Preconditioning Strategies to Enhance Neural Stem Cell-Based Therapy for Ischemic Stroke

Othman, Farah Amna; Tan, Suat Cheng

doi:10.3390/brainsci10110893

Cited by 30 publications

(16 citation statements)

References 67 publications

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“…Minocycline preconditioning increases Nrf2 expression and neuroprotective paracrine secretion. It promotes migration, proliferation, and differentiation of NSCs to improve neurological recovery after NSC transplantation[ 220 , 221 ]. The molecular mechanism involves upregulation of antioxidant genes and reduced oxidative stress grafted cell death following transplantation, resulting in low-rate cell death[ 221 ].…”

Section: Strategies To Promote Stem Cell Survival For Transplantation Therapymentioning

confidence: 99%

Programmed cell death in stem cell-based therapy: Mechanisms and clinical applications

Hu¹,

Zhang²,

Zhou³

et al. 2021

WJSC

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Stem cell-based therapy raises hopes for a better approach to promoting tissue repair and functional recovery. However, transplanted stem cells show a high death percentage, creating challenges to successful transplantation and prognosis. Thus, it is necessary to investigate the mechanisms underlying stem cell death, such as apoptotic cascade activation, excessive autophagy, inflammatory response, reactive oxygen species, excitotoxicity, and ischemia/hypoxia. Targeting the molecular pathways involved may be an efficient strategy to enhance stem cell viability and maximize transplantation success. Notably, a more complex network of cell death receives more attention than one crucial pathway in determining stem cell fate, highlighting the challenges in exploring mechanisms and therapeutic targets. In this review, we focus on programmed cell death in transplanted stem cells. We also discuss some promising strategies and challenges in promoting survival for further study.

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Section: Strategies To Promote Stem Cell Survival For Transplantation Therapymentioning

confidence: 99%

Programmed cell death in stem cell-based therapy: Mechanisms and clinical applications

Hu¹,

Zhang²,

Zhou³

et al. 2021

WJSC

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“…We did not investigate possible mechanisms underlying the effects of nicorandil. It was suggested to play an important role in neuroprotection after stroke by activating the PI3K/Akt signaling pathway [ 44 , 45 ], which remains further explored.…”

Section: Discussionmentioning

confidence: 99%

The KATP channel opener, nicorandil, ameliorates brain damage by modulating synaptogenesis after ischemic stroke

Zhao

Yang

et al. 2021

PLoS ONE

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With population growth and aging, more and more patients with cerebral infarction have varying degrees of disability. ATP-sensitive potassium (KATP) channels regulate many cellular functions by coupling metabolic status with cell membrane electrical activity. Nicorandil (N-(2-hydroxyethyl)-nicotinamide nitrate) is the first KATP channel opener approved for clinical use. It has been reported that it might exert protective effects on the cerebral infarction by increasing cerebral blood flow and reducing inflammation. However, only a few studies explored its role in synaptogenesis. We made the rat model of middle cerebral artery occlusion (MCAO). Nicorandil was administered to rats via oral administration immediately after the surgery at a dose of 7.5 mg/kg and then daily for the next days. Infarct volume, cerebral edema, neurological deficits, cognitive impairment, and the level of Synaptophysin (SYP)、Growth associated protein-43 (GAP43) and neuronal nuclear antigen (NeuN) levels were measured to evaluate the effect of nicorandil. Our data showed that nicorandil treatment could decrease brain damage, improve learning and memory, and increase SYP、GAP43 and NeuN level. Taken together, we propose that nicorandil, as an opener of the KATP channel, provides a neuroprotective role in MCAO by promoting synaptic connections.

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“…IS accounts for 70-90% of the incidence of strokes ( 1 ). It can cause irreversible neuronal damage in the ischemic area within a few minutes ( 2 ). Furthermore, studies indicated that IS is also the second leading cause of preventable deaths and the third leading cause of long-term disability among adults worldwide ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

Association of Interleukin-6–174G/C Polymorphism With Ischemic Stroke: An Updated Meta-Analysis

Chai

2022

Front. Neurol.

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Background: Although numerous epidemiological studies have investigated the association between −174G/C(rs1800795) polymorphism in the interleukin-6 (IL-6) gene-stimulatory region and the risk of ischemic stroke (IS), they failed to reach a unified conclusion. The true relationship between −174G/C(rs1800795) polymorphism and IS remains controversial and unclear. Therefore, in this meta-analysis, we aimed to analyze more precisely the association between −174G/C(rs1800795) single-nucleotide polymorphism (SNP) of IL-6 gene and IS in a larger pooled population.Methods: A comprehensive literature search was performed in PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials until June 30, 2021. A fixed or random-effects model was utilized based on heterogeneity between studies. The odds ratios (ORs) and 95% confidence intervals (Cis) were calculated in the models of allele comparison (G vs. C), homozygote comparison (GG vs. CC) and (GC vs. CC), dominant (GG vs. GC + CC), hyper dominant (GG + CC vs. GC), and recessive (GG + GC vs. CC) to determine the strength of associations.Results: This meta-analysis included 13 case-control studies in 35 articles with 5,548 individuals. Overall, no significant associations between IL-6 −174G/C(rs1800795) and IS were identified (G vs. C:OR [95% CI] = 0.99 [0.81, 1.21], P = 0.91; GG + CC vs. GC:0.97 [0.85, 1.11], P = 0.66; GG vs. GC + CC: 1.01 [0.81, 1.25], P = 0.94; GC vs. CC: OR [95% CI] = 1.01 [0.68, 1.5], P = 0.96; GG vs. CC:0.93 [0.57, 1.51], P = 0.76; GG + GC vs. CC:0.97 [0.64, 1.47], P = 0.89). In the subgroup analyses by ethnicity or HWE P-value, there was a statistically significant association between IL-6 −174G/C(rs1800795) polymorphisms and IS in the alleles model; (G vs. C: LogOR [95% CI] = 0.14 [−0.16,.45], P = 0.00), homozygote model (GG vs. CC: LogOR [95% CI] = 0.18 [−0.58,.95], P = 0.00) and (GC vs. CC: LogOR [95% CI] = 0.2 [−0.46,.85], P = 0.00), dominant model (GG vs. GC + CC: OR [95% CI] = 0.02 [−0.72, 0.77], P = 0.00), and recessive model (GG + GC vs. CC: OR [95% CI]= −0.17 [−0.86,.52], P = 0.00) of the European population and in the dominant model (GG vs. GC + CC: OR [95% CI] = −0.13 [−0.51, 0.24]) of the Asian population. No statistical significance was identified in both six models of HWE p ≥ 0.2 group (both P ≥ 0.05).Conclusion: This meta-analysis revealed no correlation between IL-6 −174G/C(rs1800795) polymorphism and IS, whereas the subgroup analysis indicated that the relationship between IL-6 −174G/C(rs1800795) polymorphism and IS susceptibility varied significantly according to ethnicity and geography.

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Preconditioning Strategies to Enhance Neural Stem Cell-Based Therapy for Ischemic Stroke

Cited by 30 publications

References 67 publications

Programmed cell death in stem cell-based therapy: Mechanisms and clinical applications

Programmed cell death in stem cell-based therapy: Mechanisms and clinical applications

The KATP channel opener, nicorandil, ameliorates brain damage by modulating synaptogenesis after ischemic stroke

Association of Interleukin-6–174G/C Polymorphism With Ischemic Stroke: An Updated Meta-Analysis

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