Neuroplastin in Neuropsychiatric Diseases

Lin, Xiao; Liang, Yi Chu; Herrera-Molina, Rodrigo; Montag, Dirk

doi:10.3390/genes12101507

Cited by 12 publications

(11 citation statements)

References 141 publications

(188 reference statements)

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“…Among them, ICAM-1 is a cell surface glycoprotein and an adhesion receptor, which is usually expressed on the cell surface and plays an important role (43). Neuroplastin is mainly involved in neuropsychiatric diseases (44). However, Galectin is the main regulatory molecule for MSCs to exert immunosuppressive function, and MSCs can express different types of galectins (45).…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α-primed mesenchymal stem cell-derived exosomes promote M2 macrophage polarization via Galectin-1 and modify intrauterine adhesion on a novel murine model

Pan

Yang

et al. 2022

Front. Immunol.

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BackgroundIntrauterine adhesion (IUA) is a condition caused due to damage or infection of the endometrium. It is characterized by continuous inflammation and following fibrosis and dysfunction. However, the current animal IUA models have several disadvantages, including complex operation, high mortality, and many extra distractions owing to opening of the abdominal cavity to expose the uterus. Mesenchymal stem cells (MSCs), which have been used in treatment of IUA, are heterogeneous and immunosuppressive. However, their therapeutic effect is not as good as expected.MethodsHere, we successfully built a new murine IUA model, called electric tool-scratching IUA model, and applied it in our experiments to investigate the efficacy of tumor necrosis factor-α (TNF-α) primed MSCs (T-MSCs). In the new model, we used a self-made electric tool that can cause mechanical damage to the endometrium without opening the abdominal cavity. ELISA and histological staining analysis were performed to evaluate pathological features of IUA. qRT-PCR, flow cytometry and immunofluoresence staining were performed to detect the phenotypes of macrophages. TMT proteomics quantification and western blotting assay were performed to analyze the differentially expressed proteins of MSC exosomes.ResultsBased on the new IUA model, we found TNF-α pretreatment could enhance the ability of MSCs to relieve inflammation and reduce endometrium fibrosis. Mechanistically, T-MSC promoted macrophage polarization to M2 phenotype through exosomes. Subsequently, we found the expression of Galectin-1 was increased in T-MSC exosomes. Finally, we analyzed the gene expression pattern of Galectin-1 treated macrophages and found Galectin-1 promoted macrophage polarization to M2 phenotype mainly through the Jak-STAT signaling pathway.ConclusionsOur studies proposed an innovative mouse model and a better MSC treatment strategy for IUA.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α-primed mesenchymal stem cell-derived exosomes promote M2 macrophage polarization via Galectin-1 and modify intrauterine adhesion on a novel murine model

Pan

Yang

et al. 2022

Front. Immunol.

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“…The two Neuroplastin isoforms (Np65 and Np55) are heavily glycosylated transmembrane proteins and members of the immunoglobulin-superfamily of cell adhesion molecules. Neuroplastin has been involved in synaptic plasticity, is essential for cognition, long-term potentiation, and associative memory formation, in addition to being implicated in Alzheimer's disease [9][10][11][12][13][14][15][16][17][18][19][20]; for a recent review see Ilic et al 2021 and Lin et al 2021 [19,20]. We reported that Neuroplastin expression is altered in the brains of mice lacking complex gangliosides [21], using a genetically engineered mouse model that lacks the GM2/GD2 synthase enzyme.…”

Section: Introductionmentioning

confidence: 86%

Plasma Membrane Calcium ATPase-Neuroplastin Complexes Are Selectively Stabilized in GM1-Containing Lipid Rafts

Ilić

Lin

Malci

et al. 2021

IJMS

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The recent identification of plasma membrane (Ca2+)-ATPase (PMCA)-Neuroplastin (Np) complexes has renewed attention on cell regulation of cytosolic calcium extrusion, which is of particular relevance in neurons. Here, we tested the hypothesis that PMCA-Neuroplastin complexes exist in specific ganglioside-containing rafts, which could affect calcium homeostasis. We analyzed the abundance of all four PMCA paralogs (PMCA1-4) and Neuroplastin isoforms (Np65 and Np55) in lipid rafts and bulk membrane fractions from GM2/GD2 synthase-deficient mouse brains. In these fractions, we found altered distribution of Np65/Np55 and selected PMCA isoforms, namely PMCA1 and 2. Cell surface staining and confocal microscopy identified GM1 as the main complex ganglioside co-localizing with Neuroplastin in cultured hippocampal neurons. Furthermore, blocking GM1 with a specific antibody resulted in delayed calcium restoration of electrically evoked calcium transients in the soma of hippocampal neurons. The content and composition of all ganglioside species were unchanged in Neuroplastin-deficient mouse brains. Therefore, we conclude that altered composition or disorganization of ganglioside-containing rafts results in changed regulation of calcium signals in neurons. We propose that GM1 could be a key sphingolipid for ensuring proper location of the PMCA-Neuroplastin complexes into rafts in order to participate in the regulation of neuronal calcium homeostasis.

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“…The adhesive and synaptic functions of neuroplastin and its role in neuronal plasticity were reviewed previously 1 https://www.ptsd.va.gov/understand/common/common_adults.asp (Owczarek and Berezin, 2012;Beesley P. W. et al, 2014). Our recent review summarizes the role of neuroplastin and its binding partners in molecular pathways underlying neuropsychiatric and neurodegenerative diseases such as schizophrenia, depression, or Alzheimer's disease (Lin et al, 2021b).…”

Section: Neuroplastin a Cell Recognition Molecule Of The Immunoglobulin Superfamily Acts Also As A Subunit Of Plasma Membrane Calcium Atpmentioning

confidence: 99%

“…As mentioned above, neuroplastin engages in numerous interactions with other molecules (for review: Lin et al, 2021b) and disturbance of these interactions might be involved in retrograde amnesia. However, the recent identification of a decisive role of neuroplastin for Ca 2+ extrusion via PMCAs suggests an attractive integrating explanation.…”

Section: The Calcium Hypothesis: a Potential Mechanism Underlying Retrograde Amnesia Caused By Neuroplastin Lossmentioning

confidence: 99%

Retrograde Amnesia – A Question of Disturbed Calcium Levels?

Montag

2021

Front. Cell. Neurosci.

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Retrograde amnesia is the inability to remember events or information. The successful acquisition and memory of information is required before retrograde amnesia may occur. Often, the trigger for retrograde amnesia is a traumatic event. Loss of memories may be caused in two ways: either by loss/erasure of the memory itself or by the inability to access the memory, which is still present. In general, memories and learning are associated with a positive connotation although the extinction of unpleasant experiences and memories of traumatic events may be highly welcome. In contrast to the many experimental models addressing learning deficits caused by anterograde amnesia, the incapability to acquire new information, retrograde amnesia could so far only be investigated sporadically in human patients and in a limited number of model systems. Apart from models and diseases in which neurodegeneration or dementia like Alzheimer’s disease result in loss of memory, retrograde amnesia can be elicited by various drugs of which alcohol is the most prominent one and exemplifies the non-specific effects and the variable duration. External or internal impacts like traumatic brain injury, stroke, or electroconvulsive treatments may similarly result in variable degrees of retrograde amnesia. In this review, I will discuss a new genetic approach to induce retrograde amnesia in a mouse model and raise the hypothesis that retrograde amnesia is caused by altered intracellular calcium homeostasis. Recently, we observed that neuronal loss of neuroplastin resulted in retrograde amnesia specifically for associative memories. Neuroplastin is tightly linked to the expression of the main Ca2+ extruding pumps, the plasma membrane calcium ATPases (PMCAs). Therefore, neuronal loss of neuroplastin may block the retrieval and storage of associative memories by interference with Ca2+ signaling cascades. The possibility to elicit retrograde amnesia in a controlled manner allows to investigate the underlying mechanisms and may provide a deeper understanding of the molecular and circuit processes of memory.

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Neuroplastin in Neuropsychiatric Diseases

Cited by 12 publications

References 141 publications

Tumor necrosis factor-α-primed mesenchymal stem cell-derived exosomes promote M2 macrophage polarization via Galectin-1 and modify intrauterine adhesion on a novel murine model

Tumor necrosis factor-α-primed mesenchymal stem cell-derived exosomes promote M2 macrophage polarization via Galectin-1 and modify intrauterine adhesion on a novel murine model

Plasma Membrane Calcium ATPase-Neuroplastin Complexes Are Selectively Stabilized in GM1-Containing Lipid Rafts

Retrograde Amnesia – A Question of Disturbed Calcium Levels?

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