周美智
Mei-Jie Jou |
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Appointments:Associate Professor |
Lab:Mitochondrial Laboratory |
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Education:Ph.D. |
School/Nation:University of Rochester, USA |
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Tel: (03)2118800 ext.5974(lab),5251(office) |
E-mail: mjjou@mail.cgu.edu.tw |
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Research website: https://meijiejou.wixsite.com/mysite |
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研究室現有: 博士後研究員 0人 |
博士班研究生 0 人 |
碩士班研究生 1人 |
專任研究助理 2人 |
大學部專題生 1 人 |
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Research outline:(1-3 pages) My lab is focused on investigating the pathophysiological mechanisms involved in mitochondria-mediated apoptosis. Fluorescence digital imaging microscopy is the basic and major technology used in this lab including conventional fluorescence digital imaging microscopy, laser scanning confocal microscopy and multi-photon imaging microscopy. Several focused on-going projects are: |
Publications: 1. Hsiao C-W, Peng T-I, Jou M-J*. (2016) mtDNA T8993G (NARP) mutation augments mCa2+-mediated mROS dependent cardiolipin depletion for lethal transient mitochondrial permeability transition: implications for pathogenesis and treatment of NARP. (in preparation) 2. Yang C-M, Yang S-H, Lee T-H, Fang J-Y, Lin C-F, Jou M-J, Hsieh H-L*. (2016) Evaluation of Anti-Inflammatory Effects of Helminthostachys zeylanica Extracts via Inhibiting Bradykinin-Induced MMP-9 Expression in Brain Astrocytes. Mol Neurobiol. (published online) (SCI,排名32/256=12.5 % (NEUROSCIENCES) ; impact factor: 5.397) 3. Huang W-I, Jou M-J, Peng T-I*.(2014) Hypoxic preconditioning-induced mitochondrial protection is not disrupted in a cell model of mtDNA T8993G mutation-induced F1F0-ATP synthase defect: the role of mitochondrial permeability transition. Free Radic. Biol. Med.,67:314-329. (SCI,排名:14/133=10.53 % (ENDOCRINOLOGY & METABOLISM) ; impact factor: 5.784) 4. Huang W-I, Jou M-J, Peng T-I*.(2013) mtDNA T8993G Mutation-Induced F1F0-ATP Synthase Defect Augments Mitochondrial Dysfunction Associated with hypoxia/reoxygenation: The Protective Role of Melatonin. PLoS One.,8(11) (published online) (SCI,排名: 11/63=17.46% (MULTIDISCIPLINARY SCIENCES ); impact factor: 3.057) 5. Peng T-I, Lin M-S*, Jou M-J*. (2013) Dual phases of respiration chain defect-augmented mROS-mediated mCa2+ stress during oxidative insult in normal and ρ0 RBA1 astrocytes. Oxidative Med. Cell. Longev. (published online) (SCI, 排名: 53/187=28.34% (CELL BIOLOGY ); impact factor:4.492) 6. Hsiao C-W, Peng T-I, Peng AC., Reiter RJ, Tanaka M, Lai Y-K and Jou M-J*. (2013) Long-term Aβ exposure augments mCa2+-independent mROS-mediated depletion of cardiolipin for the shift of a lethal transient mitochondrial permeability transition to its permanent mode in NARP cybrids: a protective targeting of melatonin. J. Pineal Res.,54:107-125. (SCI,排名: 3/83=3.61% (PHYSIOLOGY); impact factor: 9.314) 7. Yang C-M*, Tung W-H, Lin Y-H, Chen W-J, Jou M-J, Hsiao L-D. (2012) Japanese encephalitis virus induces matrix metalloproteinase-9 expression via ROS/c-Src/PDGFR/PI3K/Akt/MAPKs- dependent AP-1 pathway in rat brain astrocytes. J. Neuroinflamm.,9(1):12 (SCI,排名: 50/256=19.53% (NEUROSCIENCES); impact factor: 4.667) 8. Peng T-I, Hsiao C-W, Reiter RJ, Tanaka M, Lai Y-K and Jou M-J*. (2012) mtDNA T8993G mutation-induced mitochondrial complex V inhibition augments cardiolipin-dependent alterations in mitochondrial dynamics during oxidative, Ca2+ and lipid insults in NARP cybrids: a potential therapeutic target for melatonin. J. Pineal Res.,52(1):93-106. (SCI,排名: 3/83=3.61% (PHYSIOLOGY); impact factor: 9.314) 9. Jou M-J*. (2011) Melatonin preserves the transient mitochondrial permeability transition for protection during mitochondrial Ca2+ stress in astrocyte. J. Pineal Res., 50(4):427-435. (SCI,排名: 3/83=3.61% (PHYSIOLOGY); impact factor: 9.314)