Mesenchymal Stem Cells with Granulocyte Colony-Stimulating Factor Reduce Stress Oxidative Factors in Parkinson's Disease

Ghahari, Laya; Safari, Manouchehr; Jaberi, Khojaste Rahimi; Jafari, Behnaz; Safari, Katayoun; Madadian, Mahmoodreza

doi:10.29252/ibj.24.2.89

Cited by 19 publications

(14 citation statements)

References 31 publications

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“…Mesenchymal stem cells (MSCs) derived from human umbilical cord blood (hUCB) conferred neuroprotective and neuroregenerative benefits by improving angiogenesis and vasculogenesis [ 116 ]. MSCs plus G-CSF also decreased oxidative stress factors aggravated by HI brain injury [ 117 ]. G-CSF in combination with taurine is protective in primary cortical neurons against excitotoxicity induced by glutamate as well as suppresses endoplasmic reticulum (ER) stress [ 118 ].…”

Section: Combinational Therapy With Other Agentsmentioning

confidence: 99%

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

Dumbuya

Chen

et al. 2021

J Neuroinflammation

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Hypoxic-ischemic encephalopathy (HIE) is an important cause of permanent damage to central nervous system (CNS) that may result in neonatal death or manifest later as mental retardation, epilepsy, cerebral palsy, or developmental delay. The primary cause of this condition is systemic hypoxemia and/or reduced cerebral blood flow with long-lasting neurological disabilities and neurodevelopmental impairment in neonates. About 20 to 25% of infants with HIE die in the neonatal period, and 25-30% of survivors are left with permanent neurodevelopmental abnormalities. The mechanisms of hypoxia-ischemia (HI) include activation and/or stimulation of myriad of cascades such as increased excitotoxicity, oxidative stress, N-methyl-d-aspartic acid (NMDA) receptor hyperexcitability, mitochondrial collapse, inflammation, cell swelling, impaired maturation, and loss of trophic support. Different therapeutic modalities have been implicated in managing neonatal HIE, though translation of most of these regimens into clinical practices is still limited. Therapeutic hypothermia, for instance, is the most widely used standard treatment in neonates with HIE as studies have shown that it can inhibit many steps in the excito-oxidative cascade including secondary energy failure, increases in brain lactic acid, glutamate, and nitric oxide concentration. Granulocyte-colony stimulating factor (G-CSF) is a glycoprotein that has been implicated in stimulation of cell survival, proliferation, and function of neutrophil precursors and mature neutrophils. Extensive studies both in vivo and ex vivo have shown the neuroprotective effect of G-CSF in neurodegenerative diseases and neonatal brain damage via inhibition of apoptosis and inflammation. Yet, there are still few experimentation models of neonatal HIE and G-CSF’s effectiveness, and extrapolation of adult stroke models is challenging because of the evolving brain. Here, we review current studies and/or researches of G-CSF’s crucial role in regulating these cytokines and apoptotic mediators triggered following neonatal brain injury, as well as driving neurogenesis and angiogenesis post-HI insults.

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Section: Combinational Therapy With Other Agentsmentioning

confidence: 99%

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

Dumbuya

Chen

et al. 2021

J Neuroinflammation

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“…Also, combination therapy with MSCs and other molecules or modalities could heighten MSC-mediated neuroprotection in vivo [ 121 – 123 ]. In this regard, dextran-coated iron oxide nanoparticles showed the capability to enhance the remedial impacts of MSCs in a PD animal model [ 121 ].…”

Section: Preclinical Studies Based On Msc Therapy In Neurodegenerativ...mentioning

confidence: 99%

Therapeutic utility of mesenchymal stromal cell (MSC)-based approaches in chronic neurodegeneration: a glimpse into underlying mechanisms, current status, and prospects

et al. 2022

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Recently, mesenchymal stromal cell (MSC)-based therapy has become an appreciated therapeutic approach in the context of neurodegenerative disease therapy. Accordingly, a myriad of studies in animal models and also some clinical trials have evinced the safety, feasibility, and efficacy of MSC transplantation in neurodegenerative conditions, most importantly in Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD). The MSC-mediated desired effect is mainly a result of secretion of immunomodulatory factors in association with release of various neurotrophic factors (NTFs), such as glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF). Thanks to the secretion of protein-degrading molecules, MSC therapy mainly brings about the degradation of pathogenic protein aggregates, which is a typical appearance of chronic neurodegenerative disease. Such molecules, in turn, diminish neuroinflammation and simultaneously enable neuroprotection, thereby alleviating disease pathological symptoms and leading to cognitive and functional recovery. Also, MSC differentiation into neural-like cells in vivo has partially been evidenced. Herein, we focus on the therapeutic merits of MSCs and also their derivative exosome as an innovative cell-free approach in AD, HD, PD, and ALS conditions. Also, we give a brief glimpse into novel approaches to potentiate MSC-induced therapeutic merits in such disorders, most importantly, administration of preconditioned MSCs.

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“…Establishment of the rat PD model was performed by unilateral destruction of the nigral system with a 6-OHDA injection as previously described with minor modifications. 19 In brief, male Wistar rats weighing 200-220 g and aged 10-12 w were purchased from Experimental Animal Center of Southern Medical University (Guangzhou, China) and maintained in cages at 20-23°C under a 12:12 light: dark cycle. All experiments were carried out in accordance with the Guide For the Care and Use of Laboratory Animals and were approved by the Ethics Committee for Animal Research of Third Affiliated Hospital of Sun Yat-Sen University.…”

Section: Rat Pd Modelmentioning

confidence: 99%

Nrf2 Inhibits the Progression of Parkinson’s Disease by Upregulating AABR07032261.5 to Repress Pyroptosis

Zhong¹,

Cai²,

Li³

et al. 2022

JIR

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Objective: Parkinson's disease (PD) is associated with dysregulated neural cell death, such as pyroptosis, but its regulatory mechanisms are poorly understood. This study investigated roles of nuclear factor E2-related factor 2 (Nrf2) in regulating pyroptosis and PD development. Methods: Cellular and rat PD models established by 6-OHDA exposure were subjected to Nrf2 overexpression. Neurobehavioral functions were assessed by the traction test, Morris Water Maze, and open field test. Cell proliferation was analyzed by MTS assay, while flow cytometry was applied to quantify levels of reactive oxygen species (ROS) and apoptosis. Nissl bodies in rat brains were detected by Nissl staining, and cell apoptosis in brain tissues was assessed by terminal deoxynucleotidyl transferase dUTP nick-end labeling. Differential expression of lncRNA and mRNA was characterized by deep sequencing. Results: A cellular PD model was successfully established by inducing PC12 cell differentiation with nerve growth factor-β and exposing differentiated cells to 6-OHDA. Cells exhibited significantly increased ROS levels, enhanced pyroptosis, and inhibited Nrf2 phosphorylation. The rat PD model exhibited impaired muscle strength, increased pyroptosis, and repressed Nrf2 phosphorylation. Nrf2 overexpression effectively repressed pyroptosis in both cellular and rat PD models. Marked alterations of lncRNA and mRNA profiles were induced by Nrf2 overexpression in the cellular PD model, which involved multiple signaling pathways. Silencing of the lncRNA AABR07032261.5 significantly promoted pyroptosis in the cellular PD model. Conclusion: Nrf2 suppressed PD pathogenesis in cellular and animal models by promoting AABR07032261.5, which repressed pyroptosis.

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Mesenchymal Stem Cells with Granulocyte Colony-Stimulating Factor Reduce Stress Oxidative Factors in Parkinson's Disease

Cited by 19 publications

References 31 publications

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

Therapeutic utility of mesenchymal stromal cell (MSC)-based approaches in chronic neurodegeneration: a glimpse into underlying mechanisms, current status, and prospects

Nrf2 Inhibits the Progression of Parkinson’s Disease by Upregulating AABR07032261.5 to Repress Pyroptosis

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