Protein disulfide-isomerase A3 significantly reduces ischemia-induced damage by reducing oxidative and endoplasmic reticulum stress

Yoo, Dae Young; Cho, Su Bin; Jung, Hyo Young; Kim, Woosuk; Lee, Kwon Young; Kim, Jong Whi; Moon, Sung–Hoon; Won, Moo‐Ho; Choi, Jung Hoon; Yoon, Yeo Sung; Kim, Dae Won; Choi, Soo Young; Hwang, In Koo

doi:10.1016/j.neuint.2018.11.002

Cited by 34 publications

(56 citation statements)

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“…In addition, we found the neuroprotective actions of Tat‐PDIA3 and its mechanisms in the gerbil brain ischemia (Yoo et al, ) and rabbit spinal cord ischemia (Yoo et al, ). Especially, administration of PDIA3 protected neurons from hydrogen peroxide‐induced oxidative stress in HT22 cells and ischemic damage in the gerbil hippocampal CA1 region (Yoo et al, ). In addition, Tat‐PDIA3 significantly ameliorated ischemia‐induced changes of UPRs levels after ischemia/reperfusion (Yoo et al, ).…”

Section: Introductionmentioning

confidence: 90%

“…In previous studies, we generated Tat-PDIA3 fusion protein and observed the intracellular delivery of Tat-PDIA3 fusion protein (Yoo et al, 2017(Yoo et al, , 2019 as well as the colocalization of PDIA3 with ER tracker (Yoo et al, 2017). In addition, we found the neuroprotective actions of Tat-PDIA3 and its mechanisms in the gerbil brain ischemia (Yoo et al, 2019) and rabbit spinal cord ischemia (Yoo et and Cell Biology, College of Veterinary Medicine, Seoul National University, Seoul 08826, South Korea. Email: vetmed2@snu.ac.kr al., 2017).…”

Section: Introductionmentioning

confidence: 91%

“…In previous studies, we generated Tat‐PDIA3 fusion protein and observed the intracellular delivery of Tat‐PDIA3 fusion protein (Yoo et al, , ) as well as the colocalization of PDIA3 with ER tracker (Yoo et al, ). In addition, we found the neuroprotective actions of Tat‐PDIA3 and its mechanisms in the gerbil brain ischemia (Yoo et al, ) and rabbit spinal cord ischemia (Yoo et al, ). Especially, administration of PDIA3 protected neurons from hydrogen peroxide‐induced oxidative stress in HT22 cells and ischemic damage in the gerbil hippocampal CA1 region (Yoo et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…Especially, administration of PDIA3 protected neurons from hydrogen peroxide‐induced oxidative stress in HT22 cells and ischemic damage in the gerbil hippocampal CA1 region (Yoo et al, ). In addition, Tat‐PDIA3 significantly ameliorated ischemia‐induced changes of UPRs levels after ischemia/reperfusion (Yoo et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…Human immunodeficiency virus-1 (HIV-1) Tat would be one of best strategy for cellular delivery into central nervous system because they efficiently transport peptide or proteins which have higher molecular weights than their own (Van den Berg & Dowdy, 2011) because the efficient transduction capability has been confirmed using various peptides or proteins against ischemic damage (Jo et al, 2017;Tu et al, 2015;Zhou et al, 2015). In previous studies, we generated Tat-PDIA3 fusion protein and observed the intracellular delivery of Tat-PDIA3 fusion protein (Yoo et al, 2017(Yoo et al, , 2019 as well as the colocalization of PDIA3 with ER tracker (Yoo et al, 2017). In addition, we found the neuroprotective actions of Tat-PDIA3 and its mechanisms in the gerbil brain ischemia (Yoo et al, 2019) and rabbit spinal cord ischemia (Yoo et and Cell Biology, College of Veterinary Medicine, Seoul National University, Seoul 08826, South Korea.…”

Section: Introductionmentioning

confidence: 99%

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Differential roles of exogenous protein disulfide isomerase A3 on proliferating cell and neuroblast numbers in the normal and ischemic gerbils

et al. 2020

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Introduction We examined the effects of exogenous protein disulfide isomerase A3 (PDIA3) on hippocampal neurogenesis in gerbils under control and ischemic damage. Methods To facilitate the delivery of PDIA3 to the brain, we constructed Tat‐PDIA3 protein and administered vehicle (10% glycerol) or Tat‐PDIA3 protein once a day for 28 days. On day 24 of vehicle or Tat‐PDIA3 treatment, ischemia was transiently induced by occlusion of both common carotid arteries for 5 min. Results Administration of Tat‐PDIA3 significantly reduced ischemia‐induced spontaneous motor activity, and the number of NeuN‐positive nuclei in the Tat‐PDIA3‐treated ischemic group was significantly increased in the CA1 region compared to that in the vehicle‐treated ischemic group. Ki67‐ and DCX‐immunoreactive cells were significantly higher in the Tat‐PDIA3‐treated group compared to the vehicle‐treated control group. In vehicle‐ and Tat‐PDIA3‐treated ischemic groups, the number of Ki67‐ and DCX‐immunoreactive cells was significantly higher as compared to those in the vehicle‐ and Tat‐PDIA3‐treated control groups, respectively. In the dentate gyrus, the numbers of Ki67‐immunoreactive cells were comparable between vehicle‐ and Tat‐PDIA3‐treated ischemic groups, while more DCX‐immunoreactive cells were observed in the Tat‐PDIA3‐treated group. Transient forebrain ischemia increased the expression of phosphorylated cAMP‐response element‐binding protein (pCREB) in the dentate gyrus, but the administration of Tat‐PDIA3 robustly increased pCREB‐positive nuclei in the normal gerbils, but not in the ischemic gerbils. Brain‐derived neurotrophic factor (BDNF) mRNA expression was significantly increased in the Tat‐PDIA3‐treated group compared to that in the vehicle‐treated group. Transient forebrain ischemic increased BDNF mRNA levels in both vehicle‐ and Tat‐PDIA3‐treated groups, and there were no significant differences between groups. Conclusions These results suggest that Tat‐PDIA3 enhances cell proliferation and neuroblast numbers in the dentate gyrus in normal, but not in ischemic gerbils, by increasing BDNF mRNA and phosphorylation of pCREB.

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Section: Introductionmentioning

confidence: 90%