Phosphatidylethanolamine-binding protein 1 protects CA1 neurons against ischemic damage via ERK-CREB signaling in Mongolian gerbils

Jung, Hyo Young; Cho, Su Bin; Kim, Woosuk; Yoo, Doo-Yeol; Won, Moo‐Ho; Choi, Goang-Min; Cho, Tack-Geun; Kim, Dae Won; Hwang, In Koo; Choi, Soo Young; Moon, Sung–Hoon

doi:10.1016/j.neuint.2018.05.005

Cited by 10 publications

(37 citation statements)

References 55 publications

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“…In the previous study, we generated a PEP-1-PEBP1 fusion protein and confirmed it could penetrate the blood-brain barrier and plasma membrane of neurons [16]. In the present study, we examined the effects of PEP-1-PEBP1 treatment on H 2 O 2 -induced oxidative stress in NSC34 cells in vitro and ischemic damage in the rabbit spinal cord in vivo.…”

Section: Introductionmentioning

confidence: 73%

“…PEP-1-PEBP1 was by ligation of a TA cloning vector with human PEBP1 cDNA and expression plasmid was inserted into a pET-15 vector with His-PEP-1-PEBP1 or His-PEBP1. PEP-1-PEBP1 and control-PEBP1 proteins were produced as described in a previous study [16], and the production of PEP-1-PEBP1 and control-PEBP1 proteins was confirmed by western blot analysis for polyhistidine antibody (1:2000, His-probe, Santa Cruz Biotechnology) as described previously [16,18].…”

Section: Methodsmentioning

confidence: 99%

“…In addition, cells were treated with 3 μM PEP-1-PEBP1 and control-PEBP1 treatment and harvested at various times (0–36 h) after treatment to observe the intracellular penetration efficacy and stability of PEP-1-PEBP1 or control-PEBP1 protein. Expression of PEP-1-PEBP1 and control-PEBP1 proteins was evaluated by western blot analysis for polyhistidine antibody, as described previously [16,18].…”

Section: Methodsmentioning

confidence: 99%

“…Intracellular delivery of PEP-1-PEBP1 or control-PEBP1 protein was confirmed by immunocytochemical staining for polyhistidine, as described previously [15,16]. Briefly, cells cultured on coverslips were incubated with 3 μM PEP-1-PEBP1 or control-PEBP1 protein for 1 h at 37 °C, and the cells were fixed with 4% paraformaldehyde for 5 min.…”

Section: Methodsmentioning

confidence: 99%

“…In addition, our colleagues observed that phosphorylated PEBP1 levels significantly increase in the hippocampal CA1 region 1–2 days after ischemia. In addition, administering PEP-1-PEBP1 significantly ameliorates the pyramidal cell damage induced by ischemia in gerbils via extracellular signal-regulated kinases and phosphorylation of cyclic-AMP response element binding protein signaling [16]. However, there are only few studies on the effects of PEBP1 against ischemic damage in the spinal cord.…”

Section: Introductionmentioning

confidence: 99%

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Phosphatidylethanolamine-Binding Protein 1 Ameliorates Ischemia-Induced Inflammation and Neuronal Damage in the Rabbit Spinal Cord

Kim

Cho

Jung

et al. 2019

Cells

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In a previous study, we utilized a proteomic approach and found a significant reduction in phosphatidylethanolamine-binding protein 1 (PEBP1) protein level in the spinal cord at 3 h after ischemia. In the present study, we investigated the role of PEBP1 against oxidative stress in NSC34 cells in vitro, and ischemic damage in the rabbit spinal cord in vivo. We generated a PEP-1-PEBP1 fusion protein to facilitate the penetration of blood-brain barrier and intracellular delivery of PEBP1 protein. Treatment with PEP-1-PEBP1 significantly decreased cell death and the induction of oxidative stress in NSC34 cells. Furthermore, administering PEP-1-PEBP1 did not show any significant side effects immediately before and after ischemia/reperfusion. Administration of PEP-PEBP1 improved the Tarlov’s neurological score at 24 and 72 h after ischemia, and significantly improved neuronal survival at 72 h after ischemia based on neuronal nuclei (NeuN) immunohistochemistry, Flouro-Jade B staining, and western blot study for cleaved caspase 3. PEP-1-PEBP1 administration decreased oxidative stress based on malondialdehyde level, advanced oxidation protein products, and 8-iso-prostaglandin F2α in the spinal cord. In addition, inflammation based on myeloperoxidase level, tumor necrosis factor-α level, and high mobility group box 1 level was decreased by PEP-1-PEBP1 treatment at 72 h after ischemia. Thus, PEP-1-PEBP1 treatment, which decreases oxidative stress, inflammatory cytokines, and neuronal death, may be an effective therapeutic strategy for spinal cord ischemia.

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Section: Introductionmentioning

confidence: 73%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Phosphatidylethanolamine-Binding Protein 1 Ameliorates Ischemia-Induced Inflammation and Neuronal Damage in the Rabbit Spinal Cord

Kim

Cho

Jung

et al. 2019

Cells

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Neuroprotective Effects of Purpurin Against Ischemic Damage via MAPKs, Bax, and Oxidative Stress Cascades in the Gerbil Hippocampus

et al. 2022

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Purpurin has various effects, including anti-inflammatory effects, and can efficiently cross the blood–brain barrier. In the present study, we investigated the effects of purpurin on oxidative stress in HT22 cells and mild brain damage in the gerbil hippocampal CA1 region induced by transient forebrain ischemia. Oxidative stress induced by H2O2 was significantly ameliorated by treatment with purpurin, based on changes in cell death, DNA fragmentation, formation of reactive oxygen species, and pro-apoptotic (Bax)/anti-apoptotic (Bcl-2) protein levels. In addition, treatment with purpurin significantly reduced the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK), and p38 signaling in HT22 cells. Transient forebrain ischemia in gerbils led to a significant increase in locomotor activity 1 day after ischemia and significant decrease in number of surviving cells in the CA1 region 4 days after ischemia. Administration of purpurin reduced the travel distance 1 day after ischemia and abrogates the neuronal death in the hippocampal CA1 region 4 days after ischemia based on immunohistochemical and histochemical staining for NeuN and Fluoro-Jade C, respectively. Purpurin treatment significantly decreased the activation of microglia and astrocytes as well as the increases of nuclear factor kappa-light-chain-enhancer of activated B cells p65 in the hippocampal CA1 region 4 days after ischemia and ameliorated the ischemia-induced transient increases of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the hippocampus 6 h after ischemia. In addition, purpurin significantly alleviated the ischemia-induced phosphorylation of JNK, ERK, and p38 in the hippocampus 1 day after ischemia. Furthermore, purpurin treatment significantly mitigated the increases of Bax in the hippocampus 1 day after ischemia and the lipid peroxidation based on malondialdehyde and hydroperoxides levels 2 days after ischemia. These results suggest that purpurin can be one of the potential candidates to reduce neuronal damage and inflammatory responses after oxidative stress in HT22 cells or ischemic damage in gerbils.

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Achieving Life through Death: Redox Biology of Lipid Peroxidation in Ferroptosis

Bayır

Anthonymuthu

Tyurina

et al. 2020

Cell Chemical Biology

188

111

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Redox balance is essential for normal brain, hence dis-coordinated oxidative reactions leading to neuronal death, including programs of regulated death, are commonly viewed as an inevitable pathogenic penalty for acute neuro-injury and neurodegenerative diseases. Ferroptosis is one of these programs triggered by dyshomeostasis of three metabolic pillars: iron, thiols, and polyunsaturated phospholipids. This review focuses on: (1) lipid peroxidation (LPO) as the major instrument of cell demise, (2) iron as its catalytic mechanism, and (3) thiols as regulators of pro-ferroptotic signals, hydroperoxy lipids. Given the central role of LPO, we discuss the engagement of selective and specific enzymatic pathways versus random free radical chemical reactions in the context of the phospholipid substrates, their biosynthesis, intracellular location, and related oxygenating machinery as participants in ferroptotic cascades. These concepts are discussed in the light of emerging neuro-therapeutic approaches controlling intracellular production of pro-ferroptotic phospholipid signals and their non-cell-autonomous spreading, leading to ferroptosis-associated necroinflammation.Achieving life is not the equivalent of avoiding death.

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Phosphatidylethanolamine-binding protein 1 protects CA1 neurons against ischemic damage via ERK-CREB signaling in Mongolian gerbils

Cited by 10 publications

References 55 publications

Phosphatidylethanolamine-Binding Protein 1 Ameliorates Ischemia-Induced Inflammation and Neuronal Damage in the Rabbit Spinal Cord

Phosphatidylethanolamine-Binding Protein 1 Ameliorates Ischemia-Induced Inflammation and Neuronal Damage in the Rabbit Spinal Cord

Neuroprotective Effects of Purpurin Against Ischemic Damage via MAPKs, Bax, and Oxidative Stress Cascades in the Gerbil Hippocampus

Achieving Life through Death: Redox Biology of Lipid Peroxidation in Ferroptosis

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