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Journal of Neurorestoratology  2019, Vol. 7 Issue (3): 116-128    doi: 10.26599/JNR.2019.9040017
Review Article     
The Golgi apparatus in neurorestoration
Jianyang Liu,Jialin He,Yan Huang,Han Xiao,Zheng Jiang,Zhiping Hu(✉)()
Department of Neurology, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan, China
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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.

Key wordsGolgi apparatus      neurogenesis      synaptogenesis      angiogenesis      neurodegeneration     
Received: 16 July 2019      Published: 09 October 2019
Corresponding Authors: Zhiping Hu     E-mail:
About author: Jianyang Liu, MM, Department of Neurology of the Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China. She focuses on the neuroprotection of cerebrovascular disease. E-mail address:|Jialin He, MM, Department of Neurology of the Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China. She focuses on the neuroprotection of cerebrovascular disease. E-mail address:|Yan Huang, MD, Key laboratory of Protein Chemistry and Developmental Biology of Ministry of Education, College of Life Sciences, Hunan Normal University, Changsha, Hunan Province, China. She focuses on the role of the Golgi apparatus in the cerebrovascular disease. E-mail address:|Han Xiao, MD, Department of Neurology of the Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China. She focuses on the treatment of cerebrovascular disease. E-mail address:|Zheng Jiang, MD, Department of Neurology of the Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China. He focuses on the role of the Golgi apparatus in the cerebrovascular disease. E-mail address:|Zhiping Hu, MD, Department of Neurology of the Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China. He focuses on the molecular mechanism and molecular targeted therapy of ischemic stroke, and the role of the Golgi apparatus in neuroprotection. E-mail address:
Cite this article:

Jianyang Liu,Jialin He,Yan Huang,Han Xiao,Zheng Jiang,Zhiping Hu. The Golgi apparatus in neurorestoration. Journal of Neurorestoratology, 2019, 7: 116-128.

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Fig. 1Possible links between Golgi stress, Golgi fragmentation, and neurodegeneration. Stress signal enables the sensing of Golgi stress, which acts as a positive feedback module that enhances stress signaling. If the stress is very severe, it contributes to Golgi fragmentation and subsequently apoptosis, polarized dendrite morphogenesis abnormalities, axon transport dysfunction, and synapse degeneration, eventually resulting in neurodegeneration.
Fig. 2Signaling pathways regulating Golgi distribution and neuronal polarity during neurogenesis. (1) STK25 and Mst4, downstream effectors of LKB1, co-immunoprecipitate with STRAD and bind to the Golgi matrix protein GM130. These two effectors are enriched in the Golgi apparatus and essential for Golgi organization. (2) The lipid transfer proteins (PITPNA/PITPNB) potentiate the PI4P-dependent recruitment of GOLPH3 to the Golgi apparatus, which promotes MYO18A-directed localization of the Golgi to the apical compartment. (3) Reelin and Dab1 regulate Golgi extension into the apical process of pyramidal neurons. (4) BIG2–ARF1–RhoA–mDia1 signaling regulates dendritic Golgi deployment and dendrite growth in adult newborn hippocampal neurons.
MoleculesIn vivo modelIn vitro modelAssociation with the Golgi apparatusFunction in angiogenesisReference
Syntaxin 6Syntaxin 6-cyto-treated mouse earSyntaxin 6-deficient HUVECInhibiting syntaxin 6 increase VEGFR2 trafficking from Golgi to the lysosomes for degradation, without the inhibition of VEGFR2 synthesisSyntaxin 6 deletion reduces plasma membrane and total cellular VEGFR2 expression and blocks angiogenesis[59]
Syntaxin 16NALDL-exposed HUVECRegulates endosome–trans- Golgi network trafficking of VEGFR2Syntaxin 16 deletion increases total cellular VEGFR2 expression and may promote angiogenesis[61]
Myosin 1cNAMyosin 1c-deficient HUVECMyosin 1c depletion results in increased VEGFR2 trafficking from the Golgi to lysosomes for degradationMyosin 1c deletion reduces plasma membrane and total cellular VEGFR2 expression and blocks angiogenesis[62]
KIF13BMice injected with KIF13B-shRNA- treated MatrigelKIF13B-knockdown HUVECKIF13B interacting with VEGFR2 cargo and microtubules in the Golgi initiates VEGFR2 traffickingKIF13B deletion reduces VEGFR2 plasma membrane expression and blocks angiogenesis[64]
Src family kinasesDiabetic miceHigh-glucose- exposed HUVECSrc family kinases mediate ROS-induced VEGFR2 phosphorylation, which reduces VEGFR2 abundance in the GolgiSrc family kinases reduce cell surface VEGFR2 abundance and block angiogenesis[84]
YAP/TAZYAP/TAZ- ECKO miceYAP/TAZ-knockdown HBMECYAP/TAZ deletion impairs VEGFR2 exit from TGNYAP/TAZ deletion reduces VEGFR2 plasma membrane expression and blocks angiogenesis[63]
SENP1SENP1-ECKO miceSENP1-deficient HUVECSENP1 deletion induces VEGFR2 hyper-SUMOylation and accumulation of VEGFR2 in the GolgiSENP1 deletion reduces VEGFR2 plasma membrane expression and blocks angiogenesis[85]
Table 1Golgi apparatus-related molecular machinery regulating VEGFR2 expression in angiogenesis.
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