Experts and Doctors on brain ischemia in Jiangsu, China

Summary

Locale: Jiangsu, China
Topic: brain ischemia

Top Publications

  1. Chang L, Chen Y, Li J, Liu Z, Wang Z, Chen J, et al. Cocaine-and amphetamine-regulated transcript modulates peripheral immunity and protects against brain injury in experimental stroke. Brain Behav Immun. 2011;25:260-9 pubmed publisher
    ..Findings also suggest that the possible mechanism of CART's protective action in stroke is the regulation of the sympathetic nervous system (SNS) pathway since CAs, Treg cells and interleukin (IL)-10 are the major modulators of SNS. ..
  2. Chen M, Wang Y, Liu Y, Hou X, Zhang Q, Meng F, et al. Possible mechanisms underlying the protective effects of SY-21, an extract of a traditional Chinese herb, on transient brain ischemia/reperfusion-induced neuronal death in rat hippocampus. Brain Res. 2003;989:180-6 pubmed
    ..These results demonstrate that SY-21 has a prominent neuroprotective action against brain ischemic insult, and the mechanism may involve the regulation of the tyrosine phosphorylation of NR2A by changing the above interactions. ..
  3. He J, Zhang Y, Xu T, Zhao Q, Wang D, Chen C, et al. Effects of immediate blood pressure reduction on death and major disability in patients with acute ischemic stroke: the CATIS randomized clinical trial. JAMA. 2014;311:479-89 pubmed publisher
    ..clinicaltrials.gov Identifier: NCT01840072. ..
  4. Tang L, Li C, Hu S, Wu Y, Zong Y, Sun C, et al. S-nitrosylation of c-Src via NMDAR-nNOS module promotes c-Src activation and NR2A phosphorylation in cerebral ischemia/reperfusion. Mol Cell Biochem. 2012;365:363-77 pubmed publisher
  5. Wang R, Zhang Q, Zhang G. Activation of ERK5 is mediated by N-methyl-D-aspartate receptor and L-type voltage-gated calcium channel via Src involving oxidative stress after cerebral ischemia in rat hippocampus. Neurosci Lett. 2004;357:13-6 pubmed
    ..These results suggested that ERK5 could be significantly activated by I/R, which might be mediated by NMDA receptor and L-VGCC through Src kinase pathway involving oxidative stress in rat hippocampus. ..
  6. Tian H, Zhang G, Li H, Zhang Q. Antioxidant NAC and AMPA/KA receptor antagonist DNQX inhibited JNK3 activation following global ischemia in rat hippocampus. Neurosci Res. 2003;46:191-7 pubmed
    ..Ketamine and nifedipine had no significant effects on JNK3 activation during reperfusion. Consequently, reactive oxygen species (ROS) and AMPA/KA receptor were closely associated with JNK3 activation following global ischemia. ..
  7. Xu J, Li C, Yin X, Zhang G. Additive neuroprotection of GABA A and GABA B receptor agonists in cerebral ischemic injury via PI-3K/Akt pathway inhibiting the ASK1-JNK cascade. Neuropharmacology. 2008;54:1029-40 pubmed publisher
    ..Our results indicated that co-activation of GABA A receptor and GABA B receptor exerted neuroprotective effect via PI-3K/Akt pathway, which could inhibit the ASK1-c-Jun N-terminal protein kinase (JNK) cascade. ..
  8. Zhou C, Li C, Yu H, Zhang F, Han D, Zhang G. Neuroprotection of gamma-aminobutyric acid receptor agonists via enhancing neuronal nitric oxide synthase (Ser847) phosphorylation through increased neuronal nitric oxide synthase and PSD95 interaction and inhibited protein phosphatase activity in ce. J Neurosci Res. 2008;86:2973-83 pubmed publisher
    ..Our results suggest that GABA receptor agonists may serve as a potential and important neuroprotectant in therapy for ischemic stroke. ..
  9. Zhang Q, Tian H, Li H, Zhang G. Antioxidant N-acetylcysteine inhibits the activation of JNK3 mediated by the GluR6-PSD95-MLK3 signaling module during cerebral ischemia in rat hippocampus. Neurosci Lett. 2006;408:159-64 pubmed
    ..Taken together, these finding indicate that ischemic stimulation results in JNK3 activation through the GluR6-PSD95-MLK3 signaling module, and that the activation of JNK3 is closely related to oxidative stress. ..

More Information

Publications43

  1. Tian H, Zhang Q, Zhu G, Pei D, Guan Q, Zhang G. Activation of c-Jun NH2-terminal kinase 3 is mediated by the GluR6.PSD-95.MLK3 signaling module following cerebral ischemia in rat hippocampus. Brain Res. 2005;1061:57-66 pubmed
    ..Consequently, GluR6, one subunit of kainate receptor, plays a critical role in inducing JNK3 activation after ischemic injury. ..
  2. Yao R, Qi D, Yu H, Liu J, Yang L, Wu X. Quercetin attenuates cell apoptosis in focal cerebral ischemia rat brain via activation of BDNF-TrkB-PI3K/Akt signaling pathway. Neurochem Res. 2012;37:2777-86 pubmed publisher
    ..These results demonstrate that quercetin can decrease cell apoptosis in the focal cerebral ischemia rat brain and the mechanism may be related to the activation of BDNF-TrkB-PI3K/Akt signaling pathway. ..
  3. Wang Y, Wang Y, Li M, Xu P, Gu T, Ma T, et al. (1)H NMR-based metabolomics exploring biomarkers in rat cerebrospinal fluid after cerebral ischemia/reperfusion. Mol Biosyst. 2013;9:431-9 pubmed publisher
    ..What's more, metabolomics may, therefore, have the potential to be developed into a clinically useful diagnostic tool of ischemic brain injury. ..
  4. Yan X, Song B, Zhang G. Postsynaptic density protein 95 mediates Ca2+/calmodulin-dependent protein kinase II-activated serine phosphorylation of neuronal nitric oxide synthase during brain ischemia in rat hippocampus. Neurosci Lett. 2004;355:197-200 pubmed
    ..These data suggested that PSD95 is important for facilitating nNOS serine phosphorylation by CaMKII. ..
  5. Tian H, Zhang Q, Li H, Zhang G. Antioxidant N-acetylcysteine and AMPA/KA receptor antagonist DNQX inhibited mixed lineage kinase-3 activation following cerebral ischemia in rat hippocampus. Neurosci Res. 2003;47:47-53 pubmed
    ..We think that MLK3 activation is certainly associated with reactive oxygen species (ROS) and AMPA/KA receptor in response to ischemic insult. ..
  6. Yin X, Yan J, Yang G, Chen L, Xu X, Hong X, et al. PDZ1 inhibitor peptide protects neurons against ischemia via inhibiting GluK2-PSD-95-module-mediated Fas signaling pathway. Brain Res. 2016;1637:64-70 pubmed publisher
  7. Wang M, Qi D, Zhou C, Han D, Li P, Zhang F, et al. Ischemic preconditioning protects the brain against injury via inhibiting CaMKII-nNOS signaling pathway. Brain Res. 2016;1634:140-149 pubmed publisher
    ..Taken together, the results suggest that IPC could diminish ischemic brain injury through CaMKII-mediated up-regulation of nNOS ser847-phosphorylation signaling pathway. ..
  8. Hou X, Zhang G, Wang D, Guan Q, Yan J. Suppression of postsynaptic density protein 95 by antisense oligonucleotides diminishes postischemic pyramidal cell death in rat hippocampal CA1 subfield. Neurosci Lett. 2005;385:230-3 pubmed
    ..Our data suggest that the recruitments of ion channels and signaling molecules may be involved in the PSD-95 neurotoxicity in the postischemic hippocampus. ..
  9. Hu S, Ye J, Zong Y, Sun C, Liu D, Wu Y, et al. S-nitrosylation of mixed lineage kinase 3 contributes to its activation after cerebral ischemia. J Biol Chem. 2012;287:2364-77 pubmed publisher
  10. Zhang Q, Han D, Hu S, Li C, Yu C, Wang R, et al. Positive modulation of AMPA receptors prevents downregulation of GluR2 expression and activates the Lyn-ERK1/2-CREB signaling in rat brain ischemia. Hippocampus. 2010;20:65-77 pubmed publisher
    ..Our results revealed that positive modulation of AMPARs could exert neuroprotective effects and the possible signaling pathways underlied. ..
  11. Zhu Q, Xu Y, Du C, Hou X. SUMOylation of the kainate receptor subunit GluK2 contributes to the activation of the MLK3-JNK3 pathway following kainate stimulation. FEBS Lett. 2012;586:1259-64 pubmed publisher
    ..These results suggest that the internalization of GluK2 following SUMO modification promotes its binding with MLK3, thereby activating the MLK3-JNK3 pathway, which may be responsible for ischemic neuronal cell death. ..
  12. Qu Z, Miao W, Hu S, Li C, Zhuo X, Zong Y, et al. N-methyl-D-aspartate receptor-dependent denitrosylation of neuronal nitric oxide synthase increase the enzyme activity. PLoS ONE. 2012;7:e52788 pubmed publisher
    ..nNOS dephosphorylation may be induced by the enzyme denitrosylation, which suggest that S-nitrosylation/denitrosylation of nNOS may be an important mechanism in regulating the enzyme activity. ..
  13. Zhang J, Yan H, Wu Y, Li C, Zhang G. Activation of GluR6-containing kainate receptors induces ubiquitin-dependent Bcl-2 degradation via denitrosylation in the rat hippocampus after kainate treatment. J Biol Chem. 2011;286:7669-80 pubmed publisher
    ..Taken together, our data reveal that Bcl-2 ubiquitin-dependent degradation is induced by Bcl-2 denitrosylation during neuronal apoptosis after KA treatment. ..
  14. Zhang F, Li C, Wang R, Han D, Zhang Q, Zhou C, et al. Activation of GABA receptors attenuates neuronal apoptosis through inhibiting the tyrosine phosphorylation of NR2A by Src after cerebral ischemia and reperfusion. Neuroscience. 2007;150:938-49 pubmed
  15. Meng F, Zhang G. Autophosphorylated calcium/calmodulin-dependent protein kinase II alpha induced by cerebral ischemia immediately targets and phosphorylates N-methyl-D-aspartate receptor subunit 2B (NR2B) in hippocampus of rats. Neurosci Lett. 2002;333:59-63 pubmed
    ..These results suggest that phosphorylation of NR2B can influence the channel properties of NR2B, and the dissociation of the CaMKII alpha-NR2B complexes may be a negative feedback mechanism during longer time cerebral ischemia. ..
  16. Zhang Q, Zhang G. Activation and autophosphorylation of apoptosis signal-regulating kinase 1 (ASK1) following cerebral ischemia in rat hippocampus. Neurosci Lett. 2002;329:232-6 pubmed
  17. Meng F, Guo J, Zhang Q, Song B, Zhang G. Autophosphorylated calcium/calmodulin-dependent protein kinase II alpha (CaMKII alpha) reversibly targets to and phosphorylates N-methyl-D-aspartate receptor subunit 2B (NR2B) in cerebral ischemia and reperfusion in hippocampus of rats. Brain Res. 2003;967:161-9 pubmed
  18. Wu D, Pei D, Wang Q, Zhang G. Down-regulation of PTEN by sodium orthovanadate inhibits ASK1 activation via PI3-K/Akt during cerebral ischemia in rat hippocampus. Neurosci Lett. 2006;404:98-102 pubmed
    ..Taken together, we concluded that sodium orthovanadate could increase the tyrosine posphorylation of PTEN and further inhibit the activation of ASK1 via activating Akt during cerebral ischemia. ..
  19. Hao Z, Pei D, Guan Q, Zhang G. Calcium/calmodulin-dependent protein kinase II (CaMKII), through NMDA receptors and L-Voltage-gated channels, modulates the serine phosphorylation of GluR6 during cerebral ischemia and early reperfusion period in rat hippocampus. Brain Res Mol Brain Res. 2005;140:55-62 pubmed
    ..In conclusion, our results suggest that CaMKII, activated through NMDA receptors and L-VGCCs, mediated the serine phosphorylation of GluR6 during brain ischemia and early reperfusion period. ..
  20. Pan J, Zhang Q, Zhang G. The neuroprotective effects of K252a through inhibiting MLK3/MKK7/JNK3 signaling pathway on ischemic brain injury in rat hippocampal CA1 region. Neuroscience. 2005;131:147-59 pubmed
    ..Thus, JNK signaling may eventually emerge as a prime target for novel therapeutic approaches to treatment of ischemic stroke, and K252a may serve as a potential and important neuroprotectant in therapeutic aspect in ischemic stroke. ..
  21. Han D, Zhang Q, Yong Liu -, Li C, Zong Y, Yu C, et al. Co-activation of GABA receptors inhibits the JNK3 apoptotic pathway via the disassembly of the GluR6-PSD95-MLK3 signaling module in cerebral ischemic-reperfusion. FEBS Lett. 2008;582:1298-306 pubmed publisher
    ..Our results suggest that stimulation of the inhibitory GABA receptors can attenuate the excitatory JNK3 apoptotic signaling pathway via inhibiting the increased assembly of the GluR6-PSD-95-MLK3 signaling module in cerebral ischemia. ..
  22. Song B, Yan X, Zhang G. PSD-95 promotes CaMKII-catalyzed serine phosphorylation of the synaptic RAS-GTPase activating protein SynGAP after transient brain ischemia in rat hippocampus. Brain Res. 2004;1005:44-50 pubmed
    ..The results suggest that the serine phosphorylation of SynGAP catalyzed by CaMKII is immediately increased and that PSD95 is critical for promoting SynGAP serine phosphorylation after transient brain ischemia. ..
  23. Guo J, Meng F, Zhang G, Zhang Q. Free radicals are involved in continuous activation of nonreceptor tyrosine protein kinase c-Src after ischemia/reperfusion in rat hippocampus. Neurosci Lett. 2003;345:101-4 pubmed
    ..These results suggest that free radical production is involved in NMDA receptor-mediated continuous activation of c-Src during ischemia/reperfusion but not that during ischemia...
  24. Du C, Gao J, Tai J, Liu Y, Qi J, Wang W, et al. Increased tyrosine phosphorylation of PSD-95 by Src family kinases after brain ischaemia. Biochem J. 2009;417:277-85 pubmed publisher
    ..Thus the present study reveals an additional mechanism for the regulation of PSD-95 by tyrosine phosphorylation. This mechanism may be of pathological significance since it is associated with excitotoxicity in the ischaemic brain. ..
  25. Zhang Q, Zhang G, Meng F, Tian H. Biphasic activation of apoptosis signal-regulating kinase 1-stress-activated protein kinase 1-c-Jun N-terminal protein kinase pathway is selectively mediated by Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors involving o. Neurosci Lett. 2003;337:51-5 pubmed
  26. Xu J, Zhang Q, Li C, Zhang G. Subtoxic N-methyl-D-aspartate delayed neuronal death in ischemic brain injury through TrkB receptor- and calmodulin-mediated PI-3K/Akt pathway activation. Hippocampus. 2007;17:525-37 pubmed
  27. Du C, Tan R, Hou X. Fyn kinases play a critical role in neuronal apoptosis induced by oxygen and glucose deprivation or amyloid-? peptide treatment. CNS Neurosci Ther. 2012;18:754-61 pubmed publisher
    ..Fyn is a potential therapeutic target for the treatment of ischemic stroke and AD. ..
  28. Ma J, Zhang G. Lithium reduced N-methyl-D-aspartate receptor subunit 2A tyrosine phosphorylation and its interactions with Src and Fyn mediated by PSD-95 in rat hippocampus following cerebral ischemia. Neurosci Lett. 2003;348:185-9 pubmed
  29. Di J, Li C, Yu H, Zheng J, Zhang G. nNOS downregulation attenuates neuronal apoptosis by inhibiting nNOS-GluR6 interaction and GluR6 nitrosylation in cerebral ischemic reperfusion. Biochem Biophys Res Commun. 2012;420:594-9 pubmed publisher
    ..In summary, our results suggest that nNOS binds with GluR6 via PSD95 and then produces endogenous NO to S-nitrosylate GluR6 in cerebral ischemia-reperfusion, which provides a new approach for stroke therapy. ..
  30. Sun N, Hao J, Li X, Yin X, Zong Y, Zhang G, et al. GluR6-FasL-Trx2 mediates denitrosylation and activation of procaspase-3 in cerebral ischemia/reperfusion in rats. Cell Death Dis. 2013;4:e771 pubmed publisher
    ..This is the first evidence that cerebral I/R mediates procaspase-3 denitrosylation and activation through GluR6-FasL-Trx2 pathway, which leads to neuronal apoptosis and cell death. ..
  31. Song B, Meng F, Yan X, Guo J, Zhang G. Cerebral ischemia immediately increases serine phosphorylation of the synaptic RAS-GTPase activating protein SynGAP by calcium/calmodulin-dependent protein kinase II alpha in hippocampus of rats. Neurosci Lett. 2003;349:183-6 pubmed
  32. Wang W, Hu S, Li C, Zhou C, Qi S, Zhang G. Transduced PDZ1 domain of PSD-95 decreases Src phosphorylation and increases nNOS (Ser847) phosphorylation contributing to neuroprotection after cerebral ischemia. Brain Res. 2010;1328:162-70 pubmed publisher
    ..These results suggest that overexpression of the PDZ1 domain can perturb the binding of PSD-95 to NMDA receptor, suppress the activity of both NMDA receptor and nNOS, and thus have a neuroprotective effect. ..
  33. Jiang H, Guan Q, Pei D, Zhang G. Functional cooperation between KA2 and GluR6 subunits is involved in the ischemic brain injury. J Neurosci Res. 2007;85:2960-70 pubmed
  34. Li T, Yu X, Zhang G. Tyrosine phosphorylation of HPK1 by activated Src promotes ischemic brain injury in rat hippocampal CA1 region. FEBS Lett. 2008;582:1894-900 pubmed publisher