Publications

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2016
Kim, D. I., K. H. Lee, A. A. Gabr, G. E. Choi, J. S. Kim, S. H. Ko, and H. J. Han, "A$\beta$-Induced Drp1 phosphorylation through Akt activation promotes excessive mitochondrial fission leading to neuronal apoptosis", Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, vol. 1863, no. 11: Elsevier, pp. 2820–2834, 2016. Abstract
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Kim, D. I., K. H. Lee, A. A. Gabr, G. E. Choi, J. S. Kim, S. H. Ko, and H. J. Han, "A$\beta$-Induced Drp1 phosphorylation through Akt activation promotes excessive mitochondrial fission leading to neuronal apoptosis", Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, vol. 1863, no. 11: Elsevier, pp. 2820–2834, 2016. Abstract
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2017
Lee, K. H., S. -jung Lee, H. J. Lee, G. E. Choi, Y. H. Jung, D. I. Kim, A. A. Gabr, J. M. Ryu, and H. J. Han, "Amyloid $\beta$1-42 (A$\beta$1-42) induces the CDK2-mediated phosphorylation of tau through the activation of the mTORC1 signaling pathway while promoting neuronal cell death", Frontiers in molecular neuroscience, vol. 10: Frontiers Media SA, pp. 229, 2017. Abstract
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Onphachanh, X., H. J. Lee, J. R. Lim, Y. H. Jung, J. S. Kim, C. W. Chae, S. -jung Lee, A. A. Gabr, and H. J. Han, "Enhancement of high glucose-induced PINK1 expression by melatonin stimulates neuronal cell survival: Involvement of MT2/Akt/NF-$ąppa$B pathway", Journal of pineal research, 2017. Abstract
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Onphachanh, X., H. J. Lee, J. R. Lim, Y. H. Jung, J. S. Kim, C. W. Chae, S. -jung Lee, A. A. Gabr, and H. J. Han, "Enhancement of high glucose-induced PINK1 expression by melatonin stimulates neuronal cell survival: Involvement of MT2/Akt/NF-$ąppa$B pathway", Journal of Pineal Research, vol. 63, no. 2, pp. e12427, 2017. Abstract
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Gabr, A. A., H. J. Lee, X. Onphachanh, Y. H. Jung, J. S. Kim, C. W. Chae, and H. J. Han, "Ethanol-induced PGE2 up-regulates A$\beta$ production through PKA/CREB signaling pathway", Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, vol. 1863, no. 11: Elsevier, pp. 2942–2953, 2017. Abstract
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Lee, K. H., S. -jung Lee, H. J. Lee, G. E. Choi, Y. H. Jung, D. I. Kim, A. A. Gabr, J. M. Ryu, and H. J. Han, "Amyloid β1-42 (Aβ1-42) Induces the CDK2-Mediated Phosphorylation of Tau through the Activation of the mTORC1 Signaling Pathway While Promoting Neuronal Cell Death.", Frontiers in molecular neuroscience, vol. 10, pp. 229, 2017. Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, characterized by cognitive impairment and memory loss. Amyloid β1-42 (Aβ) and hyper-phosphorylation of microtubule-associated protein tau have been considered as major histological features in AD. However, the mechanism of how Aβ induces the hyper-phosphorylation of tau remains to be clarified. In the present study, we investigated the underlying cellular mechanisms of Aβ with regard to the cell cycle regulatory protein-mediated phosphorylation of tau in promoting neuronal cell death. The oligomer Aβ (5 μM) significantly increased the level of caspase 3 cleavage and has the ability to induce cytotoxicity in human neuroblastoma SK-N-MC cells. Aβ induced the degree of extracellular calcium influx via the L-type channel to facilitate the production of reactive oxygen species (ROS). Aβ signaling through ROS production is uniquely mediated by the activation of PI3K/Akt, which is in turn required for mammalian target of rapamycin complex 1 (mTORC1) phosphorylation. mTORC1 activated by Aβ further increased the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E), a binding protein (4E-BP1) and p70S6K1 to stimulate the HIF1α synthesis responsible for the induction of cyclinD/cyclin-dependent kinase 4 (CDK4) and cyclinE/CDK2, whereas it significantly attenuated the activation of autophagy. Aβ distinctively induced the CDK2-mediated phosphorylation of tau, which is responsible for microtubule destabilization in promoting neuronal apoptosis. In mouse hippocampal primary neurons, the apoptotic cell death induced by Aβ is highly susceptible to the mTORC1 signaling pathway. These results demonstrate that Aβ efficiently stimulates the mTORC1 signaling pathway to facilitate HIF1α synthesis and autophagy inhibition to promote the expression of cell cycle regulatory proteins, during which CDK2 uniquely stimulates tau phosphorylation for microtubule destabilization-mediated neuronal apoptosis.

Gabr, A. A., H. J. Lee, X. Onphachanh, Y. H. Jung, J. S. Kim, C. W. Chae, and H. J. Han, "Ethanol-induced PGEup-regulates Aβ production through PKA/CREB signaling pathway.", Biochimica et biophysica acta, vol. 1863, issue 11, pp. 2942-2953, 2017 Nov. Abstract

Ethanol abuse aggravates dementia-associated cognitive defects through the progression of Alzheimer's disease (AD) pathophysiology. Beta-site APP-cleaving enzyme 1 (BACE1) has been considered as a key regulator of AD pathogenesis by controlling amyloid beta peptide (Aβ) accumulation. In addition, previous studies reported that endoplasmic reticulum (ER) stress and neuroinflammation have been proposed in ethanol-induced neurodegeneration. Thus, we investigated the role of ER stress and PGE, a neuroinflammation mediator, in the ethanol-stimulated BACE1 expression and Aβ production. Using the human-derived neuroblastoma cell line SK-N-MC, the results show that ethanol up-regulated BACE1 expression in a dose-dependent manner. Ethanol stimulated reactive oxygen species (ROS) production, which induced CHOP expression and eIF2α phosphorylation. PBA (an ER stress inhibitor) attenuated the ethanol-increased cyclooxygenase-2 (COX-2) expression and PGEproduction. By using salubrinal (an eIF2α dephosphorylation inhibitor) or EIF2A siRNA, we found that eIF2α phosphorylation mediated the ethanol-induced COX-2 expression. In addition, COX-2-induced BACE1 up-regulation was abolished by NS-398 (a selective COX-2 inhibitor). And, PF-04418948 (an EP-2 receptor inhibitor) pretreatment reduced ethanol-induced PKA activation and CREB phosphorylation as well as ethanol-stimulated Aβ production. Furthermore, 14-22 amide (a PKA inhibitor) pretreatment or CREB1 siRNA transfection suppressed the ethanol-induced BACE1 expression. In conclusion, ethanol-induced eIF2α phosphorylation stimulates COX-2 expression and PGEproduction which induces the BACE1 expression and Aβ production via EP-2 receptor-dependent PKA/CREB pathway.

2020
Abd El-Hack, M. E., S. S. Elnesr, M. Alagawany, A. Gado, A. E. Noreldin, and A. A. Gabr, "Impact of green tea (Camellia sinensis) and epigallocatechin gallate on poultry", World's Poultry Science Journal, vol. 76, no. 1: Taylor & Francis, pp. 49–63, 2020. Abstract
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Abd El-Hack, M. E., S. S. Elnesr, M. Alagawany, A. Gado, A. E. Noreldin, and A. A. Gabr, "Impact of green tea (Camellia sinensis) and epigallocatechin gallate on poultry", World's Poultry Science Journal, vol. 76, no. 1: Taylor & Francis, pp. 49–63, 2020. Abstract
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Abd El-Hack, M. E., S. S. Elnesr, M. Alagawany, A. Gado, A. E. Noreldin, and A. A. Gabr, "世界家禽学会誌 (WPSJ) の紹介 家禽用飼料資材として緑茶 (Camellia sinensis) およびエピガロカテキンガレート", 日本家禽学会誌, vol. 57, no. 2: 日本家禽学会, pp. J53–55, 2020. Abstract
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2021
Pietrowski, M. J., A. A. Gabr, S. Kozlov, D. Blum, A. Halle, and K. Carvalho, "Glial purinergic signaling in neurodegeneration", Frontiers in neurology, vol. 12: Frontiers Media SA, pp. 654850, 2021. Abstract
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Alagawany, M., S. S. Elnesr, M. R. Farag, M. E. Abd El-Hack, R. A. Barkat, A. A. Gabr, M. A. Foda, A. E. Noreldin, A. F. Khafaga, K. El-Sabrout, et al., "Potential role of important nutraceuticals in poultry performance and health-A comprehensive review", Research in Veterinary Science, vol. 137: WB Saunders, pp. 9–29, 2021. Abstract
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