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周美智

 

周美智( Mei-Jie Jou

職稱副教授

研究室名稱粒線體研究室

最高學歷Ph.D.

學校/國家羅徹斯特大學/美國

分機號碼03-2118800#5974(lab),5251(office)

電子郵件帳號 mjjou@mail.cgu.edu.tw

個人網頁網址: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

 

研究方向研究室特色

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

我的實驗室目前主要致力於研究粒線體功能的調節與病變機轉,以及粒線體掌控的細胞凋亡。研究特色乃專注於利用傳統影相系統、單光子共軛焦及多光子雷射掃描顯微影相系統來進行單一活細胞內粒線體之動態觀察與研究。目前執行的研究如下: 
a. 
探究粒線體在細胞凋亡過程的仲裁角色,包括粒線體運動、粒線體高活性氧族及一氧化氮的生成、粒線體鈣離子的平衡、粒線體膜電位的調節以及在細胞凋亡過程中粒線體過度性通透孔通道的開關。
b. 
探究粒線體在光照、光觸媒及光照動力學作用下引起的毒性中所扮演的角色,並探討新一代的光敏感劑的毒性與臨床應用。
c. 
探究粒線體DNA突變及斷損所造成的粒線體功能病變以及細胞凋亡的病理機轉。特殊粒線體DNA突變及斷損的融合細胞株乃是由世界各地的研究合作者所提供。治療方向目前著重在臨床上對於點突變引起之粒線體疾病頗具治療潛力的基因療法。
d. 
整合型計劃在於1)探究新一代的奈米半導體及奈米粒子包括奈米光粒子、奈米碳粒子及奈米磁粒子等對細胞及粒線體功能影響與臨床應用2)探究有關於粒線體在SARS蛋白引起的細胞凋亡中的作用機轉。

 

 

最近五年所發表論文:

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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