NG2-glia cell proliferation and differentiation by glial growth factor 2 (GGF2), a strategy to promote functional recovery after ischemic stroke

Li, Fēi; Liu, Wen-Cao; Wang, Qi; Sun, Yuanheng; Wang, Hongbo; Jin, Xinchun

doi:10.1016/j.bcp.2019.113720

Cited by 25 publications

(23 citation statements)

References 79 publications

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“…Brain ischemia causes severe damage to white matter, especially in the ischemic core. This white matter damage accounts for almost half of the infarct volume and is a major cause of functional disability and cognitive dysfunction [ 199 , 200 ]. Some recent reports suggest that changes in white matter infarct volume, particularly in the deep subcortical area, have clinical relevance as predictors of long-term severity after cerebral ischemia [ 201 , 202 ].…”

Section: Oligodendrocytesmentioning

confidence: 99%

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

Hernández

Villa-González

Martín

et al. 2021

Cells

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Ischemic stroke is the second cause of mortality and the first cause of long-term disability constituting a serious socioeconomic burden worldwide. Approved treatments include thrombectomy and rtPA intravenous administration, which, despite their efficacy in some cases, are not suitable for a great proportion of patients. Glial cell-related therapies are progressively overcoming inefficient neuron-centered approaches in the preclinical phase. Exploiting the ability of microglia to naturally switch between detrimental and protective phenotypes represents a promising therapeutic treatment, in a similar way to what happens with astrocytes. However, the duality present in many of the roles of these cells upon ischemia poses a notorious difficulty in disentangling the precise pathways to target. Still, promoting M2/A2 microglia/astrocyte protective phenotypes and inhibiting M1/A1 neurotoxic profiles is globally rendering promising results in different in vivo models of stroke. On the other hand, described oligodendrogenesis after brain ischemia seems to be strictly beneficial, although these cells are the less studied players in the stroke paradigm and negative effects could be described for oligodendrocytes in the next years. Here, we review recent advances in understanding the precise role of mentioned glial cell types in the main pathological events of ischemic stroke, including inflammation, blood brain barrier integrity, excitotoxicity, reactive oxygen species management, metabolic support, and neurogenesis, among others, with a special attention to tested therapeutic approaches.

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Section: Oligodendrocytesmentioning

confidence: 99%

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

Hernández

Villa-González

Martín

et al. 2021

Cells

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“…The disruption of white matter integrity, including oligodendrocyte death, myelin loss, and axonal damage, significantly worsens neurological function after ischemic stroke; the impaired proliferation and differentiation of the oligodendrocyte precursor cell may also hamper the functional recovery. Consistently, Id2 is a critical component for regulating the differentiation of oligodendrocyte precursor cells in cerebral ischemia [ 55 ].…”

Section: Id Proteins With Various Pathophysiological Functionsmentioning

confidence: 99%

Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer’s Disease: Cell Cycle Reentry and Beyond

Chen

Yang

Lin

et al. 2020

Cells

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Inhibitor of DNA-binding/differentiation (Id) proteins, a family of helix-loop-helix (HLH) proteins that includes four members of Id1 to Id4 in mammalian cells, are critical for regulating cell growth, differentiation, senescence, cell cycle progression, and increasing angiogenesis and vasculogenesis, as well as accelerating the ability of cell migration. Alzheimer’s disease (AD), the most common neurodegenerative disease in the adult population, manifests the signs of cognitive decline, behavioral changes, and functional impairment. The underlying mechanisms for AD are not well-clarified yet, but the aggregation of amyloid-beta peptides (Aβs), the major components in the senile plaques observed in AD brains, contributes significantly to the disease progression. Emerging evidence reveals that aberrant cell cycle reentry may play a central role in Aβ-induced neuronal demise. Recently, we have shown that several signaling mediators, including Id1, hypoxia-inducible factor-1 (HIF-1), cyclin-dependent kinases-5 (CDK5), and sonic hedgehog (Shh), may contribute to Aβ-induced cell cycle reentry in postmitotic neurons; furthermore, Id1 and CDK5/p25 mutually antagonize the expression/activity of each other. Therefore, Id proteins may potentially have clinical applications in AD. In this review article, we introduce the underlying mechanisms for cell cycle dysregulation in AD and present some examples, including our own studies, to show different aspects of Id1 in terms of cell cycle reentry and other signaling that may be crucial to alter the neuronal fates in this devastating neurodegenerative disease. A thorough understanding of the underlying mechanisms may provide a rationale to make an earlier intervention before the occurrence of cell cycle reentry and subsequent apoptosis in the fully differentiated neurons during the progression of AD or other neurodegenerative diseases.

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“…Interestingly, patients without apparent improvement still exhibited complex changes over time due to motor network connectivity [ 91 ]. Investigated mechanisms of motor functional recovery include axonal sprouting [ 92 , 93 ], white matter repair [ 94 ], neurogenesis [ 95 ], and ipsilesional/contralesional network reorganization [ 96 ]. Just as consequences of stroke disability maladaptively alter cortical mapping and hinder recovery [ 97 ], interventions targeting beneficial neuroplastic reorganization can strengthen tracts and improve recovery [ 98 , 99 ].…”

Section: Motor Pathway Disruptionmentioning

confidence: 99%

Beyond the Brain: The Systemic Pathophysiological Response to Acute Ischemic Stroke

et al. 2020

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Stroke research has traditionally focused on the cerebral processes following ischemic brain injury, where oxygen and glucose deprivation incite prolonged activation of excitatory neurotransmitter receptors, intracellular calcium accumulation, inflammation, reactive oxygen species proliferation, and ultimately neuronal death. A recent growing body of evidence, however, points to far-reaching pathophysiological consequences of acute ischemic stroke. Shortly after stroke onset, peripheral immunodepression in conjunction with hyperstimulation of autonomic and neuroendocrine pathways and motor pathway impairment result in dysfunction of the respiratory, urinary, cardiovascular, gastrointestinal, musculoskeletal, and endocrine systems. These end organ abnormalities play a major role in the morbidity and mortality of acute ischemic stroke. Using a pathophysiology-based approach, this current review discusses the pathophysiological mechanisms following ischemic brain insult that result in end organ dysfunction. By characterizing stroke as a systemic disease, future research must consider bidirectional interactions between the brain and peripheral organs to inform treatment paradigms and develop effective, comprehensive therapeutics for acute ischemic stroke.

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NG2-glia cell proliferation and differentiation by glial growth factor 2 (GGF2), a strategy to promote functional recovery after ischemic stroke

Cited by 25 publications

References 79 publications

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury

Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer’s Disease: Cell Cycle Reentry and Beyond

Beyond the Brain: The Systemic Pathophysiological Response to Acute Ischemic Stroke

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