Mn-Induced Neurocytes Injury and Autophagy Dysfunction in Alpha-Synuclein Wild-Type and Knock-Out Mice: Highlighting the Role of Alpha-Synuclein

Yan, Dong-Ying; Liu, Chang; Tan, Xuan; Ma, Zhuo; Wang, Can; Deng, Yu; Liu, Wei; Xu, Zhenbo; Xu, Bin

doi:10.1007/s12640-019-00016-y

Cited by 32 publications

(29 citation statements)

References 37 publications

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“…Although Tre did not improve Mn‐induced locomotor activity impairment in mice, our results support the idea strongly that Tre could enhance mitophagy and protect mitochondrial damage. Occupational or environmental exposure to Mn can affect nigrostriatal neuronal circuitry and subsequent behavioural and motor impairments . Mn neurotoxicity appears to be regulated by multiple factors, including oxidative injury, mitochondrial dysfunction, protein misfolding and neuroinflammation .…”

Section: Discussionmentioning

confidence: 99%

“…Tre was given earlier than the Mn injection for 7 days. The volume of MnCl 2 injection was 2 mL/kg body‐weight, five times per week for 6 weeks . The concentration of blood glucose in mice during 7 weeks of Tre administration was detected using the Kit from Solarbio.…”

Section: Methodsmentioning

confidence: 99%

“…Then, immunomagnetic beads (A + G) were mixed in antigen‐antibody complex and incubated for 4 hours at 4℃. The mixture was aggregated by magnetic separation and followed by Western blot analysis …”

Section: Methodsmentioning

confidence: 99%

“…The volume of MnCl 2 injection was 2 mL/kg body-weight, five times per week for 6 weeks. 18 The concentration of blood glucose in mice during 7 weeks of Tre administration was detected using the Kit from Solarbio. The animal experiment was conducted in accordance with the National Institutes of Health Guidelines for the Care and Use of Laboratory Animals and approved by the Laboratory Animal Center of China Medicine University (approval NO.…”

Section: Animalsmentioning

confidence: 99%

“…To evaluate the formation of autophagic vesicles, singlecell suspension was prepared from striatal tissue and cells (1 × 10 6 ) were stained with monodansylcadaverine (MDC) (50 mM in a solution of DMSO, 50 μM final concentration) at 37℃ away from light for 45 minutes. 18 Then, the cells were finally resuspended in 0.5 mL binding buffer. The fluorescence intensity was performed with a flow cytometer (BD FACS Canto II).…”

Section: Detection Of Autophagic Vacuolesmentioning

confidence: 99%

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Effect of trehalose on manganese‐induced mitochondrial dysfunction and neuronal cell damage in mice

Liu

Jing

Liu

et al. 2019

Basic Clin Pharma Tox

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Chronic overexposure to manganese (Mn) has been verified to induce mitochondrial dysfunction, which is related to oxidative damage. The autophagic‐lysosomal degradation pathway plays a vital role in the removal of impaired mitochondria through a specific quality control mechanism termed mitophagy. However, trehalose functions as an inducer of autophagy by an mTOR‐independent mechanism, and little data report its effect on Mn‐induced mitochondrial dysfunction. To explore the possibility that trehalose could be effective in interfering with the Mn‐induced mitochondrial dysfunction, we used trehalose (2% and 4% (g/vol (mL))) in a mouse model of manganism. Our data showed that mice developed weary motor and behavioural deficits after exposure to Mn for 6 weeks. Overexposure to Mn resulted in mitochondrial dysfunction and neuronal cell damage in the basal nuclei of mice, which could be ameliorated by trehalose pre‐treatment. Moreover, our results indicated that trehalose pre‐treatment significantly reduced the oxidative damage and enhanced the activation of mitophagy. The findings clearly demonstrated that trehalose could relieve Mn‐induced mitochondrial and neuronal cell damage through its antioxidative and mitophagy‐inducing effects.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Animalsmentioning

confidence: 99%

Section: Detection Of Autophagic Vacuolesmentioning

confidence: 99%

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Effect of trehalose on manganese‐induced mitochondrial dysfunction and neuronal cell damage in mice

Liu

Jing

Liu

et al. 2019

Basic Clin Pharma Tox

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Transition metals and metal complexes in autophagy and diseases

Luo

Huang

et al. 2021

Journal Cellular Physiology

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Transition metals refer to the elements in the d and ds blocks of the periodic table. Since the success of cisplatin and auranofin, transition metal‐based compounds have become a prospective source for drug development, particularly in cancer treatment. In recent years, extensive studies have shown that numerous transition metal‐based compounds could modulate autophagy, promising a new therapeutic strategy for metal‐related diseases and the design of metal‐based agents. Copper, zinc, and manganese, which are common components in physiological pathways, play important roles in the progression of cancer, neurodegenerative diseases, and cardiovascular diseases. Furthermore, enrichment of copper, zinc, or manganese can regulate autophagy. Thus, we summarized the current advances in elucidating the mechanisms of some metals/metal‐based compounds and their functions in autophagy regulation, which is conducive to explore the intricate roles of autophagy and exploit novel therapeutic drugs for human diseases.

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Involvement of calcium homeostasis and unfolded protein response in autophagy co-induced by molybdenum and cadmium in duck (Anas platyrhyncha) brain

Lin

Nie

et al. 2022

Environ Sci Pollut Res

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Mn-Induced Neurocytes Injury and Autophagy Dysfunction in Alpha-Synuclein Wild-Type and Knock-Out Mice: Highlighting the Role of Alpha-Synuclein

Cited by 32 publications

References 37 publications

Effect of trehalose on manganese‐induced mitochondrial dysfunction and neuronal cell damage in mice

Effect of trehalose on manganese‐induced mitochondrial dysfunction and neuronal cell damage in mice

Transition metals and metal complexes in autophagy and diseases

Involvement of calcium homeostasis and unfolded protein response in autophagy co-induced by molybdenum and cadmium in duck (Anas platyrhyncha) brain

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