Effects of low doses of Tat-PIM2 protein against hippocampal neuronal cell survival

Woo, Su Jung; Shin, Min Jea; Kim, Dae Won; Jo, Hyo Sang; Yong, Ji; Ryu, Eun Ji; Ju, Hyun; Kim, Sang Jin; Yeo, Hyeon Ji; Cho, Su Bin; Park, Jung Hwan; Lee, Chi Hern; Yeo, Eun Ji; Choi, Yeon Joo; Park, Sung‐Yeon; Im, Seung Kwon; Kim, Duk‐Soo; Kwon, Oh Nam; Park, Jinseu; Eum, Won Sik; Choi, Soo Young

doi:10.1016/j.jns.2015.08.1549

Cited by 8 publications

(6 citation statements)

References 56 publications

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“…Also, GSTpi protein provided protection against dopaminergic neuronal cell death in MPTP-induced PD mouse models (41 , 42) . In previous studies, we have demonstrated that the PTD fused therapeutic protein crossed the BBB and significantly inhibited against ischemic injury (24 - 26) .…”

Section: Resultsmentioning

confidence: 98%

“…However, many studies have shown that therapeutic proteins transduce into the cells and provide protective effects against various diseases using protein transduction domains (PTDs) or cell-penetrating peptides (CPPs) as delivery systems (20 - 23) . Our previous studies have demonstrated that PTD fused proteins transduce into cells or tissues and significantly increase the cell survival against oxidative stress-induced neuronal cell death, as well as attenuate Parkinson’s disease and ischemic injury in an animal model (24 - 26) .…”

Section: Introductionmentioning

confidence: 99%

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PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage

et al. 2016

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Reactive oxygen species generated under oxidative stress are involved in neuronal diseases, including ischemia. Glutathione S-transferase pi (GSTpi) is a member of the GST family and is known to play important roles in cell survival. We investigated the effect of GSTpi against oxidative stress-induced hippocampal HT-22 cell death, and its effects in an animal model of ischemic injury, using a cell-permeable PEP-1-GSTpi protein. PEP-1-GSTpi was transduced into HT-22 cells and significantly protected against H2O2-treated cell death by reducing the intracellular toxicity and regulating the signal pathways, including MAPK, Akt, Bax, and Bcl-2. PEP-1-GSTpi transduced into the hippocampus in animal brains, and markedly protected against neuronal cell death in an ischemic injury animal model. These results indicate that PEP-1-GSTpi acts as a regulator or an antioxidant to protect against oxidative stress-induced cell death. Our study suggests that PEP-1-GSTpi may have potential as a therapeutic agent for the treatment of ischemia and a variety of oxidative stress-related neuronal diseases. [BMB Reports 2016; 49(7): 382-387]

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Section: Resultsmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage

et al. 2016

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“…In a previous study, we constructed recombinant PIM2 protein using Tat-peptide [ 34 ]. The purified Tat-PIM2 and control PIM2 were identified using SDS-PAGE and Western blotting ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…All other reagents used were of guaranteed or analytical grade. Tat-PIM2 protein purified as previously described [ 34 ].…”

Section: Methodsmentioning

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

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“…Moreover, low doses of PIM2 protein have been demonstrated to have a protective effect on oxidative stress-induced neuronal cell death ( 17 ), and PIM2 expression is significantly upregulated in lipopolysaccharide (LPS)-induced mouse macrophages ( 18 ). Knockdown of PIM2 causes a marked reduction in the expression of IL-1β and NLR family pyrin domain-containing 3 (NLRP3) inflammasome in LPS-induced macrophages, thereby alleviating LPS-induced ARDS ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Role of PIM2 in acute lung injury induced by sepsis

et al. 2022

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Pediatric sepsis can cause lung damage leading to death in children. In addition, its complicated pathogenesis currently presents a difficult problem in the medical field. Proviral integrations of Moloney virus 2 (PIM2) is a prognostic marker of pediatric sepsis; therefore, the aim of the present study was to investigate the role of PIM2 in lung injury caused by pediatric sepsis. To meet this aim, the expression of PIM2 in lipopolysaccharide (LPS)-induced BEAS-2B pulmonary epithelial cells was detected using reverse transcription-quantitative (RT-q)PCR and western blotting. Subsequently, the expression of PIM2 was inhibited using the cell transfection technique. Cell Counting Kit-8, TUNEL and western blotting, use of a fluorescence kit, ELISA detection kits were used to detect the expression of inflammatory-and cell injury-associated indicators following PIM2 inhibition. In addition, the expression of proteins known to be associated with the Toll-like receptor 2 (TLR2)/myeloid differentiation primary response 88 (MyD88) pathway were also assessed using western blotting. Finally, the simultaneous inhibition of PIM2 expression and overexpression of TLR2 were investigated in an attempt to elucidate the underlying mechanism. The expression level of PIM2 was revealed to be increased in LPS-induced BEAS-2B cells. Interference with PIM2 expression led to an increase in BEAS-2B cell viability, the inhibition of apoptosis and a reduction in oxidative stress and the inflammatory response. These processes were also revealed to be accomplished via downregulation of the TLR2/MyD88 signaling pathway. Overall, the present study demonstrated that knockdown of PIM2 alleviated LPS-induced bronchial epithelial cell injury by inhibiting the TLR2/MyD88 pathway.

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Effects of low doses of Tat-PIM2 protein against hippocampal neuronal cell survival

Cited by 8 publications

References 56 publications

PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage

PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage

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

Role of PIM2 in acute lung injury induced by sepsis

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