M
Mitra Kooshki
Researcher at Wake Forest University
Publications - 25
Citations - 745
Mitra Kooshki is an academic researcher from Wake Forest University. The author has contributed to research in topics: Medicine & Hippocampal formation. The author has an hindex of 14, co-authored 20 publications receiving 664 citations. Previous affiliations of Mitra Kooshki include Wake Forest Baptist Medical Center.
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PPARα ligands inhibit radiation-induced microglial inflammatory responses by negatively regulating NF-κB and AP-1 pathways
TL;DR: Pretreatment with peroxisomal proliferator-activated receptor (PPAR)alpha agonists is hypothesized to ameliorate the proinflammatory responses seen in the microglia following in vitro radiation, and data support the hypothesis that activation of PPARalpha can modulate the radiation-induced microglial proinflammatory response.
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THE PPARα AGONIST FENOFIBRATE PRESERVES HIPPOCAMPAL NEUROGENESIS AND INHIBITS MICROGLIAL ACTIVATION AFTER WHOLE-BRAIN IRRADIATION
TL;DR: A novel role for PPARalpha ligands in improving neurogenesis after WBI is highlighted and the promise of improving the quality of life for brain cancer patients receiving radiotherapy is offered.
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Chronic Administration of the Angiotensin-Converting Enzyme Inhibitor, Ramipril, Prevents Fractionated Whole-Brain Irradiation-Induced Perirhinal Cortex-Dependent Cognitive Impairment
Tammy C. Lee,Dana Greene-Schloesser,Valerie Payne,Debra I. Diz,Fang-Chi Hsu,Mitra Kooshki,Rashida Mustafa,David R. Riddle,Weiling Zhao,Michael D. Chan,Mike E. Robbins +10 more
TL;DR: Continuous administration of ramipril before, during, and after irradiation prevented the fractionated whole-brain irradiation-induced changes in perirhinal cortex-dependent cognitive function, as well as in microglial activation in the dentate gyrus.
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PPARδ prevents radiation-induced proinflammatory responses in microglia via transrepression of NF-κB and inhibition of the PKCα/MEK1/2/ERK1/2/AP-1 pathway.
TL;DR: The hypothesis that PPARδ activation can modulate radiation-induced oxidative stress and inflammatory responses in microglia is supported.
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Decreasing peroxiredoxin II expression decreases glutathione, alters cell cycle distribution, and sensitizes glioma cells to ionizing radiation and H2O2
Pameeka S. Smith-Pearson,Mitra Kooshki,Douglas R. Spitz,Leslie B. Poole,Weiling Zhao,Mike E. Robbins +5 more
TL;DR: It is shown that rat and human glioma cells overexpress the antioxidant enzyme peroxiredoxin II (Prx II), which supports the hypothesis that inhibiting Prx II sensitizes gliomas cells to oxidative stress, presenting Prxs as potential therapeutic targets.