VPS35 regulates developing mouse hippocampal neuronal morphogenesis by promoting retrograde trafficking of BACE1

Wang, C. L.; Tang, Fu Lei; Peng, Yun; Shen, Cheng Yong; Mei, Lin; Xiong, Wen Cheng

doi:10.1242/bio.20122451

Cited by 69 publications

(83 citation statements)

References 46 publications

(71 reference statements)

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“…Modulating the localization of BACE1 in synaptic terminals is an alternative approach for decreasing amyloid deposition. Recent studies showed that either increased axonal transport of BACE1 by calsyntenin 1 (53) or retrograde transport by vps35 significantly altered amyloid deposition (56). Transgenic mice overexpressing RTN3 have reduced amyloid deposition (23,35,36,57), and this reduction is partially attributable to reduced BACE1 in presynaptic terminals in response to overexpression of RTN3 in mouse neurons.…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Reticulon 3 in Neurons Leads to Reduced Axonal Transport of β Site Amyloid Precursor Protein-cleaving Enzyme 1

Deng

Tan

et al. 2013

Journal of Biological Chemistry

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Background: Axonal transport of BACE1 and the regulation of BACE1 synaptic localization remain to be fully characterized. Results: Colocalization of BACE1 with synaptophysin was reduced by overexpression of RTN3. This reduction was due to reduced BACE1 axonal transport. Conclusion: Increased interaction of RTN3 with BACE1 in the soma impacts axonal transport of BACE1. Significance: Changes of BACE1 synaptic localization potentially alter synaptic A␤ generation and amyloid deposition.

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Section: Discussionmentioning

confidence: 99%

Increased Expression of Reticulon 3 in Neurons Leads to Reduced Axonal Transport of β Site Amyloid Precursor Protein-cleaving Enzyme 1

Deng

Tan

et al. 2013

Journal of Biological Chemistry

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“…Briefly, VPS35 knockdown (KD) in mouse embryonic hippocampal neurons results in shortened apical dendrites, reduced dendritic spines and swollen commissural axons [97].…”

Section: Evidence For a Developmental Component Of Pd: Deregulated Emmentioning

confidence: 99%

“…Little is known about the role of VPS35 in neurogenesis partly because homozygous KO mice die early during embryonic development, before E10 and before the onset of neurogenesis [231]. In one study focusing on Alzheimer's disease by Wang et al [97], VPS35 was shown to promote apical dendritic growth and maturation and axonal protein transport in developing mouse hippocampal neurons. The authors demonstrated that embryonic hippocampal CA1 neurons with reduced VPS35 expression (via electroporation with microRNAs) display shortened apical dendrites, less dendritic spines and swollen commissural axons.…”

Section: Vps35 (Park17)mentioning

confidence: 99%

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

Grand

Gonzalez-Cano

Pavlou

et al. 2014

Cell. Mol. Life Sci.

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Parkinson's disease (PD) is the second most common neurodegenerative disorder, leading to a variety of motor and non-motor symptoms. Interestingly, nonmotor symptoms often appear a decade or more before the first signs of motor symptoms. Some of these non-motor symptoms are remarkably similar to those observed in cases of impaired neurogenesis and several PD-related genes have been shown to play a role in embryonic or adult neurogenesis. Indeed, animal models deficient in Nurr1, Pitx3, SNCA and PINK1 display deregulated embryonic neurogenesis and LRRK2 and VPS35 have been implicated in neuronal development-related processes such as Wnt/bcatenin signaling and neurite outgrowth. Moreover, adult neurogenesis is affected in both PD patients and PD animal models and is regulated by dopamine and dopaminergic (DA) receptors, by chronic neuroinflammation, such as that observed in PD, and by differential expression of wild-type or mutant forms of PD-related genes. Indeed, an increasing number of in vivo studies demonstrate a role for SNCA and LRRK2 in adult neurogenesis and in the generation and maintenance of DA neurons. Finally, the roles of PDrelated genes, SNCA, LRRK2, VPS35, Parkin, PINK1 and DJ-1 have been studied in NSCs, progenitor cells and induced pluripotent stem cells, demonstrating a role for some of these genes in stem/progenitor cell proliferation and maintenance. Together, these studies strongly suggest a link between deregulated neurogenesis and the onset and progression of PD and present strong evidence that, in addition to a neurodegenerative disorder, PD can also be regarded as a developmental disorder.

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“…2). Later, studies showed that Vps35 depletion in neurons makes impairment of BACE1 retrieval and redistribution of BACE1 [59]. Sortilin, a Vps10p domain-sorting receptor, also participates in BACE1 retrograde trafficking.…”

Section: The Role Of Retromer Complex In Bace1 Traffickingmentioning

confidence: 99%

The Role of Retromer in Alzheimer’s Disease

Zhang

Tan

et al. 2015

Mol Neurobiol

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The retromer complex is an important component of the endosomal protein sorting machinery and mediates protein cargoes from endosomes to the trans-Golgi network (TGN) by retrograde pathway or to the cell surface through recycling pathway. Studies show that retromer and its receptors can make amyloid precursor protein (APP)/β-site APP-cleaving enzyme 1 (BACE1) away endosomes that reduces the production of amyloid β (Aβ). And, tetramer is also found to regulate phagocytic receptors to the plasma membrane of microglia, where some phagocytic receptors take part in Aβ clearance. Therefore, disruption of retromer will increase the production of Aβ. Recently, a plausible relationship between disturbance of retromer and tauopathies is raised. Retromer dysfunction may result in decreasing the clearance of extracellular tau and the level of cathepsin D, which enables tau-induced neurotoxicity. This review article summarizes the structure and function of retromer and its role in pathogenesis of AD. In the end, retromer may provide a potential therapeutic strategy for the treatment of AD.

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VPS35 regulates developing mouse hippocampal neuronal morphogenesis by promoting retrograde trafficking of BACE1

Cited by 69 publications

References 46 publications

Increased Expression of Reticulon 3 in Neurons Leads to Reduced Axonal Transport of β Site Amyloid Precursor Protein-cleaving Enzyme 1

Increased Expression of Reticulon 3 in Neurons Leads to Reduced Axonal Transport of β Site Amyloid Precursor Protein-cleaving Enzyme 1

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

The Role of Retromer in Alzheimer’s Disease

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