Wnt signaling pathways participate in Astragalus injection-induced differentiation of bone marrow mesenchymal stem cells

Zhong, Jingfei; Cao, Hui; Chen, Zhonghua; Zhou, Fei; Xiangling, Tan

doi:10.1016/j.neulet.2013.08.007

Cited by 10 publications

(12 citation statements)

References 26 publications

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“…The results were also in agreement with the findings of Cheng et al [ 13 ], which demonstrated that astragaloside plays a dual role in peripheral nerve regeneration, wherein a low dose induced a higher rate of regeneration, whereas a high dose did not. Other reports have described that Huangqi or its extract induced differentiation of bone marrow mesenchymal stem cells [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of Astragaloside IV on Neural Stem Cell Transplantation in Alzheimer’s Disease Rat Models

Rensong

Jin

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Stem cell-based therapy is a promising treatment strategy for neurodegenerative diseases such as Alzheimer's disease (AD). However, the mechanism underlying the maintenance of renewal and replacement capabilities of endogenous progenitor cells or engrafted stem cells in a pathological environment remains elusive. To investigate the effect of astragaloside IV (ASI) on the proliferation and differentiation of the engrafted neural stem cells (NSCs), we cultured NSCs from the hippocampus of E14 rat embryos, treated the cells with ASI, and then transplanted the cells into the hippocampus of rat AD models. In vitro experimentation showed that 10−5 M ASI induced NSCs to differentiate into β-tubulin III+ and GFAP+ cells. NSCs transplantation into rat AD models resulted in improvements in learning and memory, especially in the ASI-treated groups. ASI treatment resulted in an increase in the number of β-tubulin III+ cells in the hippocampus. Further investigation showed that ASI inhibited PS1 expression in vitro and in vivo. The high-dose ASI downregulated the Notch intracellular domain, whereas the low-dose ASI increased Notch-1 and NICD. In conclusion, ASI treatment resulted in improvements in learning and memory of AD models by promoting NSC proliferation and differentiation partly through the Notch signal pathway.

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Section: Discussionmentioning

confidence: 99%

Effect of Astragaloside IV on Neural Stem Cell Transplantation in Alzheimer’s Disease Rat Models

Rensong

Jin

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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“…While NSE is thought to be an important molecule that directly assesses damage to neurons, it may also be involved in neuronal repair. NSE has been shown to control neuronal survival, differentiation, and neurite regeneration by activating the PI3K/Akt and MAPK/ERK signaling pathways [ 18 , 25 ]. NSE-mediated activation of both PI3K and ERK1/2 pathways is required for neurite outgrowth, which may be attenuated by inhibition of MEK (MAPK/ERK kinase) and PI3K.…”

Section: Introductionmentioning

confidence: 99%

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection

et al. 2018

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Neurodegeneration is a complex process that leads to irreversible neuronal damage and death in spinal cord injury (SCI) and various neurodegenerative diseases, which are serious, debilitating conditions. Despite exhaustive research, the cause of neuronal damage in these degenerative disorders is not completely understood. Elevation of cell surface α-enolase activates various inflammatory pathways, including the production of pro-inflammatory cytokines, chemokines, and some growth factors that are detrimental to neuronal cells. While α-enolase is present in all neurological tissues, it can also be converted to neuron specific enolase (NSE). NSE is a glycolytic enzyme found in neuronal and neuroendocrine tissues that may play a dual role in promoting both neuroinflammation and neuroprotection in SCI and other neurodegenerative events. Elevated NSE can promote ECM degradation, inflammatory glial cell proliferation, and actin remodeling, thereby affecting migration of activated macrophages and microglia to the injury site and promoting neuronal cell death. Thus, NSE could be a reliable, quantitative, and specific marker of neuronal injury. Depending on the injury, disease, and microenvironment, NSE may also show neurotrophic function as it controls neuronal survival, differentiation, and neurite regeneration via activation of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways. This review discusses possible implications of NSE expression and activity in neuroinflammation, neurodegeneration, and neuroprotection in SCI and various neurodegenerative diseases for prognostic and therapeutic potential.

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“…[51] Monocytes [52], neurons [16], astrocytes [16,53], microglia [54], skeletal muscle [55], fibroblasts, mesenchymal cells, endothelial cells [56] Functions Cell proliferation, differentiation, migration, apoptosis inhibition, astrocyte activation after injury [57], neuronal survival enhancement [58], neurogenesis [59], cell line proliferation [60], apoptosis [61] Axonal transport and homoeostasis maintenance after injury [62], neuronal survival, neuronal differentiation, neurite regeneration [63,64] Maintenance of astrocyte stability, reactive astrogliosis, glial scar formation, blood brain barrier integrity [65] Immune regulation, hematopoiesis, inflammation, oncogenesis [66], bone metabolism, neural development [67], astrocyte differentiation [68] Reason for biomarker level change within compartment after traumatic head impact Hypothesis for CSF: diffusion via cellular breakdown or breakdown of BBB [31,69] Blood: transport from CSF via glymphatic system [35] Hypothesis for blood: transport from CSF via glymphatic system [35] Hypothesis: upregulation of GFAP following head impact depending on brain swelling [70], brain parenchyma destruction causes leakage into CSF [71] Hypothesis: increased mRNA expression in post-mortem brain samples suggests active upregulation after TBI [72,73]; serum: diffusion via trauma-induced BBB disruption [74] Age-dependency CSF: no [30,31] Serum: no [7,30,31] CSF: no [30,31] Serum: no [30,31] CSF and serum: no…”

Section: Survival Time Estimationmentioning

confidence: 99%

Forensic biomarkers of lethal traumatic brain injury

et al. 2022

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Traumatic brain injury (TBI) is a major cause of death and its accurate diagnosis is an important concern of daily forensic practice. However, it can be challenging to diagnose TBI in cases where macroscopic signs of the traumatic head impact are lacking and little is known about the circumstances of death. In recent years, several post-mortem studies investigated the possible use of biomarkers for providing objective evidence for TBIs as the cause of death or to estimate the survival time and time since death of the deceased. This work systematically reviewed the available scientific literature on TBI-related biomarkers to be used for forensic purposes. Post-mortem TBI-related biomarkers are an emerging and promising resource to provide objective evidence for cause of death determinations as well as survival time and potentially even time since death estimations. This literature review of forensically used TBI-biomarkers revealed that current markers have low specificity for TBIs and only provide limited information with regards to survival time estimations and time since death estimations. Overall, TBI fatality-related biomarkers are largely unexplored in compartments that are easily accessible during autopsies such as urine and vitreous humor. Future research on forensic biomarkers requires a strict distinction of TBI fatalities from control groups, sufficient sample sizes, combinations of currently established biomarkers, and novel approaches such as metabolomics and mi-RNAs.

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Wnt signaling pathways participate in Astragalus injection-induced differentiation of bone marrow mesenchymal stem cells

Cited by 10 publications

References 26 publications

Effect of Astragaloside IV on Neural Stem Cell Transplantation in Alzheimer’s Disease Rat Models

Effect of Astragaloside IV on Neural Stem Cell Transplantation in Alzheimer’s Disease Rat Models

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection

Forensic biomarkers of lethal traumatic brain injury

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