Rab11-mediated recycling endosome role in nervous system development and neurodegenerative diseases

Zhang, Jiajia; Su, Gang; Wu, Qionghui; Liu, Jifei; Tian, Ye; Liu, Xiaoyan; Zhou, Jian; Gao, Juan; Chen, Wei; Chen, Deyi; Zhang, Zhenchang

doi:10.1080/00207454.2020.1761354

Cited by 15 publications

(14 citation statements)

References 74 publications

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“…Rab9 and Rab11 are important for energy metabolism: Rab9 overexpression reduces lipid storage [ 118 ]; Rab11, by affecting insulin sensitivity, is involved in diabetes pathogenesis [ 119 ]; [ 120 – 122 ] Rab1, Rab6, Rab9, and Rab11 participate in cancer progression: Rab1 regulates the development of hepatocellular carcinoma by modulating the mTOR pathway [ 120 ]; Rab6 interact with myosin II and acts as a negative regulator in multiple cancer cells, including lung cancer and osteosarcoma [ 121 ]; the progression of gastric cancer can be suppressed by inhibiting the Akt pathway via Rab9 silencing [ 122 ]; and the overexpression of Rab11 indicates poor survival time in patients with colorectal carcinoma [ 123 ]. In addition, Rab1 and Rab11 play crucial roles in the development of the nervous system[ 124 , 125 ]: Rab1 protects against neuron loss in an animal model of Parkinson’s disease [ 124 ]; decreased Rab11 is observed in multiple neurodegenerative diseases; and overexpression of Rab11 slows down the progress of these diseases [ 125 ]. Rab1, Rab6, Rab11, Rab30, and Rab33B are involved in pathogen infections: the Legionella pneumophila effector SetA modifies the GDP-bound form of Rab1, thus, regulating its activity [ 126 ]; Rab6 affects the proliferation of Staphylococcus aureus in macrophages [ 127 ]; Rab11 contributes to the assembly of the core of influenza A [ 128 ]; Rab30 is involved in the immune response to GAS infection [ 93 ]; and Rab33B participates in hepatitis B virus assembly by regulating its nucleocapsid formation and trafficking [ 129 ].…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Golgi-associated Rab GTPases implicated in autophagy

Wang

Yang

2021

Cell Biosci

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Autophagy is a conserved cellular degradation process in eukaryotes that facilitates the recycling and reutilization of damaged organelles and compartments. It plays a pivotal role in cellular homeostasis, pathophysiological processes, and diverse diseases in humans. Autophagy involves dynamic crosstalk between different stages associated with intracellular vesicle trafficking. Golgi apparatus is the central organelle involved in intracellular vesicle trafficking where Golgi-associated Rab GTPases function as important mediators. This review focuses on the recent findings that highlight Golgi-associated Rab GTPases as master regulators of autophagic flux. The scope for future research in elucidating the role and mechanism of Golgi-associated Rab GTPases in autophagy and autophagy-related diseases is discussed further.

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Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Golgi-associated Rab GTPases implicated in autophagy

Wang

Yang

2021

Cell Biosci

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“…Being the most polarized, morphologically diverse and not-dividing cell type, neurons are extremely active in membrane trafficking to maintain proper functions. Perturbation of trafficking regulation related to Cu transporters' cellular distribution and dysfunctional endocytic machinery are often observed in neurodegenerative neurons [12,[242][243][244][245][246]. Hampered by neurons' compact and complex morphology, the studies of Cu transporters' organization and response in live neurons have not been achieved.…”

Section: Conclusion Remarks and Perspectivesmentioning

confidence: 99%

Crossroads between membrane trafficking machinery and copper homeostasis in the nerve system

et al. 2021

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Imbalanced copper homeostasis and perturbation of membrane trafficking are two common symptoms that have been associated with the pathogenesis of neurodegenerative and neurodevelopmental diseases. Accumulating evidence from biophysical, cellular and in vivo studies suggest that membrane trafficking orchestrates both copper homeostasis and neural functions—however, a systematic review of how copper homeostasis and membrane trafficking interplays in neurons remains lacking. Here, we summarize current knowledge of the general trafficking itineraries for copper transporters and highlight several critical membrane trafficking regulators in maintaining copper homeostasis. We discuss how membrane trafficking regulators may alter copper transporter distribution in different membrane compartments to regulate intracellular copper homeostasis. Using Parkinson's disease and MEDNIK as examples, we further elaborate how misregulated trafficking regulators may interplay parallelly or synergistically with copper dyshomeostasis in devastating pathogenesis in neurodegenerative diseases. Finally, we explore multiple unsolved questions and highlight the existing challenges to understand how copper homeostasis is modulated through membrane trafficking.

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“…This process is essential for exosomes release and may help neurons to clear out amyloid species from inside cell to avoid engul ng lysosome machineries [45]. On the other hand, it was demonstrated that lack of expression of Rab11A may counteract the settling of tissue AD phenotypes by lowering pathological EV cargo tra c that favours the widespread of toxic species [46][47]. Loss of Rab11A expression in neurons decreases also intracellular Aβ by downregulation of its endocytosis and of axon localization of BACE1, the beta secretase that along with gamma secretase is responsible for the cleavage of APP to produce Aβ species [48][49].…”

Section: Discussionmentioning

confidence: 99%

Rab11A depletion in microglia-derived extracellular vesicle proteome upon beta-amyloid treatment

Mignogna,

Fabrizi,

Correani

et al. 2022

Preprint

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Microglia, the macrophage-like glial cells, behave as sentinels against exogenous pathogens invading the neural tissue. Their commitment is not only confined to the defensive function, but they also perform balancing trophic activities such as neuronal postnatal development, remodelling and pruning of synapses. Likewise, microglia-derived extracellular vesicles (EVs) can play strategic roles in maintaining health brain by modulating neuronal activity and by controlling neurite outgrowth as well as innate immune response. Nevertheless, strong evidence also points to their role in the development of neurodegenerative pathologies such as Alzheimer’s disease (AD). Here, we explored EV protein content released by BV2 microglial cells in resting state and after stimulation with beta-amyloid peptides (Ab), mimicking conditions occurring in AD. In the resting BV2 cells, we extended the list of proteins present in mouse microglia EV cargo with respect to those reported in Vesiclepedia exosome database while, in amyloid-triggered microglia, we highlighted a pronounced drop in EV protein content. Focusing on Rab11A, a key factor in the recycling routes of amyloid species, we observed a dramatic decrease of this protein in Aβ-treated microglia EV cargo with respect to the EVs from the untreated sample. This decrease might affect the delivery of Rab11A to neurons thus increasing the harmful amyloid burden in neuronal cells that eventually may lead to their death. We tentatively proposed that alterations observed in EVs derived from Aβ-treated microglia may represent molecular features that, among other, shape the disease-associated microglia phenotype, a recently proposed subset of microglial population, present in neurodegenerative pathologies.

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Rab11-mediated recycling endosome role in nervous system development and neurodegenerative diseases

Cited by 15 publications

References 74 publications

Golgi-associated Rab GTPases implicated in autophagy

Golgi-associated Rab GTPases implicated in autophagy

Crossroads between membrane trafficking machinery and copper homeostasis in the nerve system

Rab11A depletion in microglia-derived extracellular vesicle proteome upon beta-amyloid treatment

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