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Barbara Miller

As seen in: Cell Reports, Cell Press, Cell Reports Medicine
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Articles

TRPM2 overactivation drives hyperlipidemia-induced dysfunction of myeloid cells and neurovascular units

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By Pengyu Zong, Cindy Li, Jianlin Feng, Zhichao Yue, Nicholas Legere, Albert Yu, Fahad Shah, Adrianna Perez, Zhu Li, Evan R. Jellison, Yasuo Mori, Barbara Miller, Rajkumar Verma, Bruce T. Liang, Lixia Yue
| Cell Reports Medicine Verified
Keywords TRPM2 hyperlipidemia oxLDL stroke myeloid cell activation endothelial dysfunction blood-brain-barrier damage BBB Introduction Hyperlipidemia is a prevalent condition affecting over 50%–70% of adults in the developed countries, with a significant proportion of patients having a poor management of their elevated blood lipid levels.1,2,3 This condition is strongly associated with many diseases, particularly myocardial infarction and ischemic stroke,4 the leading causes of disability and...
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TRPM2 enhances ischemic excitotoxicity by associating with PKCγ

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By Nicholas Legere, Cindy Li, Barbara Miller
| Cell Reports Verified
Highlights • TRPM2’s PBM directly binds to PKCγ’s C2 domain • TRPM2-PKCγ binding promotes the activation of each other • TRPM2-PKCγ coupling enhances ischemic excitotoxicity • Uncoupling TRPM2-PKCγ interaction by TAT-M2PMB mitigates ischemic brain injury Summary N-methyl-D-aspartate receptor (NMDAR)-mediated glutamate excitotoxicity significantly contributes to ischemic neuronal death and post-recanalization infarction expansion.
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By Pengyu Zong, Jianlin Feng, Yunfeng Li, Zhichao Yue, Yanlin He, Barbara Miller, Albert Yu, Jia Xie, Yasuo Mori, Zhichao Yue, Gongxiong Wu, Baonan Sun, Zhongping Su, Lixia Yue
| Cell Press Verified
Alim I. Teves L. Li R. Mori Y. Tymianski M. Modulation of NMDAR subunit expression by TRPM2 channels regulates neuronal vulnerability to ischemic cell death. J. Neurosci. 2013; 33: 17264-17277https://doi.org/10.1523/JNEUROSCI.1729-13.2013 Bading H. Nuclear calcium signalling in the regulation of brain function. Nat. Rev. Neurosci. 2013; 14: 593-608https://doi.org/10.1038/nrn3531 Bayer K.U. De Koninck P. Leonard A.S. Hell J.W. Schulman H.
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