M
Mei-Jie Jou
Researcher at Chang Gung University
Publications - 24
Citations - 2154
Mei-Jie Jou is an academic researcher from Chang Gung University. The author has contributed to research in topics: Mitochondrion & Mitochondrial permeability transition pore. The author has an hindex of 19, co-authored 24 publications receiving 1953 citations.
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Journal ArticleDOI
Oxidative stress caused by mitochondrial calcium overload
Tsung-I Peng,Mei-Jie Jou +1 more
TL;DR: The reciprocal interactions between Ca2+ induced ROS increase and ROS modulatedCa2+ upsurge may cause a feedforward, self‐amplified loop createing cellular damage far beyond direct Ca2- induced damage.
Journal ArticleDOI
Visualization of the antioxidative effects of melatonin at the mitochondrial level during oxidative stress-induced apoptosis of rat brain astrocytes
TL;DR: The powerful mitochondrial protection provided by melatonin reinforces its therapeutic potential to combat a variety of oxidative stress‐induced mitochondrial dysfunctions as well as mitochondria‐mediated apoptosis in various diseases.
Journal ArticleDOI
Melatonin protects against common deletion of mitochondrial DNA-augmented mitochondrial oxidative stress and apoptosis.
Mei-Jie Jou,Tsung I. Peng,Pai Zu Yu,Shuo Bin Jou,Russel J. Reiter,Jin Yi Chen,Hong Yueh Wu,Chih Chun Chen,Lee Fen Hsu +8 more
TL;DR: Melatonin significantly prevents CD‐augmented mROS formation under basal conditions as well as at early time‐points upon secondary oxidative stress induced by H2O2 exposure, and may serve as a therapeutic drug to benefit many clinical conditions that involve malfunction of the mitochondria.
Journal ArticleDOI
Visualization of melatonin’s multiple mitochondrial levels of protection against mitochondrial Ca2+-mediated permeability transition and beyond in rat brain astrocytes
Mei-Jie Jou,Tsung I. Peng,Lee Fen Hsu,Shuo Bin Jou,Russel J. Reiter,Chuen Mao Yang,Chuan Chin Chiao,Yi Fan Lin,Chun Chia Chen +8 more
TL;DR: These multiple mitochondrial layers of protection provided by melatonin against mCa2+‐and/or mROS‐mediated apoptosis in astrocytes may be crucial for future therapeutic prevention and treatment of astroCyte‐mediated neurodegenerative diseases in the CNS.
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Involvement of p42/p44 MAPK, p38 MAPK, JNK and nuclear factor-kappa B in interleukin-1beta-induced matrix metalloproteinase-9 expression in rat brain astrocytes.
TL;DR: Results suggest that in RBA‐1 cells, activation of p42/p44 MAPK, p38, JNK and NF‐κB pathways is essential for IL‐1β‐induced MMP‐9 gene expression via transcription and translation processes.