Dimethyloxalylglycine preconditioning enhances protective effects of bone marrow-derived mesenchymal stem cells in Aβ- induced Alzheimer disease

Esmaeilzade, Banafshe; Artimani, Tayebe; Amiri, Iraj; Najafi, Rezvan; Shahidi, Siamak; Sabec, Marie H.; Farzadinia, Parviz; Zare, Mohammad-Ali; Zahiri, Maria; Asl, Sara Soleimani

doi:10.1016/j.physbeh.2018.11.034

Cited by 32 publications

(21 citation statements)

References 44 publications

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“…However, low migration, survival, and neural differentiation rates are the key factors in determining therapeutic efficacy in translational studies (Chakari-Khiavi et al, 2019). Accumulating evidence has demonstrated that the preconditioning of stem cells prior to transplantation could promote cell survival and efficacy (Pourjafar et al, 2017;Hu and Li, 2018;Esmaeilzade et al, 2019). Resveratrol, an activator of SIRT1, is an antiaging regent which could protect cells against oxidative stress and nutrient stressors FIGURE 5 | MSCs and RES-MSCs regulated the expression of APP in mouse hippocampus.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

Wang

et al. 2020

Front. Cell. Neurosci.

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Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) are promising for the treatment of Alzheimer's disease (AD). However, their low rate of migration and survival in the brain limit their clinical applicability. This study is designed to improve the therapeutic potential of hUC-MSCs by preincubating them with resveratrol, a natural polyphenol capable of regulating cell destiny. Herein, we demonstrate that resveratrol preincubation enhances the migration of hUC-MSCs in vitro, as well as their survival and homing into the hippocampus of AD mice in vivo. Moreover, resveratrol-primed MSCs were better able to inhibit amyloid-β peptide (Aβ) deposition, Tau hyperphosphorylation, and oxidative stress, all while improving learning and memory. Notably, we found that hUC-MSCs inhibited neuroinflammation by reacting with astrocytes and microglial cells and suppressing mitogen-activated protein kinases (MAPKs), extracellular signal kinases (ERK), p38 kinases (p38), and c-Jun N-terminal kinases (JNK) signaling pathways in the hippocampus of AD mice. Furthermore, resveratrol pretreatment enhanced these effects. Conclusively, the current study revealed that resveratrol preconditioning protected hUC-MSCs against the hostile microenvironment characteristic of AD and enhanced their viability and homing into the brain of AD mice. The use of resveratrol-pretreated hUC-MSCs is thereby proposed to be a promising therapy for AD.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

Wang

et al. 2020

Front. Cell. Neurosci.

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“…Treatment with dimethyloxalylglycine in Aβ injected rats reversed memory impairment in the MWM and increased Nrf2 activation [109]. Activation of the Nrf2 pathway with SFN improved memory in the MWM in a mouse model of AD [110].…”

Section: The Role Of Nrf2 In Memorymentioning

confidence: 88%

Role of Nrf2 in Synaptic Plasticity and Memory in Alzheimer’s Disease

Davies

Adlimoghaddam

Albensi

2021

Cells

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Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important transcription factor that reduces oxidative stress. When reactive oxygen species (ROS) or reactive nitrogen species (RNS) are detected, Nrf2 translocates from the cytoplasm into the nucleus and binds to the antioxidant response element (ARE), which regulates the expression of antioxidant and anti-inflammatory genes. Nrf2 impairments are observed in the majority of neurodegenerative disorders, including Alzheimer’s disease (AD). The classic hallmarks of AD include β-amyloid (Aβ) plaques, and neurofibrillary tangles (NFTs). Oxidative stress is observed early in AD and is a novel therapeutic target for the treatment of AD. The nuclear translocation of Nrf2 is impaired in AD compared to controls. Increased oxidative stress is associated with impaired memory and synaptic plasticity. The administration of Nrf2 activators reverses memory and synaptic plasticity impairments in rodent models of AD. Therefore, Nrf2 activators are a potential novel therapeutic for neurodegenerative disorders including AD.

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“…The preconditioning MSCs with dimethyloxalylglycine enhance the therapeutic efficiency of Aβ-induced animal models. 62 Other preconditioning methods, such as hypoxia, LPS, inflammatory cytokines, vitamin E, electromagnetic stimulation and low-level lasers, can also improve the viability and immunomodulatory activity of MSCs. 25 , 63 Chemokine receptor CXCR4 is involved in the homing processes to injured tissues.…”

Section: Autocrine and Paracrine Cytokinesmentioning

confidence: 99%

“… 64 The expression of CXCR4, CCR2, Nrf2 and HIF-1α is upregulated in the MSCs, which mediates the rescue of learning and memory function in Aβ-injected rats. 62 When anti-apoptotic microRNA Let-7f-5p is used in APP/PS1 transgenic mice, the prolonged survival of BMMSCs can increase the therapeutic effect of BMMSCs. 65 Paracrine effects are reflected by the secretion of soluble cytokines, such as TGF-β, IL-10, VEGF, BDNF, NGF, and neurotrophin-3 in human MSCs.…”

Section: Autocrine and Paracrine Cytokinesmentioning

confidence: 99%

“… 84 , 85 Moreover, the transplanted BMMSCs could elevate the expression of Nrf2 and seladin-1 in Aβ-injected AD rats as well as aluminium chloride-induced AD rats. 62 , 86 The function of Nrf2 was to regulate the levels of antioxidant proteins and protect neurons from oxidative damage. 5 Seladin-1 inhibited the activation of caspase-3 and mediated neuronal apoptosis, improving neuroprotective effects.…”

Section: Transplanted Bmmscs Inhibit Neuroinflammationmentioning

confidence: 99%

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Functional Mechanism of Bone Marrow-Derived Mesenchymal Stem Cells in the Treatment of Animal Models with Alzheimer’s Disease: Inhibition of Neuroinflammation

Qin¹,

Li²,

Wang³

2021

JIR

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The transplantation of bone marrow-derived mesenchymal stem cells (BMMSCs) alleviates neuropathology and improves cognitive deficits in animal models with Alzheimer’s disease. However, the underlying mechanisms remain to be determined. Available data demonstrate transplanted BMMSCs can inhibit neuroinflammation, which may be related to microglial M1/M2 polarization and is regulated by the secretion of autocrine and paracrine cytokines. BMMSCs also mitigate Aβ plaques and Tau tangles in the brain, which may be associated with the recruitment of peripheral blood monocytes and the subsequent comprehensive effects. The therapeutic effects of stem cells involve potential mechanisms such as immunomodulation, apoptosis, and proliferation. BMMSC-mediated functional reconstruction through dynamic remodeling develops a novel balance. Herein, present review recapitulates the molecular basis of BMMSC-assisted biological processes and summarizes the possible mechanisms related to the interaction between BMMSCs and microglia. The transplanted BMMSCs can suppress neuroinflammation that plays a key role in the pathogenesis of Alzheimer’s disease.

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Dimethyloxalylglycine preconditioning enhances protective effects of bone marrow-derived mesenchymal stem cells in Aβ- induced Alzheimer disease

Cited by 32 publications

References 44 publications

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

RETRACTED: Resveratrol Preincubation Enhances the Therapeutic Efficacy of hUC-MSCs by Improving Cell Migration and Modulating Neuroinflammation Mediated by MAPK Signaling in a Mouse Model of Alzheimer’s Disease

Role of Nrf2 in Synaptic Plasticity and Memory in Alzheimer’s Disease

Functional Mechanism of Bone Marrow-Derived Mesenchymal Stem Cells in the Treatment of Animal Models with Alzheimer’s Disease: Inhibition of Neuroinflammation

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