Deletion of JDP2 improves neurological outcomes of traumatic brain injury (TBI) in mice: Inactivation of Caspase-3

Wang, Xiaohong; Liu, Qiang; Shao, Zetao

doi:10.1016/j.bbrc.2018.08.055

Cited by 6 publications

(4 citation statements)

References 34 publications

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“…In addition, JDP2 expression is activated by hypoxia in a murine model of MI and is regulated by testis-specific transcript, Y-linked 15-targeted microRNA-455-5p to prevent cardiomyocyte apoptosis and rescue cell migration and invasion (39). In mice with traumatic brain injury, LPS stimulates the expression of JDP2, and JDP2 overexpression aggravates LPS-induced inflammation and apoptosis of mouse astrocytes (40). Consistent with these findings, the results of the present study demonstrated that JDP2 overexpression attenuated the ameliorative effect of PDE4B knockdown on cell viability, cytotoxicity, oxidative stress and apoptosis in H/R-stimulated H9c2 cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Transcription factor JDP2 activates PDE4B to participate in hypoxia/reoxygenation‑induced H9c2 cell injury

Chen

Jia

et al. 2022

Exp Ther Med

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Myocardial ischemia/reperfusion (I/R) injury is a clinical challenge in the treatment of acute myocardial infarction (AMI). Phosphodiesterase 4B (PDE4B) expression is upregulated in AMI tissues. Thus, the present study aimed to investigate the role of PDE4B in myocardial I/R injury. H9c2 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) to establish an in vitro myocardial I/R model. PDE4B expression was detected via reverse transcription-quantitative PCR (RT-qPCR) and western blotting before and after transfection with PDE4B interference plasmids in H/R-stimulated H9c2 cells. Cell viability and cytotoxicity were assessed using the Cell Counting Kit-8 and lactate dehydrogenase assays, respectively. Furthermore, oxidative stress was assessed using malondialdehyde, superoxide dismutase and glutathione/glutathione oxidized ratio detection kits. Cell apoptosis was detected via a TUNEL assay and western blotting. c-Jun dimerization protein 2 (JDP2) expression was also detected via RT-qPCR and western blotting. The dual luciferase reporter and chromatin immunoprecipitation assays were performed to verify the interaction between JDP2 and PDE4B. Following co-transfection with PDE4B interference plasmid and JDP2 overexpression plasmid, cell viability, cytotoxicity, oxidative stress and cell apoptosis were assessed. The results demonstrated that PDE4B knockdown reversed H/R-induced loss of viability and cytotoxicity of H9c2 cells. H/R-induced oxidative stress and cardiomyocyte apoptosis were also alleviated by PDE4B knockdown. In addition, the transcription factor JDP2 was expressed at high levels in H/R-stimulated H9c2 cells, and JDP2 overexpression upregulated PDE4B expression. Notably, JDP2 overexpression partly reversed the ameliorative effect of PDE4B knockdown on H/R-induced H9c2 injury. Taken together, the results of the present study suggested that JDP2-activated PDE4B contributed to H/R-induced H9c2 cell injury.

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Section: Discussionmentioning

confidence: 99%

Transcription factor JDP2 activates PDE4B to participate in hypoxia/reoxygenation‑induced H9c2 cell injury

Chen

Jia

et al. 2022

Exp Ther Med

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Section: Ferroptosismentioning

confidence: 99%

“…The upregulated transcription factor activator protein-1 (AP-1) promotes the catalysis of heme by heme oxygenase 1, which produces a large amount of Fe 2+ after brain injury [58,59]. Moreover, cognitive function was improved in AP-1-deficient mice [58]. During the inflammatory response, iron (especially NTBI) is preferentially transported into cells via the upregulated divalent metal transporter-1 [60].…”

Section: Ferroptosismentioning

confidence: 99%

Metabolic disorders on cognitive dysfunction after traumatic brain injury

Lai¹,

Shi²,

Lin³

et al. 2022

Trends in Endocrinology & Metabolism

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“…In one study, Evidence-Based Complementary and Alternative Medicine scientists reported that the level of IL-6, an inflammatory factor closely related to inflammation, in AD patients was significantly elevated [44]. Investigators have also found that downgrading the expression of CASP3 could reduce the inflammation induced by LPS in astrocytes associated with neurotic plaques in AD [45,46]. In addition, one study found that VEGFA, an instigator of inflammation, was involved in the therapeutic regulatory network of AD and had a neuroprotective function [47].…”

Section: Evidence-based Complementary and Alternative Medicinementioning

confidence: 99%

Network Pharmacology Study of Heat‐Clearing and Detoxifying Traditional Chinese Medicine for Alzheimer′s Disease

Zhang

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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This study aims to explore the possible homologous mechanism of 7 frequently‐used herbs for heat-clearing and detoxification in traditional Chinese medicine (HDTCM) for treating Alzheimer's disease (AD), one of the most common types of dementia, based on network pharmacology. Herbs that satisfied the criteria of containing chlorogenic acid, relating to AD and aligning with HDTCM, were simultaneously collected to determine whether they have anti-AD effect based on a survey of the literature. Herb-ingredient-target-disease networks were constructed by collecting information from the TCMSP and GeneCards public databases. The common targets of the herbs and AD were identified for conducting a Gene Ontology (GO) analyses and a Reactome pathway enrichment analysis. The results showed that PTGS1, IL-6, CASP3, and VEGFA were the predicted key gene targets. The IL-4 and IL-13 signaling pathway, the ESR-mediated signaling pathway, and the extranuclear estrogen signaling pathway were the significant pathways associated with the 7 herbs. This study revealed that the analogous anti-AD mechanism of the 7 herbs of HDTCM may be associated with anti-inflammation, which is a common effect of the chlorogenic acid and quercetin components.

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Deletion of JDP2 improves neurological outcomes of traumatic brain injury (TBI) in mice: Inactivation of Caspase-3

Cited by 6 publications

References 34 publications

Transcription factor JDP2 activates PDE4B to participate in hypoxia/reoxygenation‑induced H9c2 cell injury

Transcription factor JDP2 activates PDE4B to participate in hypoxia/reoxygenation‑induced H9c2 cell injury

Metabolic disorders on cognitive dysfunction after traumatic brain injury

Network Pharmacology Study of Heat‐Clearing and Detoxifying Traditional Chinese Medicine for Alzheimer′s Disease

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