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SHA Weimeng
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071006 神经生物学
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07 理学
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References List

[1] E. J. Benjamin et al., “Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association,” Circulation, vol. 135, no. 10, Mar. 2017, doi: 10.1161/CIR.0000000000000485.
[2] D. W. Choi and S. M. Rothman, “The Role of Glutamate Neurotoxicity in Hypoxic-Ischemic Neuronal Death,” Annu Rev Neurosci, vol. 13, no. 1, pp. 171–182, Mar. 1990, doi: 10.1146/annurev.ne.13.030190.001131.
[3] C. Yang, K. E. Hawkins, S. Doré, and E. Candelario-Jalil, “Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke,” American Journal of Physiology-Cell Physiology, vol. 316, no. 2, pp. C135–C153, Feb. 2019, doi: 10.1152/ajpcell.00136.2018.
[4] M. R. Halstead and R. G. Geocadin, “The Medical Management of Cerebral Edema: Past, Present, and Future Therapies,” Neurotherapeutics, vol. 16, no. 4, pp. 1133–1148, Oct. 2019, doi: 10.1007/s13311-019-00779-4.
[5] T. Clément, B. Rodriguez-Grande, and J. Badaut, “Aquaporins in brain edema,” J Neurosci Res, vol. 98, no. 1, pp. 9–18, Jan. 2020, doi: 10.1002/jnr.24354.
[6] N. J. Abbott, L. Rönnbäck, and E. Hansson, “Astrocyte–endothelial interactions at the blood–brain barrier,” Nat Rev Neurosci, vol. 7, no. 1, pp. 41–53, Jan. 2006, doi: 10.1038/nrn1824.
[7] D. J. Begley and M. W. Brightman, “Structural and functional aspects of the blood-brain barrier,” in Peptide Transport and Delivery into the Central Nervous System, Basel: Birkhäuser Basel, 2003, pp. 39–78. doi: 10.1007/978-3-0348-8049-7_2.
[8] W. M. Pardridge, “CSF, blood-brain barrier, and brain drug delivery,” Expert Opin Drug Deliv, vol. 13, no. 7, pp. 963–975, Jul. 2016, doi: 10.1517/17425247.2016.1171315.
[9] E. Neuwelt et al., “Strategies to advance translational research into brain barriers,” Lancet Neurol, vol. 7, no. 1, pp. 84–96, Jan. 2008, doi: 10.1016/S1474-4422(07)70326-5.
[10] B. Obermeier, R. Daneman, and R. M. Ransohoff, “Development, maintenance and disruption of the blood-brain barrier,” Nat Med, vol. 19, no. 12, pp. 1584–1596, Dec. 2013, doi: 10.1038/nm.3407.
[11] J. D. Huber, R. D. Egleton, and T. P. Davis, “Molecular physiology and pathophysiology of tight junctions in the blood–brain barrier,” Trends Neurosci, vol. 24, no. 12, pp. 719–725, Dec. 2001, doi: 10.1016/S0166-2236(00)02004-X.
[12] P. Borst and A. H. Schinkel, “P-glycoprotein ABCB1: a major player in drug handling by mammals,” Journal of Clinical Investigation, vol. 123, no. 10, pp. 4131–4133, Oct. 2013, doi: 10.1172/JCI70430.
[13] N. Strazielle and J.-F. Ghersi-Egea, “Potential Pathways for CNS Drug Delivery Across the Blood-Cerebrospinal Fluid Barrier,” Curr Pharm Des, vol. 22, no. 35, pp. 5463–5476, Nov. 2016, doi: 10.2174/1381612822666160726112115.
[14] I. Klatzo, “Presidential Address *,” J Neuropathol Exp Neurol, vol. 26, no. 1, pp. 1–14, Jan. 1967, doi: 10.1097/00005072-196701000-00001.
[15] T. H. Milhorat, “Classification of the cerebral edemas with reference to hydrocephalus and pseudotumor cerebri,” Child’s Nervous System, vol. 8, no. 6, pp. 301–306, Sep. 1992, doi: 10.1007/BF00296558.
[16] J. A. Stokum, D. B. Kurland, V. Gerzanich, and J. M. Simard, “Mechanisms of Astrocyte-Mediated Cerebral Edema,” Neurochem Res, vol. 40, no. 2, pp. 317–328, Feb. 2015, doi: 10.1007/s11064-014-1374-3.
[17] Y. Liu et al., “The protective role of Tongxinluo on blood–brain barrier after ischemia–reperfusion brain injury,” J Ethnopharmacol, vol. 148, no. 2, pp. 632–639, Jul. 2013, doi: 10.1016/j.jep.2013.05.018.
[18] J. Huang, Y. Li, Y. Tang, G. Tang, G.-Y. Yang, and Y. Wang, “CXCR4 Antagonist AMD3100 Protects Blood–Brain Barrier Integrity and Reduces Inflammatory Response After Focal Ischemia in Mice,” Stroke, vol. 44, no. 1, pp. 190–197, Jan. 2013, doi: 10.1161/STROKEAHA.112.670299.
[19] C. Iacovetta, E. Rudloff, and R. Kirby, “The role of aquaporin 4 in the brain,” Vet Clin Pathol, p. n/a-n/a, Jan. 2012, doi: 10.1111/j.1939-165X.2011.00390.x.
[20] H. Hirai, Y. Maru, K. Hagiwara, J. Nishida, and F. Takaku, “A Novel Putative Tyrosine Kinase Receptor Encoded by the eph Gene,” Science (1979), vol. 238, no. 4834, pp. 1717–1720, Dec. 1987, doi: 10.1126/science.2825356.
[21] J. Zhao et al., “EphA4 Regulates Hippocampal Neural Precursor Proliferation in the Adult Mouse Brain by d-Serine Modulation of N-Methyl-d-Aspartate Receptor Signaling,” Cerebral Cortex, vol. 29, no. 10, pp. 4381–4397, Sep. 2019, doi: 10.1093/cercor/bhy319.
[22] S. Kuijper, C. J. Turner, and R. H. Adams, “Regulation of Angiogenesis by Eph–Ephrin Interactions,” Trends Cardiovasc Med, vol. 17, no. 5, pp. 145–151, Jul. 2007, doi: 10.1016/j.tcm.2007.03.003.
[23] A. Martínez and E. Soriano, “Functions of ephrin/Eph interactions in the development of the nervous system: Emphasis on the hippocampal system,” Brain Res Rev, vol. 49, no. 2, pp. 211–226, Sep. 2005, doi: 10.1016/j.brainresrev.2005.02.001.
[24] A. Davy and P. Soriano, “Ephrin signaling in vivo: Look both ways,” Developmental Dynamics, vol. 232, no. 1, pp. 1–10, Jan. 2005, doi: 10.1002/dvdy.20200.
[25] M. Aoki, T. Yamashita, and M. Tohyama, “EphA Receptors Direct the Differentiation of Mammalian Neural Precursor Cells through a Mitogen-activated Protein Kinase-dependent Pathway,” Journal of Biological Chemistry, vol. 279, no. 31, pp. 32643–32650, Jul. 2004, doi: 10.1074/jbc.M313247200.
[26] E. M. Lisabeth, G. Falivelli, and E. B. Pasquale, “Eph Receptor Signaling and Ephrins,” Cold Spring Harb Perspect Biol, vol. 5, no. 9, pp. a009159–a009159, Sep. 2013, doi: 10.1101/cshperspect.a009159.
[27] D. Vreeken, H. Zhang, A. J. van Zonneveld, and J. M. van Gils, “Ephs and Ephrins in Adult Endothelial Biology,” Int J Mol Sci, vol. 21, no. 16, p. 5623, Aug. 2020, doi: 10.3390/ijms21165623.
[28] Eph Nomenclature Committee, “Unified Nomenclature for Eph Family Receptors and Their Ligands, the Ephrins,” Cell, vol. 90, no. 3, pp. 403–404, Aug. 1997, doi: 10.1016/S0092-8674(00)80500-0.
[29] H. Liu, K. Devraj, K. Möller, S. Liebner, M. Hecker, and T. Korff, “EphrinB-mediated reverse signalling controls junctional integrity and pro-inflammatory differentiation of endothelial cells,” Thromb Haemost, vol. 112, no. 07, pp. 151–163, Dec. 2014, doi: 10.1160/TH13-12-1034.
[30] E. B. Pasquale, “Eph-Ephrin Bidirectional Signaling in Physiology and Disease,” Cell, vol. 133, no. 1, pp. 38–52, Apr. 2008, doi: 10.1016/j.cell.2008.03.011.
[31] E. B. Pasquale, “Eph receptor signalling casts a wide net on cell behaviour,” Nat Rev Mol Cell Biol, vol. 6, no. 6, pp. 462–475, Jun. 2005, doi: 10.1038/nrm1662.
[32] S. Tanasic et al., “Desipramine targets astrocytes to attenuate synaptic plasticity via modulation of the ephrinA3/EphA4 signalling,” Neuropharmacology, vol. 105, pp. 154–163, Jun. 2016, doi: 10.1016/j.neuropharm.2016.01.021.
[33] H. U. Wang, Z.-F. Chen, and D. J. Anderson, “Molecular Distinction and Angiogenic Interaction between Embryonic Arteries and Veins Revealed by ephrin-B2 and Its Receptor Eph-B4,” Cell, vol. 93, no. 5, pp. 741–753, May 1998, doi: 10.1016/S0092-8674(00)81436-1.
[34] I. Konstantinova et al., “EphA-Ephrin-A-Mediated β Cell Communication Regulates Insulin Secretion from Pancreatic Islets,” Cell, vol. 129, no. 2, pp. 359–370, Apr. 2007, doi: 10.1016/j.cell.2007.02.044.
[35] Z. Miao et al., “VEGF Increases Paracellular Permeability in Brain Endothelial Cells via Upregulation of EphA2,” Anat Rec, vol. 297, no. 5, pp. 964–972, May 2014, doi: 10.1002/ar.22878.
[36] G. Ende et al., “TNF-α-mediated adhesion of monocytes to endothelial cells—The role of ephrinA1,” J Mol Cell Cardiol, vol. 77, pp. 125–135, Dec. 2014, doi: 10.1016/j.yjmcc.2014.10.010.
[37] A. Kania and R. Klein, “Mechanisms of ephrin–Eph signalling in development, physiology and disease,” Nat Rev Mol Cell Biol, vol. 17, no. 4, pp. 240–256, Apr. 2016, doi: 10.1038/nrm.2015.16.
[38] T. M. Woodruff et al., “Epha4-Fc Treatment Reduces Ischemia/Reperfusion-Induced Intestinal Injury by Inhibiting Vascular Permeability,” Shock, vol. 45, no. 2, pp. 184–191, Feb. 2016, doi: 10.1097/SHK.0000000000000494.
[39] T. Gong et al., “EphrinB2/EphB4 Signaling Regulates DPSCs to Induce Sprouting Angiogenesis of Endothelial Cells,” J Dent Res, vol. 98, no. 7, pp. 803–812, Jul. 2019, doi: 10.1177/0022034519843886.
[40] D. M. Poitz et al., “EphrinB2/EphA4-mediated activation of endothelial cells increases monocyte adhesion,” Mol Immunol, vol. 68, no. 2, pp. 648–656, Dec. 2015, doi: 10.1016/j.molimm.2015.10.009.
[41] D. Pfaff et al., “Involvement of endothelial ephrin-B2 in adhesion and transmigration of EphB-receptor-expressing monocytes,” J Cell Sci, vol. 121, no. 22, pp. 3842–3850, Nov. 2008, doi: 10.1242/jcs.030627.
[42] F. Chen et al., “Activation of EphA4 induced by EphrinA1 exacerbates disruption of the blood brain barrier following cerebral ischemia reperfusion via the Rho/ROCK signaling pathway,” Exp Ther Med, Jul. 2018, doi: 10.3892/etm.2018.6460.
[43] R. Lemmens, T. Jaspers, W. Robberecht, and V. N. Thijs, “Modifying expression of EphA4 and its downstream targets improves functional recovery after stroke,” Hum Mol Genet, vol. 22, no. 11, pp. 2214–2220, Jun. 2013, doi: 10.1093/hmg/ddt073.
[44] E. M. Weekman and D. M. Wilcock, “Matrix Metalloproteinase in Blood-Brain Barrier Breakdown in Dementia,” Journal of Alzheimer’s Disease, vol. 49, no. 4, pp. 893–903, Nov. 2015, doi: 10.3233/JAD-150759.
[45] Y. Goldshmit and J. Bourne, “Upregulation of EphA4 on Astrocytes Potentially Mediates Astrocytic Gliosis after Cortical Lesion in the Marmoset Monkey,” J Neurotrauma, vol. 27, no. 7, pp. 1321–1332, Jul. 2010, doi: 10.1089/neu.2010.1294.
[46] L. Wu, X. Yu, and L. Feng, “Connexin 43 stabilizes astrocytes in a stroke-like milieu to facilitate neuronal recovery,” Acta Pharmacol Sin, vol. 36, no. 8, pp. 928–938, Aug. 2015, doi: 10.1038/aps.2015.39.
[47] M. M. Elgebaly, “Ephrin–Eph Signaling as a Novel Neuroprotection Path in Ischemic Stroke,” Journal of Molecular Neuroscience, vol. 70, no. 12, pp. 2001–2006, Dec. 2020, doi: 10.1007/s12031-020-01603-x.
[48] B. Okyere et al., “EphA4/Tie2 crosstalk regulates leptomeningeal collateral remodeling following ischemic stroke,” Journal of Clinical Investigation, vol. 130, no. 2, pp. 1024–1035, Jan. 2020, doi: 10.1172/JCI131493.
[49] Y. Goldshmit et al., “EphA4 Blockers Promote Axonal Regeneration and Functional Recovery Following Spinal Cord Injury in Mice,” PLoS One, vol. 6, no. 9, p. e24636, Sep. 2011, doi: 10.1371/journal.pone.0024636.
[50] J. Zhao, L. T. Cooper, A. W. Boyd, and P. F. Bartlett, “Decreased signalling of EphA4 improves functional performance and motor neuron survival in the SOD1G93A ALS mouse model,” Sci Rep, vol. 8, no. 1, p. 11393, Dec. 2018, doi: 10.1038/s41598-018-29845-1.
[51] R. Lemmens, T. Jaspers, W. Robberecht, and V. N. Thijs, “Modifying expression of EphA4 and its downstream targets improves functional recovery after stroke,” Hum Mol Genet, vol. 22, no. 11, pp. 2214–2220, Jun. 2013, doi: 10.1093/hmg/ddt073.

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沙溦濛. EphA4-Fc在小鼠脑中动脉局灶缺血中神经保护作用的研究[D]. 深圳. 南方科技大学,2022.
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