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Graduate Institute of Biomedical Sciences

:::

周美智

 

 

Mei-Jie Jou

AppointmentsAssociate Professor

LabMitochondrial Laboratory

EducationPh.D.

School/NationUniversity of Rochester, USA

Tel: (03)2118800 ext.5974(lab),5251(office)

E-mail: mjjou@mail.cgu.edu.tw

Research website: https://meijiejou.wixsite.com/mysite

研究室現有: 博士後研究員 0

博士班研究生 0

碩士班研究生 1

專任研究助理  2

大學部專題生 1

 

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:
a. to study how mitochondria arbitrate or regulate apoptosis via mechanisms of mitochondrial ROS and NO formation, mitochondrial calcium homeostasis, mitochondrial membrane potential regulation and modulationof the opening of the mitochondrial permeability transition pore
b. to study the pathological mechanisms involved in mitochondrial DNA defect induced mitochondrial dysfunction and apoptosis. Several mtDNA mutant cybrids provided from worldwide collaborators are used for study. Potential therapeutic strategies including photodynamic therapy and gene therapy are currently under investigation with a long term goal of clinical treatment of mitochondrial diseases.
c. to study the mechanistic role of mitochondria in light-induced phototoxicity and photodynamic effect using new generation of photosensitizers and nano-particles
 
d. 1) to study mitochondria-targeted biomedical application of nano particles
  2) to study the mitochondrial mechanisms involved in the SARS peptides induced apoptosis

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)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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