S
Sheu Ran Choi
Researcher at Seoul National University
Publications - 27
Citations - 631
Sheu Ran Choi is an academic researcher from Seoul National University. The author has contributed to research in topics: Neuropathic pain & Astrocyte. The author has an hindex of 14, co-authored 27 publications receiving 522 citations.
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Journal ArticleDOI
Spinal interleukin-1β inhibits astrocyte cytochrome P450c17 expression which controls the development of mechanical allodynia in a mouse model of neuropathic pain
TL;DR: Investigation of the possible involvement of interleukin-1β in altering P450c17 expression during the induction phase of neuropathic pain implies that spinal IL-1 β plays an important role as an early, but transient, control mechanism in the development of peripheral neuropathicPain via the inhibition of astrocyte P450 c17 expression and astroCyte activation.
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Peripheral neurosteroids enhance P2X receptor-induced mechanical allodynia via a sigma-1 receptor-mediated mechanism
Soon Gu Kwon,Seo Yeon Yoon,Dae Hyun Roh,Sheu Ran Choi,Hoon Seong Choi,Jiyoung Moon,Suk Yun Kang,Alvin J. Beitz,Jang Hern Lee +8 more
TL;DR: It is shown that peripheral neurosteroids potentiate P2X-induced mechanical allodynia and that this action is mediated by sigma-1, but not by GABAA nor NMDA, receptors.
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Spinal Sigma-1 Receptor-mediated Dephosphorylation of Astrocytic Aromatase Plays a Key Role in Formalin-induced Inflammatory Nociception.
TL;DR: Results suggest that dephosphorylation is an important regulatory mechanism involved in the rapid activation of aromatase and that spinal sigma-1 receptors mediate this deph phosphorylation of arom atase through an intrinsic calcineurin pathway.
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Spinal Nitric Oxide Synthase Type II Increases Neurosteroid-metabolizing Cytochrome P450c17 Expression in a Rodent Model of Neuropathic Pain.
TL;DR: Results provide strong support for the hypothesis that activation of NOS-II increases the mRNA and protein levels of P450c17 in the spinal cord, ultimately leading to the development of central sensitization and neuropathic pain induced by peripheral nerve injury.
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nNOS-PSD95 interactions activate the PKC-ε isoform leading to increased GluN1 phosphorylation and the development of neuropathic mechanical allodynia in mice
TL;DR: Results demonstrate that spinal nNOS-PSD95 interactions play an important role in PKC-dependent GluN1 phosphorylation via activation of thePKC-ε isoform, and ultimately contributes to the development of MA in peripheral neuropathy.