain as a target organ for this hormone. Our group was one of the first to investigate brain outcomes resulting from primarily restricting dietary vitamin D during brain development. With the advent of new molecular and neurochemical techniques in neuroscience, there has been increasing interest in the potential neuroprotective actions of vitamin D in response to a variety of adverse exposures and how this hormone could affect brain development and function. Rather than provide an exhaustive summary of this data and a listing of neurological or psychiatric conditions that vitamin D deficiency has been associated with, here, we provide an update on the actions of this vitamin in the brain and cellular processes vitamin D may be targeting in psychiatry and neurology.

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“…It also regulates gene expression of the low-affinity NGF receptor, p75NRT [ 85 ]. Moreover, 1,25(OH)2D3 was shown to be neuroprotective in an in vitro model of Alzheimer’s Disease through the restoration of Aβ-induced decrease in GDNF level and activation of the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) pathway [ 86 ]. Both epidemiological data and results from animal experiments suggest that vitamin D3 deficiency may be a significant factor in increasing the risk of multiple sclerosis, diabetes, schizophrenia, and certain cancers, as well as SARS-CoV-2 virus infections [ 87 , 88 ].…”

Section: The Effects Of Vitamin D3 In the Cnsmentioning

confidence: 99%

Vitamin D3 and Ischemic Stroke: A Narrative Review

et al. 2022

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Ischemic stroke is one of the major causes of death and permanent disability worldwide. The only efficient treatment to date is anticoagulant therapy and thrombectomy, which enable restitution of blood flow to ischemic tissues. Numerous promising neuroprotectants have failed in clinical trials. Given the complex pathomechanism of stroke, a multitarget pharmacotherapy seems a more rational approach in stroke prevention and treatment than drugs acting on single molecular targets. Recently, vitamin D3 has emerged as a potential treatment adjunct for ischemic stroke, as it interferes with the key prosurvival pathways and shows neuroprotective, anti-inflammatory, regenerative and anti-aging properties in both neuronal and vascular tissue. Moreover, the stimulatory effect of vitamin D3 on brain-derived neurotrophic factor (BDNF) signaling and neuroplasticity may play a role not only in the recovery of neurological functions, but also in ameliorating post-stroke depression and anxiety. This narrative review presents advances in research on the biochemical mechanisms of stroke-related brain damage, and the genomic and non-genomic effects of vitamin D3 which may interfere with diverse cell death signaling pathways. Next, we discuss the results of in vitro and in vivo experimental studies on the neuroprotective potential of 1alpha,25-dihydroxyvitamin D3 (calcitriol) in brain ischemia models. Finally, the outcomes of clinical trials on vitamin D3 efficiency in ischemic stroke patients are briefly reviewed. Despite the mixed results of the clinical trials, it appears that vitamin D3 still holds promise in preventing or ameliorating neurological and psychiatric consequences of ischemic stroke and certainly deserves further study.

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1,25(OH)2D3 Alleviates Aβ(25-35)-Induced Tau Hyperphosphorylation, Excessive Reactive Oxygen Species, and Apoptosis Through Interplay with Glial Cell Line-Derived Neurotrophic Factor Signaling in SH-SY5Y Cells

Cited by 26 publications

References 74 publications

Calcitriol Alleviates MPP+- and MPTP-Induced Parthanatos Through the VDR/PARP1 Pathway in the Model of Parkinson’s Disease

Calcitriol Alleviates MPP+- and MPTP-Induced Parthanatos Through the VDR/PARP1 Pathway in the Model of Parkinson’s Disease

Vitamin D and the Central Nervous System: Causative and Preventative Mechanisms in Brain Disorders

Vitamin D3 and Ischemic Stroke: A Narrative Review

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