Tat-HSP70 protects neurons from oxidative damage in the NSC34 cells and ischemic damage in the ventral horn of rabbit spinal cord

Kim, Woosuk; Kwon, Hyun Jung; Jung, Hyo Young; Yoo, Doo-Yeol; Moon, Sung–Hoon; Kim, Dae Won; Hwang, In Koo

doi:10.1016/j.neuint.2019.104477

Cited by 13 publications

(12 citation statements)

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“…Oxidative stress in NSC34 cells was induced by treatment with 1 mM H 2 O 2 , and the neuroprotective effects of Tat-PGAM1 and Control-PGAM1 were assessed using WST-1 and TUNEL assays, as described in a previous study [ 49 ]. Briefly, various concentrations (0.5–5.0 µM) or 3.0 µM of Tat-PGAM1 and Control-PGAM1 were added to NSC34 cells for 60 min, followed by 1 mM H 2 O 2 , and then incubated for 3 h or 5 h for TUNEL and WST-1 assays, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…The intracellular ROS levels were visualized by monitoring the DCF formation from DCF-DA as described previously [ 8 , 49 ]. Briefly, 3.0 µM of Tat-PGAM1 and Control-PGAM1 were added to NSC34 cells for 60 min, followed by 1 mM H 2 O 2 , and then incubated for 10 min.…”

Section: Methodsmentioning

confidence: 99%

“…In addition, the mean arterial pressure (MAP) was measured from the coccygeal artery. The neurological status was evaluated based on the Tarlov criteria [ 51 ] 24 and 72 h after reperfusion as described in previous studies [ 8 , 49 ], because postural abnormalities were found 12–24 h after ischemia; complete paraplegia was seen 48 h after ischemia [ 52 , 53 ].…”

Section: Methodsmentioning

confidence: 99%

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Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

Jung

Kwon

Kim

et al. 2020

IJMS

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Phosphoglycerate mutase 1 (PGAM1) is a glycolytic enzyme that increases glycolytic flux in the brain. In the present study, we examined the effects of PGAM1 in conditions of oxidative stress and ischemic damage in motor neuron-like (NSC34) cells and the rabbit spinal cord. A Tat-PGAM1 fusion protein was prepared to allow easy crossing of the blood-brain barrier, and Control-PGAM1 was synthesized without the Tat peptide protein transduction domain. Intracellular delivery of Tat-PGAM1, not Control-PGAM1, was achieved in a time- and concentration-dependent manner. Immunofluorescent staining confirmed the intracellular expression of Tat-PGAM1 in NSC34 cells. Tat-PGAM1, but not Control-PGAM1, significantly alleviated H2O2-induced oxidative stress, neuronal death, mitogen-activated protein kinase, and apoptosis-inducing factor expression in NSC34 cells. After ischemia induction in the spinal cord, Tat-PGAM1 treatment significantly improved ischemia-induced neurological impairments and ameliorated neuronal cell death in the ventral horn of the spinal cord 72 h after ischemia. Tat-PGAM1 treatment significantly mitigated the ischemia-induced increase in malondialdehyde and 8-iso-prostaglandin F2α production in the spinal cord. In addition, Tat-PGAM1, but not Control-PGAM1, significantly decreased microglial activation and secretion of pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α induced by ischemia in the ventral horn of the spinal cord. These results suggest that Tat-PGAM1 can be used as a therapeutic agent to reduce spinal cord ischemia-induced neuronal damage by lowering the oxidative stress, microglial activation, and secretion of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

Jung

Kwon

Kim

et al. 2020

IJMS

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“…Male New Zealand white rabbits (1.2–1.5 kg) were purchased from Experimental Animal Center (Cheonan Yonam College, Cheonan, South Korea) and were housed as described in the previous studies [15,21]. The Institutional Animal Care and Use Committee (IACUC) of Seoul National University approved the animal procedures (SNU-160613-18).…”

Section: Methodsmentioning

confidence: 99%

“…Neurological function of animals was assessed by modified Tarlov criteria, as described in previous studies [15,21], with two independent observers for each experiment 24 h and 72 h after reperfusion because the animals showed neurological deficits 12–24 h after reperfusion [22,23].…”

Section: Methodsmentioning

confidence: 99%

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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Potential of oligonucleotide- and protein/peptide-based therapeutics in the management of toxicant/stressor-induced diseases

Sadeghian,

Akbarpour,

Chafjiri

et al. 2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Tat-HSP70 protects neurons from oxidative damage in the NSC34 cells and ischemic damage in the ventral horn of rabbit spinal cord

Cited by 13 publications

References 45 publications

Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

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

Potential of oligonucleotide- and protein/peptide-based therapeutics in the management of toxicant/stressor-induced diseases

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Tat-HSP70 protects neurons from oxidative damage in the NSC34 cells and ischemic damage in the ventral horn of rabbit spinal cord

Cited by 13 publications

References 45 publications

Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

Phosphoglycerate Mutase 1 Prevents Neuronal Death from Ischemic Damage by Reducing Neuroinflammation in the Rabbit Spinal Cord

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

Potential of oligonucleotide- and protein/peptide-based therapeutics in the management of toxicant/stressor-induced diseases

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Product

Resources

About

Tat-HSP70 protects neurons from oxidative damage in the NSC34 cells and ischemic damage in the ventral horn of rabbit spinal cord