Silencing of Id2 attenuates hypoxia/ischemia-induced neuronal injury via inhibition of neuronal apoptosis

Guo, Liemei; Yang, Xi; Lin, Xi Zhang; Lin, Yingying; Lin, Senjie; Nie, Qiang; Ren, Li; Guo, Qinhua; Que, Shuanglin; Qiu, Yongming

doi:10.1016/j.bbr.2015.07.018

Cited by 15 publications

(11 citation statements)

References 45 publications

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“…The suppression of Id2 expression protects the cerebellar granule neurons from apoptosis, whereas the overexpression of Id2 induces neuronal death [ 52 ]. In another study, the overexpression and knockdown of Id2 respectively increased and attenuated hypoxia/ischemia-induced neuronal apoptosis [ 53 , 54 ]. The effect of Id2 may involve an interaction with tumor suppressor protein Rb, and transcription factor E2F1 and Id2 knockdown could induce G0/G1 cell cycle arrest [ 54 ].…”

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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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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“…A 28-gauge stainless steel injection cannula was paved into the right lateral ventricle as previously described. 10 Then the rats received a single injection of Id2-siRNA or misRNA at a rate of .5 μL/min using amicor infusion pump and a 10 μL microsyringe. Once the infusion was done, the cannula remained in place for 5 minutes, then withdrawn at a rate of 1 mm/min.…”

Section: Middle Cerebral Artery Occlusion/reperfusion Animal Modelmentioning

confidence: 99%

Suppression of Glutamate Carboxypeptidase II Ameliorates Neuronal Apoptosis from Ischemic Brain Injury

Zhang

et al. 2016

Journal of Stroke and Cerebrovascular Diseases

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“…CoCl 2 can mimic hypoxic/ischemic conditions, including ROS generation, in various cultured cells. 4,5) H9c2 embryonic rat cardiac cells, a subclone of an original clonal cell line, are derived from rat embryonic hearts and have been used as in vitro models for exploring the mechanisms underlying hypoxia-induced apoptosis of cardiomyocytes. 6) Therefore, in the present study, we used CoCl 2 -treated H9c2 cells as a model with which to investigate whether CsA protects H9c2 cells from chemical hypoxia-induced injury and reduces oxidative stress and mitochondrial damage by the inhibition of MAPK signaling pathways.…”

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confidence: 99%

Cyclosporin A Protects H9c2 Cells Against Chemical Hypoxia-Induced Injury via Inhibition of MAPK Signaling Pathway

et al. 2016

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This study aimed to investigate the effects and molecular mechanism of cyclosporin A (CsA) on cobalt chloride (CoCl2)-induced injury in H9c2 embryonic rat cardiac cells. The results showed that CsA could protect H9c2 cells against CoCl2-induced hypoxic injury. CsA effectively improved cell viability, and decreased LDH leakage, cell apoptosis, MDA concentration, and ROS generation, and increased SOD activity, GSH production, and CAT activity in a dosedependent manner. In addition, CsA treatment blocked the CoCl2-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways. The results also suggested that CsA protected H9c2 cells against CoCl2-induced hypoxic injury, possibly by suppressing the MAPK signaling pathway. Thus, CsA is a potential therapeutic agent for cardiac hypoxic injury.

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Silencing of Id2 attenuates hypoxia/ischemia-induced neuronal injury via inhibition of neuronal apoptosis

Cited by 15 publications

References 45 publications

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

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

Suppression of Glutamate Carboxypeptidase II Ameliorates Neuronal Apoptosis from Ischemic Brain Injury

Cyclosporin A Protects H9c2 Cells Against Chemical Hypoxia-Induced Injury via Inhibition of MAPK Signaling Pathway

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