PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression

Kim, Duk‐Soo; Sohn, Eun Jeong; Kim, Dae Won; Kim, Young Nam; Eom, Seon Ae; Yoon, Ga Hyeon; Cho, Sung‐Woo; Lee, Jangwook; Hwang, Hyun Sook; Cho, Yoon Shin; Park, Jinseu; Eum, Won Sik; Choi, Soo Young

doi:10.5483/bmbrep.2012.45.9.083

Cited by 16 publications

(10 citation statements)

References 29 publications

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“…transduction efficiency is known to be affected by several factors such as the target protein, the cell types, and the PTDs (van den Berg and Dowdy, 2011), Tat-BLVRA protein efficiently transduced into cells unaffected by these factors. Although the exact means by which transduction takes place is not fully understood, many studies including those done by our group have demonstrated that Tat fusion protein transduction has potential for the therapeutic application of proteins in number of diseases Ahn et al, 2013;Kim et al, 2013a,b;Embury et al, 2001;Kubo et al, 2008;Kim et al, 2012).…”

Section: Discussionmentioning

confidence: 97%

Tat-biliverdin reductase A inhibits inflammatory response by regulation of MAPK and NF-κB pathways in Raw 264.7 cells and edema mouse model

Kim

et al. 2015

Molecular Immunology

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Section: Discussionmentioning

confidence: 97%

Tat-biliverdin reductase A inhibits inflammatory response by regulation of MAPK and NF-κB pathways in Raw 264.7 cells and edema mouse model

Kim

et al. 2015

Molecular Immunology

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“…After the plasmids were transformed into E. coli BL21 (DE3) cells, the PEP-1-PON1 and control PON1 proteins were induced by adding 0.5 mM isopropyl-β-D-thio-galactoside (Duchefa, Haarlem, Netherlands) at 37°C for 6 h. Recombinant proteins obtained from harvested cells were lysed by sonication after which the proteins were purified by Ni 2+ -nitrilotriacetic acid Sepharose affinity column chromatography (Qiagen, Valencia, CA, USA) and PD-10 column chromatography (Amersham, Brauncschweig, Germany) according to the manufacturer’s instructions [28]–[36]. To remove endotoxins of proteins, purified control PON1 and PEP-1-PON1 were treated with a Detoxi-Gel™ endotoxin removing gel (Pierce, Rockford, IL, USA) as per manufacturer’s instructions [34].…”

Section: Methodsmentioning

confidence: 99%

“…However, many studies have shown that the delivery of therapeutic proteins to cells and tissues using protein transduction domains (PTDs) is a powerful tool in clinical protein application [21]–[27]. In previous studies, we showed that PTD fusion proteins transduced into cells and tissues as well as protected against various diseases including skin inflammation and neuronal diseases [28]–[36].…”

Section: Introductionmentioning

confidence: 99%

PEP-1-PON1 Protein Regulates Inflammatory Response in Raw 264.7 Macrophages and Ameliorates Inflammation in a TPA-Induced Animal Model

et al. 2014

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Paraoxonase 1 (PON1) is an antioxidant enzyme which plays a central role in various diseases. However, the mechanism and function of PON1 protein in inflammation are poorly understood. Since PON1 protein alone cannot be delivered into cells, we generated a cell permeable PEP-1-PON1 protein using protein transduction domains, and examined whether it can protect against cell death in lipopolysaccharide (LPS) or hydrogen peroxide (H2O2)-treated Raw 264.7 cells as well as mice with 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced skin inflammation. We demonstrated that PEP-1-PON1 protein transduced into Raw 264.7 cells and markedly protected against LPS or H2O2-induced cell death by inhibiting cellular reactive oxygen species (ROS) levels, the inflammatory mediator’s expression, activation of mitogen-activated protein kinases (MAPKs) and cellular apoptosis. Furthermore, topically applied PEP-1-PON1 protein ameliorates TPA-treated mice skin inflammation via a reduction of inflammatory response. Our results indicate that PEP-1-PON1 protein plays a key role in inflammation and oxidative stress in vitro and in vivo. Therefore, we suggest that PEP-1-PON1 protein may provide a potential protein therapy against oxidative stress and inflammation.

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“…An MTT assay was performed as described previously (Kim et al, 2012). SH-SY5Y cells were seeded into 96 well plates at the density of 10,000 cells/well overnight.…”

Section: Methodsmentioning

confidence: 99%

Tat-Fused Recombinant Human SAG Prevents Dopaminergic Neurodegeneration in a MPTP-Induced Parkinson’s Disease Model

Sohn

Shin²,

Kim³

et al. 2014

Molecules and Cells

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Excessive reactive oxygen species (ROS) generated from abnormal cellular process lead to various human diseases such as inflammation, ischemia, and Parkinson’s disease (PD). Sensitive to apoptosis gene (SAG), a RING-FINGER protein, has anti-apoptotic activity and anti-oxidant activity. In this study, we investigate whether Tat-SAG, fused with a Tat domain, could protect SH-SY5Y neuroblastoma cells against 1-methyl-4-phenylpyridinium (MPP+) and dopaminergic (DA) neurons in the substantia nigra (SN) against 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP) toxicity. Western blot and immunohistochemical analysis showed that, unlike SAG, Tat-SAG transduced efficiently into SH-SY5Y cells and into the brain, respectively. Tat-SAG remarkably suppressed ROS generation, DNA damage, and the progression of apoptosis, caused by MPP+ in SH-SY5Y cells. Also, immunohistochemical data using a tyrosine hydroxylase antibody and cresyl violet staining demonstrated that Tat-SAG obviously protected DA neurons in the SN against MPTP toxicity in a PD mouse model. Tat-SAG-treated mice showed significant enhanced motor activities, compared to SAG- or Tat-treated mice. Therefore, our results suggest that Tat-SAG has potential as a therapeutic agent against ROS-related diseases such as PD.

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PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression

Cited by 16 publications

References 29 publications

Tat-biliverdin reductase A inhibits inflammatory response by regulation of MAPK and NF-κB pathways in Raw 264.7 cells and edema mouse model

Tat-biliverdin reductase A inhibits inflammatory response by regulation of MAPK and NF-κB pathways in Raw 264.7 cells and edema mouse model

PEP-1-PON1 Protein Regulates Inflammatory Response in Raw 264.7 Macrophages and Ameliorates Inflammation in a TPA-Induced Animal Model

Tat-Fused Recombinant Human SAG Prevents Dopaminergic Neurodegeneration in a MPTP-Induced Parkinson’s Disease Model

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