Mechanism of Action of Autophagy on the Cerebral Ischemia-Reperfusion Injury

doi:10.3969/j.issn.2095-1396.2016.01.006

Abstract

Abstract: Autophagy is a life phenomenon widely existing in eukaryotic cells and a special metabolic pathway of decomposition. It controls the degradation of protein and organelles and is essential for cell survival and tissue homeostasis. At present，autophagy has become a hot research topic in the field of biological medicine，and the studies have demonstrated the association with various diseases. To date，ischemic cerebral stroke responsible for human death and disability may cause the ischemia-reperfusion （I/R） injury，which is common and receives much more concern. This review states autophagy and its mechanisms on the I/R injury to provide the theoretical basis for further therapy on ischemic cerebrovascular disorder.

Key words: autophagy, cerebral ischemia-reperfusion injury, mechanism

CLC Number:

R743

WANG Xiao-ru，AN Fang. Mechanism of Action of Autophagy on the Cerebral Ischemia-Reperfusion Injury[J]. Acta Neuropharmacologica, 2016, 6(1): 41-48.

References

[1] Knut Biber, Erik Boddeke. Neuronal CC chemokines: the distinct roles of CCL21 and CCL2 in neuropathic pain [J]. Frontiers Cell Neurosci, 2014, 8: 210.

[2] Van Steenwinckel J, Reaux-Le Goazigo A, Pommier B, et al. CCL2 released from neuronal synaptic vesicles in the spinal cord is a major mediator of local inflammation and pain after peripheral nerve injury[J]. J Neurosci, 2011, 31(15): 5865-5875.

[3] Moser B, Pius Loetscher. Lymphocyte traffic control by chemokines [J]. Nat Immunol, 2001, 2(2): 123-128.

[4] Satish L Deshmane, Sergey Kremlev, Shohreh Amini, et al. Monocytechemoattractant protein-1 (MCP-1): an overview [J]. J Interferon & Cytokine Res, 2009, 29 (6): 313-326.

[5] Marc-Andre Dansereau, Romain-Daniel Gosselin, Michel Pohl, et al. Spinal CCL2 pronociceptive action is no longer effective in CCR2 receptor antagonist-treated rats [J]. J Neurochemistry, 2008, 106(2): 757-769.

[6]   Michael A Thacker, Anna K Clark, Thomas Bishop, et al. CCL2 is a key mediator of microglia activation in neuropathic pain states [J]. J European Pain, 2009, 13 (3): 263-272.

[7] Menetski J, Mistry S, Lu M, et al. Mice overexpressing chemokine ligand 2 (CCL2) in astrocytes display enhanced nociceptive responses [J]. Neuroscience, 2007, 149(3): 706-714.

[8] Catherine Abbadie, Jill A Lindia, Anne Marie Cumiskey, et al. Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2 [J]. Science Signalling, 2003, 100(13): 7947-7952.

[9] Zhang Zhi-jun, Dong Yu-lin, Lu Ying, et al. Chemokine CCL2 and its receptor CCR2 in the medullary dorsal horn are involved in trigeminal neuropathic pain [J]. J Neuroinflammation, 2012, 9(1): 136.

[10] Norikazu Kiguchi, Yuka Kobayashi, Shiroh Kishioka. Chemokines and cytokines in neuroinflammation leading to neuropathic pain [J]. Current Opinion Pharmacol, 2012, 12(1): 55-61.

[11] Guo Wei, Wang Hu, Zou Shi-ping, et al. Chemokine signaling involving chemokine (CC motif) ligand 2 plays a role in descending pain facilitation [J]. Neuroscience Bulletin, 2012, 21(2): 1-15.

[12] Jung Hosung, Peter T Toth, Fletcher A White, et al. Monocyte chemoattractant protein‐1 functions as a neuromodulator in dorsal root ganglia neurons [J]. J Neurochemistry, 2008, 104(1): 254-263.

[13] Gregory Conductier, Nicolas Blondeau, Alice Guyon, et al. The role of monocyte chemoattractant protein MCP1/CCL2 in neuroinflammatory diseases [J]. J Neuroimmunol, 2010, 224(1-2): 93-100.

[14] Mounir Belkouch, Marc-Andre Dansereau, Annabelle Réaux-Le Goazigo, et al. The chemokine CCL2 increases Nav1.8 sodium channel activity in primary sensory neurons through a Gβγ -dependent mechanism [J]. J Neuroscience 2011, 31(50): 18381-18390.

[15] Gao Yong-jing, Zhang Ling, Omar Abdel Samad, et al. JNK-induced MCP-1 production in spinal cord astrocytes contributes to central sensitization and neuropathic pain [J].J Neurosci, 2009, 29(13): 4096-4108.

[16] Elizabeth A Old, Marzia Malcangio. Chemokine mediated neuron–glia communication and aberrant signalling in neuropathic pain states [J]. Current Opin Pharmacology, 2012, 12(1): 67-73.

[17] Joachim Scholz, Clifford J Woolf. The neuropathic pain triad: neurons, immune cells and glia [J]. Nature Neuroscience, 2007, 10(11): 1361-1368.

[18] Makoto Tsuda, Yukari Shigemoto-Mogami, Schuichi Koizumi, et al. P2X4 receptors induced in spinal microglia gate tactile allodynia after nerve injury [J]. Nature, 2003, 424(6950): 778-783.

[19] 杜雯, 孙益. 小胶质细胞在神经病理性疼痛中的作用[J]. 细胞生物学杂志, 2007, 29(1): 11-16.

[20] 高永静, 纪如荣. 星形胶质细胞调节慢性疼痛的分子机制[J]. 中国疼痛医学杂志, 2013, 19 (9): 545-552

[21] Vyklicky L, Novakova-Tousova K, Benedikt J, et al. Calcium-dependent desensitization of vanilloid receptor TRPV1: a mechanism possibly involved in analgesia induced by topical application of capsaicin [J]. Physiol Res, 2008, 57(Suppl 3): S59-S68.

[22] 韩重阳, 王晓良. 瞬时受体电位通道研究进展[J]. 生理科学进展, 2008, 39 (1): 27-32.

[23] Michael S Gold, Gerald F Gebhart. Nociceptor sensitization in pain pathogenesis [J]. Nature Medicine, 2010, 16(11): 1248-1257.

[24] Sun J H, Yang B, Donnelly D F, et al. MCP-1 enhances excitability of nociceptive neurons in chronically compressed dorsal root ganglia [J]. J Neurophysiol, 2006, 96(5): 2189-2199.

[25] Der-Jang Kao, Allen H Li, Jin-Chung Chen, et al. CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons [J]. J Neuroinflammation, 2012, 9(1): 189.

[26] Diana Spicarova, Pavel Adamek, Nataliia Kalynovska, et al. TRPV1 receptor inhibition decreases CCL2-induced hyperalgesia [J]. Neuropharmacology, 2014, 81: 75-84.

[27] Der-Jang Kao, Alien H Li, Jin-Chung Chen, et al. CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons [J]. Journal of Neuroinflammation, 2012, 9 (1): 189. (与25条重复)

[28] Han Ying, Li Yan, Xiao Xing, et al. Formaldehyde up-regulates TRPV1 through MAPK and PI3K signaling pathways in a rat model of bone cancer pain [J]. Neuroscience bulletin, 2012, 28(2): 165-172.

[29] Zhuang Zhi-ye, Xu Hao-xing, David E Clapham, et al. Phosphatidylinositol 3-kinase activates ERK in primary sensory neurons and mediates inflammatory heat hyperalgesia through TRPV1 sensitization [J]. J Neuroscience, 2004, 24(38): 8300-8309.

[30] Renuka Ramachandra, Stephanie Y McGrew, James C Baxter, et al. NaV1.8 channels are expressed in large, as well as small, diameter sensory afferent neurons [J]. Channels, 2013, 7(1): 0-1.

[31] Amaya F, Wang H, Costigan M, et al. The voltage-gated sodium channel Nav1. 9 is an effector of peripheral inflammatory pain hypersensitivity [J]. J Neurosci, 2006, 26(50): 12852-12860.

[32] Sulayman D Dib-Hajj, Theodore R Cummins, Joel A Black, et al. Sodium channels in normal and pathological pain [J]. Annual Review of Neuroscience, 2010, 33: 325-347.

[33] Wu Dai-fei, Dave Chandra, Thomas McMahon, et al. PKCε phosphorylation of the sodium channel NaV1.8 increases channel function and produces mechanical hyperalgesia in mice [J]. J Clinical Investigation, 2012, 122(3): 1306-1315.

[34] 肖杭, 戴晓青, 毛霞, 等. 铅抑制大鼠背根神经元外向延迟整流钾通道[J]. 中华预防医学杂志, 2001, 35(2): 108-110.

[35] B Hille. Ion channels of excitable membranes [M]. 507, USA, Sinauer Sunderland, MA, 2001

[36] Zhu Xiang, Liu Jin-qian, Gao Yong-jing, et al. ATP-sensitive potassium channels alleviate postoperative pain through JNK-dependent MCP-1 expression in spinal cord [J]. Int J Mol Med, 2015, 35(5): 1257-1265.

[37] Sang-Min Jeon, Kyung-Min Lee, Hee-Jung Cho. Expression of monocyte chemoattractant protein-1 in rat dorsal root ganglia and spinal cord in experimental models of neuropathic pain [J]. Brain Res, 2009, 1251: 103-111.

[38] Wang Chang-hui, Zou Li-jing, Zhang Yi-li, et al. The excitatory effects of the chemokine CCL2 on DRG somata are greater after an injury of the ganglion than after an injury of the spinal or peripheral nerve [J]. Neuroscience Lett, 2010, 475 (1): 48-52.

[39]   Tatsuro Kohno, Hai-bin Wang, Fumimasa Amaya, et al. Bradykinin enhances AMPA and NMDA receptor activity in spinal cord dorsal horn neurons by activating multiple kinases to produce pain hypersensitivity [J]. J Neuroscience, 2008, 28(17): 4533-4540.

[40]   Randi? M, He?imovi? H, Ryu P. Substance P modulates glutamate-induced currents in acutely isolated rat spinal dorsal horn neurons[J]. Neuroscience Lett, 1990, 117(1-2): 74-80.

[41]   Aaron Y Lai, Richard D Swayze, Alaa El-Husseini, et al. Interleukin-1 beta modulates AMPA receptor expression and phosphorylation in hippocampal neurons[J]. J Neuroimmunol, 2006, 175(1-2): 97-106.

[42]   Chung-Yu Huang, Chen Ying-ling, Allen H Li, et al. Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons[J]. J Neuroinflammation, 2014, 11: 7.

[43] Fletcher A White, Sun Ji-hu, Stephen M Waters, et al. Excitatory monocyte chemoattractant protein-1 signaling is up-regulated in sensory neurons after chronic compression of the dorsal root ganglion [J]. Proc Natl Acad Sci of the USA, 2005, 102(39): 14092-14097.

[44] Zhou Yan, Tang Hong-mei, Liu Jia-nuo, et al. Chemokine CCL2 modulation of neuronal excitability and synaptic transmission in rat hippocampal slices [J]. J Neurochemistry, 2011, 116(3): 406-414.

[45] Gao Yong-jing, Ji Ru-rong. Chemokines, neuronal–glial interactions, and central processing of neuropathic pain [J]. Pharmacology & Therapeutics, 2010, 126(1): 56-68.

[46] Cao Jing, Yang Xian, Liu Yan-ni, et al. GABAergic disinhibition induced pain hypersensitivity by upregulating NMDA receptor functions in spinal dorsal horn [J]. Neuropharmacology, 2011, 60(6): 921-929.

[47] Arbazia Baamonde, Ana Hidalgo, Luis Menéndez. Involvement of glutamate NMDA and AMPA receptors, glial cells and IL-1β in the spinal hyperalgesia evoked by the chemokine CCL2 in mice [J]. Neuroscience Lett, 2011, 502(3): 178-181.

[48] Herman Friedman, Susan Pross, Thomas W Klein. Addictive drugs and their relationship with infectious diseases [J]. FEMS Immunology & Medical Microbiology, 2006, 47(3): 330-342.

[49] Avi Nath, Kurt F Hauser, Valerie Wojna, et al. Molecular basis for interactions of HIV and drugs of abuse [J]. JAIDS J Acquired Immune Deficiency Syndromes, 2002, 31(Suppl 2): S62-S69.

[50] Toby K Eisenstein, Mary E Hilburger. Opioid modulation of immune responses: effects on phagocyte and lymphoid cell populations [J]. J Neuroimmunology, 1998, 83(1-2): 36-44.

[51] Michele A Wetzel, Amber D Steele, Toby K Eisenstein, et al. µ-Opioid induction of monocyte chemoattractant protein-1, RANTES, and IFN-γ-inducible protein-10 expression in human peripheral blood mononuclear cells [J]. J Immunology, 2000, 165(11): 6519-6524.

[52] Supriya D Mahajan, Stanley A Schwartz, Ravikumar Aalinkeel, et al. Morphine modulates chemokine gene regulation in normal human astrocytes [J]. Clinical Immunology, 2005, 115(3): 323-332.

[53] R Bryan Rock, Hu Shu-xian, Wen S Sheng, et al. Morphine stimulates CCL2 production by human neurons [J]. J Neuroinflammation, 2006, 3:32.

[54] Christine Happel, Michele Kutzler, Thomas J Rogers. Opioid-induced chemokine expression requires NF-κB activity: the role of PKCζ [J]. J Leukoc Biol, 2011, 89(2): 301-309.

[55] Imre Szabo, Chen Xiao-hong, Xin Lin, et al. Heterologous desensitization of opioid receptors by chemokines inhibits chemotaxis and enhances the perception of pain [J]. Proc Natl Acad Sci USA, 2002, 99(16): 10276-10281.

[56] Jon-Kar Zubieta, Smith Y R, Bueller J A, et al. Regional mu opioid receptor regulation of sensory and affective dimensions of pain [J]. Science, 2001, 293(5528): 311-315.

[57] Zhang Ning, Thomas J Rogers, Michael Caterina, et al. Proinflammatory chemokines, such as CC chemokine ligand 3, desensitize µ-opioid receptors on dorsal root ganglia neurons [J]. J Immunology, 2004, 173(1): 594-599.

[58] Marzia Melcangic, Norman G Bowery. GABA and its receptors in the spinal cord [J]. Trends in pharmacological sciences, 1996, 17 (12): 457-462.

[59] T Philip Malan, Heriberto P Mata, Frank Porreca. Spinal GABAA and GABAB receptor pharmacology in a rat model of neuropathic pain [J]. Anesthesiology, 2002, 96(5): 1161-1167.

[60] Young S Gwak, Claire E Hulsebosch. GABA and central neuropathic pain following spinal cord injury [J]. Neuropharmacology, 2011, 60(5): 799-808.

[61] Romain Daniel Gosselin, Carolina Varela, Banisadr G, et al. Constitutive expression of CCR2 chemokine receptor and inhibition by MCP‐1/CCL2 of GABA‐induced currents in spinal cord neurones [J]. J Neurochemistry, 2005, 95(4): 1023-1034.

[62] Hu Ji-hua, Zheng Xiao-yan, Yang Jian-ping, et al. Involvement of spinal monocyte chemoattractant protein-1 (MCP-1) in cancer-induced bone pain in rats [J]. Neuroscience Letters, 2012, 517(1): 60-63.