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Review Article | Open Access

The Golgi apparatus in neurorestoration

Jianyang LiuJialin HeYan HuangHan XiaoZheng JiangZhiping Hu( )
Department of Neurology, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan, China
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Abstract

The central role of the Golgi apparatus in critical cellular processes such as the transport, processing, and sorting of proteins and lipids has placed it at the forefront of cell science. Golgi apparatus dysfunction caused by primary defects within the Golgi or pharmacological and oxidative stress has been implicated in a wide range of neurodegenerative diseases. In addition to participating in disease progression, the Golgi apparatus plays pivotal roles in angiogenesis, neurogenesis, and synaptogenesis, thereby promoting neurological recovery. In this review, we focus on the functions of the Golgi apparatus and its mediated events during neurorestoration.

References

[1]
HH Mollenhauer, DwJ Morré. Perspectives on Golgi apparatus form and function. J Electron Microsc Tech. 1991, 17(1): 2-14.
[2]
Z Mourelatos, NK Gonatas, A Stieber, et al. The Golgi apparatus of spinal cord motor neurons in transgenic mice expressing mutant Cu, Zn superoxide dismutase becomes fragmented in early, preclinical stages of the disease. Proc Natl Acad Sci USA. 1996, 93(11): 5472-5477.
[3]
G Joshi, ME 2nd Bekier, YZ Wang. Golgi fragmentation in Alzheimer’s disease. Front Neurosci. 2015, 9: 340.
[4]
WO Rendón, E Martínez-Alonso, M Tomás, et al. Golgi fragmentation is Rab and SNARE dependent in cellular models of Parkinson’s disease. Histochem Cell Biol. 2013, 139(5): 671-684.
[5]
C Golgi. On the structure of nerve cells. 1898. J Microsc. 1989, 155(Pt 1): 3-7.
[6]
A Sesso, FP de Faria, ES Iwamura, et al. A three- dimensional reconstruction study of the rough ER- Golgi interface in serial thin sections of the pancreatic acinar cell of the rat. J Cell Sci. 1994, 107(Pt 3): 517-528.
[7]
RM Rios, M Bornens. The Golgi apparatus at the cell centre. Curr Opin Cell Biol. 2003, 15(1): 60-66.
[8]
KJ Day, LA Staehelin, BS Glick. A three-stage model of Golgi structure and function. Histochem Cell Biol. 2013, 140(3): 239-249.
[9]
C Darido, SM Jane. Golgi feels its own wound. Adv Wound Care. 2013, 2(3): 87-92.
[10]
V Sundaramoorthy, JM Sultana, JD Atkin. Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences. Front Neurosci. 2015, 9: 400.
[11]
NK Gonatas, A Stieber, JO Gonatas. Fragmentation of the Golgi apparatus in neurodegenerative diseases and cell death. J Neurol Sci. 2006, 246(1/2): 21-30.
[12]
GE Shull, ML Miller, V Prasad. Secretory pathway stress responses as possible mechanisms of disease involving Golgi Ca2+ pump dysfunction. Biofactors. 2011, 37(3): 150-158.
[13]
T Yoshida, T Kamiya, K Imanaka-Yoshida, et al. Low cytoplasmic pH causes fragmentation and dispersal of the Golgi apparatus in human hepatoma cells. Int J Exp Pathol. 1999, 80(1): 51-57.
[14]
XY Zhang, YZ Wang. Glycosylation quality control by the Golgi structure. J Mol Biol. 2016, 428(16): 3183-3193.
[15]
CE Machamer. The Golgi complex in stress and death. Front Neurosci. 2015, 9: 421.
[16]
K Sasaki, H Yoshida. Organelle autoregulation-stress responses in the ER, Golgi, mitochondria and lysosome. J Biochem. 2015, 157(4): 185-195.
[17]
M. Taniguchi, H Yoshida. TFE3, HSP47, and CREB3 pathways of the mammalian Golgi stress response. Cell Struct Funct. 2017, 42(1): 27-36.
[18]
C Gomes, AS Palma, R Almeida, et al. Establishment of a cell model of ALS disease: Golgi apparatus disruption occurs independently from apoptosis. Biotechnol Lett. 2008, 30(4): 603-610.
[19]
N Furuta, K Makioka, Y Fujita, et al. Reduced expression of BTBD10 in anterior horn cells with Golgi fragmentation and pTDP-43-positive inclusions in patients with sporadic amyotrophic lateral sclerosis. Neuropathology. 2013, 33(4): 397-404.
[20]
AN Strehlow, JZ Li, RM Myers. Wild-type huntingtin participates in protein trafficking between the Golgi and the extracellular space. Hum Mol Genet. 2007, 16(4): 391-409.
[21]
A Sakurai, K Okamoto, Y Fujita, et al. Fragmentation of the Golgi apparatus of the ballooned neurons in patients with corticobasal degeneration and creutzfeldt- Jakob disease. Acta Neuropathol. 2000, 100(3): 270-274.
[22]
A Sakurai, K Okamoto, M Yaguchi, et al. Pathology of the inferior olivary nucleus in patients with multiple system atrophy. Acta Neuropathol. 2002, 103(6): 550-554.
[23]
G Haase, C Rabouille. Golgi fragmentation in ALS motor neurons. new mechanisms targeting microtubules, tethers, and transport vesicles. Front Neurosci. 2015, 9: 448.
[24]
SW Hicks, CE Machamer. Golgi structure in stress sensing and apoptosis. Biochim Biophys Acta. 2005, 1744(3): 406-414.
[25]
FL Tang, JR Erion, Y Tian, et al. VPS35 in dopamine neurons is required for endosome-to-Golgi retrieval of Lamp2a, a receptor of chaperone-mediated autophagy that is critical for α-synuclein degradation and prevention of pathogenesis of Parkinson’s disease. J Neurosci. 2015, 35(29): 10613-10628.
[26]
TK Graves, S Patel, PS Dannies, et al. Misfolded growth hormone causes fragmentation of the Golgi apparatus and disrupts endoplasmic reticulum-to-Golgi traffic. J Cell Sci. 2001, 114(Pt 20): 3685-3694.
[27]
Y Kaneko, R Sullivan, T Dailey, et al. Kainic acid- induced Golgi complex fragmentation/dispersal shifts the proteolysis of reelin in primary rat neuronal cells: an in vitro model of early stage epilepsy. Mol Neurobiol. 2016, 53(3): 1874-1883.
[28]
S Nakagomi, MJ Barsoum, E Bossy-Wetzel, et al. A Golgi fragmentation pathway in neurodegeneration. Neurobiol Dis. 2008, 29(2): 221-231.
[29]
F Doetsch, I Caillé, DA Lim, et al. Subventricular zone astrocytes are neural stem cells in the adult mammalian brain. Cell. 1999, 97(6): 703-716.
[30]
MS Kaplan, JW Hinds. Neurogenesis in the adult rat: electron microscopic analysis of light radioautographs. Science. 1977, 197(4308): 1092-1094.
[31]
GL Ming, HJ Song. Adult neurogenesis in the mammalian central nervous system. Annu Rev Neurosci. 2005, 28: 223-250.
[32]
CD Clelland, M Choi, C Romberg, et al. A functional role for adult hippocampal neurogenesis in spatial pattern separation. Science. 2009, 325(5937): 210-213.
[33]
L Santarelli, M Saxe, C Gross, et al. Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants. Science. 2003, 301(5634): 805-809.
[34]
CM Zhao, EM Teng, RG Summers Jr, et al. Distinct morphological stages of dentate granule neuron maturation in the adult mouse Hippocampus. J Neurosci. 2006, 26(1): 3-11.
[35]
CM Zhao, W Deng, FH Gage. Mechanisms and functional implications of adult neurogenesis. Cell. 2008, 132(4): 645-660.
[36]
S Rao, GW Kirschen, J Szczurkowska, et al. Repositioning of somatic Golgi apparatus is essential for the dendritic establishment of adult-born hippocampal neurons. J Neurosci. 2018, 38(3): 631-647.
[37]
W Huang, L She, XY Chang, et al. Protein kinase LKB1 regulates polarized dendrite formation of adult hippocampal newborn neurons. Proc Natl Acad Sci USA. 2014, 111(1): 469-474.
[38]
E Taverna, WB Huttner. The Golgi apparatus in polarized neuroepithelial stem cells and their progeny: canonical and noncanonical features. Results Probl Cell Differ. 2019, 67: 359-375.
[39]
Y Arai, E Taverna. Neural progenitor cell polarity and cortical development. Front Cell Neurosci. 2017, 11: 384.
[40]
E Taverna, F Mora-Bermúdez, PJ Strzyz, et al. Non-canonical features of the Golgi apparatus in bipolar epithelial neural stem cells. Sci Rep. 2016, 6: 21206.
[41]
T Matsuki, RT Matthews, JA Cooper, et al. Reelin and stk25 have opposing roles in neuronal polarization and dendritic Golgi deployment. Cell. 2010, 143(5): 826-836.
[42]
E Förster. Reelin, neuronal polarity and process orientation of cortical neurons. Neuroscience. 2014, 269: 102-111.
[43]
M Frotscher. Role for reelin in stabilizing cortical architecture. Trends Neurosci. 2010, 33(9): 407-414.
[44]
ZG Xie, SK Hur, L Zhao, et al. A Golgi lipid signaling pathway controls apical Golgi distribution and cell polarity during neurogenesis. Dev Cell. 2018, 44(6): 725-740.e4.
[45]
EH Hong, JY Kim, JH Kim, et al. BIG2-ARF1-RhoA- mDia1 signaling regulates dendritic Golgi polarization in hippocampal neurons. Mol Neurobiol. 2018, 55(10): 7701-7716.
[46]
B Ye, Y Zhang, W Song, et al. Growing dendrites and axons differ in their reliance on the secretory pathway. Cell. 2007, 130(4): 717-729.
[47]
M Bisbal, C Conde, M Donoso, et al. Protein kinase d regulates trafficking of dendritic membrane proteins in developing neurons. J Neurosci. 2008, 28(37): 9297-9308.
[48]
C Yeaman, MI Ayala, JR Wright, et al. Protein kinase D regulates basolateral membrane protein exit from trans-Golgi network. Nat Cell Biol. 2004, 6(2): 106-112.
[49]
DM Yin, YH Huang, YB Zhu, et al. Both the establishment and maintenance of neuronal polarity require the activity of protein kinase D in the Golgi apparatus. J Neurosci. 2008, 28(35): 8832-8843.
[50]
AC Horton, B Rácz, EE Monson, et al. Polarized secretory trafficking directs cargo for asymmetric dendrite growth and morphogenesis. Neuron. 2005, 48(5): 757-771.
[51]
T Dresbach, V Torres, N Wittenmayer, et al. Assembly of active zone precursor vesicles: obligatory trafficking of presynaptic cytomatrix proteins Bassoon and Piccolo via a trans-Golgi compartment. J Biol Chem. 2006, 281(9): 6038-6047.
[52]
V Sytnyk, I Leshchyns’ka, A Dityatev, et al. Trans-Golgi network delivery of synaptic proteins in synaptogenesis. J Cell Sci. 2004, 117(Pt 3): 381-388.
[53]
A Gardiol, C Racca, A Triller. Dendritic and postsynaptic protein synthetic machinery. J Neurosci. 1999, 19(1): 168-179.
[54]
AC Horton, MD Ehlers. Dual modes of endoplasmic reticulum-to-Golgi transport in dendrites revealed by live-cell imaging. J Neurosci. 2003, 23(15): 6188-6199.
[55]
MO Caracci, LM Fuentealba, MP Marzolo. Golgi complex dynamics and its implication in prevalent neurological disorders. Front Cell Dev Biol. 2019, 7: 75.
[56]
CG Chung, MJ Kwon, KH Jeon, et al. Golgi outpost synthesis impaired by toxic polyglutamine proteins contributes to dendritic pathology in neurons. Cell Rep. 2017, 20(2): 356-369.
[57]
CY Liu, M Mei, QL Li, et al. Loss of the golgin GM130 causes Golgi disruption, Purkinje neuron loss, and ataxia in mice. Proc Natl Acad Sci USA. 2017, 114(2): 346-351.
[58]
N Ferrara. Vascular endothelial growth factor. Arterioscler Thromb Vasc Biol. 2009, 29(6): 789-791.
[59]
V Manickam, A Tiwari, JJ Jung, et al. Regulation of vascular endothelial growth factor receptor 2 trafficking and angiogenesis by Golgi localized t-SNARE syntaxin 6. Blood. 2011, 117(4): 1425-1435.
[60]
O Laufman, WJ Hong, S Lev. The COG complex interacts directly with Syntaxin 6 and positively regulates endosome-to-TGN retrograde transport. J Cell Biol. 2011, 194(3): 459-472.
[61]
FY Jin, N Hagemann, U Brockmeier, et al. LDL attenuates VEGF-induced angiogenesis via mechanisms involving VEGFR2 internalization and degradation following endosome-trans-Golgi network trafficking. Angiogenesis. 2013, 16(3): 625-637.
[62]
A Tiwari, JJ Jung, SM Inamdar, et al. The myosin motor Myo1c is required for VEGFR2 delivery to the cell surface and for angiogenic signaling. Am J Physiol Heart Circ Physiol. 2013, 304(5): H687-H696.
[63]
XH Wang, A Freire Valls, G Schermann, et al. YAP/TAZ orchestrate VEGF signaling during developmental angiogenesis. Dev Cell. 2017, 42(5): 462-478.e7.
[64]
KH Yamada, Y Nakajima, M Geyer, et al. KIF13B regulates angiogenesis through Golgi to plasma membrane trafficking of VEGFR2. J Cell Sci. 2014, 127(Pt 20): 4518-4530.
[65]
Martínez-Menárguez, M Tomás, N Martínez-Martínez, et al. Golgi fragmentation in neurodegenerative diseases: is there a common cause? Cells. 2019, 8(7): E748.
[66]
SC Su, LH Tsai. Cyclin-dependent kinases in brain development and disease. Annu Rev Cell Dev Biol. 2011, 27: 465-491.
[67]
WY Fu, Y Chen, M Sahin, et al. Cdk5 regulates EphA4-mediated dendritic spine retraction through an ephexin1-dependent mechanism. Nat Neurosci. 2007, 10(1): 67-76.
[68]
KH Sun, Y de Pablo, F Vincent, et al. Novel genetic tools reveal Cdk5’s major role in Golgi fragmentation in Alzheimer’s disease. Mol Biol Cell. 2008, 19(7): 3052-3069.
[69]
G Joshi, YJ Chi, ZP Huang, et al. Aβ-induced Golgi fragmentation in Alzheimer’s disease enhances aβ production. Proc Natl Acad Sci USA. 2014, 111(13): E1230-E1239.
[70]
FF Miao, CC Kong, Y Wu, et al. Golgi fragmentation induced by overactivated cyclin-dependent kinase 5 is associated with isoflurane-induced neurotoxicity. Neuroreport. 2018, 29(4): 241-246.
[71]
G Quassollo, J Wojnacki, DA Salas, et al. A RhoA signaling pathway regulates dendritic Golgi outpost formation. Curr Biol. 2015, 25(8): 971-982.
[72]
J Leemhuis, E Bouché, M Frotscher, et al. Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation. J Neurosci. 2010, 30(44): 14759-14772.
[73]
S Salian, TJ Cho, SR Phadke, et al. Additional three patients with Smith-McCort dysplasia due to novel RAB33B mutations. Am J Med Genet. 2017, 173(3): 588-595.
[74]
KP Harris, U Tepass. Cdc42 and vesicle trafficking in polarized cells. Traffic. 2010, 11(10): 1272-1279.
[75]
H Farhan, VW Hsu. Cdc42 and cellular polarity: emerging roles at the Golgi. Trends Cell Biol. 2016, 26(4): 241-248.
[76]
M Meseke, G Rosenberger, E Förster. Reelin and the Cdc42/ Rac1 guanine nucleotide exchange factor αPIX/Arhgef6 promote dendritic Golgi translocation in hippocampal neurons. Eur J Neurosci. 2013, 37(9): 1404-1412.
[77]
D Wang, CC Chan, S Cherry, et al. Membrane trafficking in neuronal maintenance and degeneration. Cell Mol Life Sci. 2013, 70(16): 2919-2934.
[78]
HA Lashuel, H Hirling. Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson’s disease. ACS Chem Biol. 2006, 1(7): 420-424.
[79]
AA Cooper, AD Gitler, A Cashikar, et al. Alpha- synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson’s models. Science. 2006, 313(5785): 324-328.
[80]
PG Coune, JC Bensadoun, P Aebischer, et al. Rab1A over-expression prevents Golgi apparatus fragmentation and partially corrects motor deficits in an alpha- synuclein based rat model of Parkinson’s disease. J Parkinsons Dis. 2011, 1(4): 373-387.
[81]
PH Kuhn, HH Wang, B Dislich, et al. ADAM10 is the physiologically relevant, constitutive alpha-secretase of the amyloid precursor protein in primary neurons. EMBO J. 2010, 29(17): 3020-3032.
[82]
R Epis, E Marcello, F Gardoni, et al. Blocking ADAM10 synaptic trafficking generates a model of sporadic Alzheimer’s disease. Brain. 2010, 133(11): 3323-3335.
[83]
C Saraceno, E Marcello, D Di Marino, et al. SAP97- mediated ADAM10 trafficking from Golgi outposts depends on PKC phosphorylation. Cell Death Dis. 2014, 5: e1547. .
[84]
CM Warren, S Ziyad, A Briot, et al. A ligand- independent VEGFR2 signaling pathway limits angiogenic responses in diabetes. Sci Signal. 2014, 7(307): ra1.
[85]
HJ Zhou, Z Xu, ZR Wang, et al. SUMOylation of VEGFR2 regulates its intracellular trafficking and pathological angiogenesis. Nat Commun. 2018, 9(1): 3303.
Journal of Neurorestoratology
Pages 116-128
Cite this article:
Liu J, He J, Huang Y, et al. The Golgi apparatus in neurorestoration. Journal of Neurorestoratology, 2019, 7(3): 116-128. https://doi.org/10.26599/JNR.2019.9040017

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Received: 16 July 2019
Revised: 08 September 2019
Accepted: 19 September 2019
Published: 09 October 2019
© The authors 2019

This article is published with open access at http://jnr.tsinghuajournals.com

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