PEP-1-GLRX1 Reduces Dopaminergic Neuronal Cell Loss by Modulating MAPK and Apoptosis Signaling in Parkinson’s Disease

Choi, Yeon Joo; Kim, Dae Won; Shin, Min Jea; Yeo, Hyeon Ji; Yeo, Eun Ji; Lee, Lee Re; Song, Yejin; Kim, Duk‐Soo; Han, Kyu Hyung; Park, Jinseu; Lee, Moon Hyoung; Park, Jong Kook; Eum, Won Sik; Choi, Soo Young

doi:10.3390/molecules26113329

Cited by 7 publications

(10 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lin also demonstrated that IL-13Rα2 was over-expressed in GBM and that a nano-delivery system constructed utilizing Pep-1 was efficient at impeding tumor proliferation via the regulation of the JNK signaling pathway ( Lin et al, 2021 ). In our work,Pep-1carried NPs could permeate U87 cells and enter the cell nucleus via transmembrane mechanisms ( Pandya et al, 2012 ; Wang et al, 2015 ; Jiang et al, 2016 ; Lv et al, 2016 ; Jiang et al, 2017 ; Jiao et al, 2017 ; Wang et al, 2017 ; Guo et al, 2019 ; Wang et al, 2020 ; Choi et al, 2021 ) According to cell experiments, we tracked the endocytosis of PDA-TMZ NPs and Pep-1@PDA-TMZ NPs by coumarin-6 labeling. The results showed that Pep-1@PDA-TMZ NPs were successfully endocytosed into the nucleus of U87 cells.…”

Section: Discussionmentioning

confidence: 94%

Polydopamine-based loaded temozolomide nanoparticles conjugated by peptide-1 for glioblastoma chemotherapy and photothermal therapy

Zhang²,

Liu³

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

Purpose: Nanoparticles (NPs) of the polydopamine (PDA)-based,loaded with temozolomide (TMZ) and conjugated with Pep-1 (Peptide-1) as a feasible nano-drug delivery system were constructed and utilized for chemotherapy (CT) and photothermal therapy (PTT) of glioblastoma (GBM).Method: PDA NPs were synthesized from dopamine (DA) hydrochloride and reacted with TMZ to obtain the PDA-TMZ NPs and then the PDA NPs and the PDA-TMZ NPs were conjugated and modified by Pep-1 to obtain the Pep-1@PDA NPs and Pep-1@PDA-TMZ NPs via the Schiff base reaction (SBR), respectively.Their dimensions, charge, and shape were characterized by dynamic light scattering (DLS) and scanning electron microscope (SEM). The assembly of TMZ was verified by Fourier-transform infrared spectroscopy (FT-IR) and ultraviolet and visible spectroscopy (UV-Vis). The biostability of both the nanocarrier and the synthetic NPs were validated using water and fetal bovine serum (FBS). The antitumor activities of the PDA-TMZ NPs and Pep-1@PDA-TMZ NPs were verified in U87 cells and tumor-bearing nude mice.Results: The prepared PDA NPs, PDA-TMZ NPs, Pep-1@PDA NPs, and Pep-1@PDA-TMZ NPs were regular and spherical, with dimension of approximately 122, 131, 136, and 140 nm, respectively. The synthetic nanoparticles possessed good dispersity, stability,solubility, and biocompatibility. No obvious toxic side effects were observed, and the loading rate of TMZ was approximately 50%.In vitro research indicated that the inhibition ratio of the Pep-1@PDA-TMZ NPs combined with 808 nm laser was approximately 94% for U87 cells and in vivo research was approximately 77.13%, which was higher than the ratio of the other groups (p < 0.05).Conclusion: Pep-1 was conjugated and modified to PDA-TMZ NPs, which can serve as a new targeted drug nano-delivery system and can offer a CT and PTT integration therapy against GBM. Thus, Pep-1@PDA-TMZ NPs could be a feasible approach for efficient GBM therapy, and further provide some evidence and data for clinical transformation so that gradually conquer GBM.

show abstract

Section: Discussionmentioning

confidence: 94%

Polydopamine-based loaded temozolomide nanoparticles conjugated by peptide-1 for glioblastoma chemotherapy and photothermal therapy

Zhang²,

Liu³

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…injected. The valid concentration of Tat-PIM2 (2 mg/kg) was decided following our previous studies [ 33 , 35 ]. After 12 h, the mice brain was sectioned and stained using an immunohistochemical method as previously described [ 33 , 35 ].…”

Section: Methodsmentioning

confidence: 99%

“…Protein transduction domains (PTDs) facilitate the transduction of proteins into cells as well as various tissues including the brain [ [27] , [28] , [29] ] and we previously demonstrated that several PTD fusion proteins penetrated into cells and brain tissues passing through the BBB and showed inhibition of apoptosis [ [30] , [31] , [32] , [33] ]. Therefore, cell permeable Tat-PIM2 was prepared and investigated the protective effects of this fusion protein against MPP + - and MPTP-induced oxidative damage in dopaminergic neurons using in vitro and in vivo PD models.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of cell permeable Tat-PIM2 protein on oxidative stress induced dopaminergic neuronal cell death

Shin

Eum

Youn

et al. 2023

Heliyon

Self Cite

View full text Add to dashboard Cite

“…Thereafter, the entire brain was frozen and sectioned with a cryostat into 30 lm sections and consecutive sections were placed in six-well plates-containing PBS. Every sixth section in the series throughout the entire substantia nigra (SN) from selected animals was used for the immunohistochemistry and double immunofluorescence staining as previous studies [67,68].…”

Section: Immunohistochemistrymentioning

confidence: 99%

Protective effect of GK2 fused BLVRA protein against oxidative stress‐induced dopaminergic neuronal cell damage

et al. 2023

Self Cite

View full text Add to dashboard Cite

It is well known that oxidative stress is highly associated with Parkinson's disease (PD), and biliverdin reductase A (BLVRA) is known to have antioxidant properties against oxidative stress. In this study, we developed a novel N-acetylgalactosamine kinase (GK2) protein transduction domain (PTD) derived from adenosine A2A and fused with BLVRA to determine whether the GK2-BLVRA fusion protein could protect dopaminergic neuronal cells (SH-SY5Y) from oxidative stress in vitro and in vivo using a PD animal model. GK2-BLVRA was transduced into various cells, including SH-SY5Y cells, without cytotoxic effects, and this fusion protein protected SH-SY5Y cells and reduced reactive oxygen species production and DNA damage after 1-methyl-4-phenylpyridinium (MPP + ) exposure. GK2-BLVRA suppressed mitogen-activated protein kinase (MAPK) activation and modulated apoptosis-related protein (Bcl-2, Bax, cleaved Caspase-3 and -9) expression levels. In the PD animal model, GK2-BLVRA transduced into the substantia nigra crossed the blood-brain barrier and markedly reduced dopaminergic neuronal cell death in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced animals. These results indicate that our novel PTD GK-2 is useful for the transduction of protein, and GK2-BLVRA exhibits a beneficial effect against dopaminergic neuronal cell death in vitro and in vivo, suggesting that BLVRA can be used as a therapeutic agent for PD.

show abstract

PEP-1-GLRX1 Reduces Dopaminergic Neuronal Cell Loss by Modulating MAPK and Apoptosis Signaling in Parkinson’s Disease

Cited by 7 publications

References 66 publications

Polydopamine-based loaded temozolomide nanoparticles conjugated by peptide-1 for glioblastoma chemotherapy and photothermal therapy

Polydopamine-based loaded temozolomide nanoparticles conjugated by peptide-1 for glioblastoma chemotherapy and photothermal therapy

Protective effects of cell permeable Tat-PIM2 protein on oxidative stress induced dopaminergic neuronal cell death

Protective effect of GK2 fused BLVRA protein against oxidative stress‐induced dopaminergic neuronal cell damage

Contact Info

Product

Resources

About