Cell‐ and region‐specific expression of depression‐related protein p11 (S100a10) in the brain

Milosevic, Ana; Liebmann, Thomas; Knudsen, Margarete Grace; Schintu, Nicoletta; Svenningsson, Per; Greengard, Paul

doi:10.1002/cne.24113

Cited by 39 publications

(33 citation statements)

References 94 publications

(157 reference statements)

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“…p11 in hippocampal cells is essential in mediating the response to antidepressants (12). In this brain region, p11 is highly enriched in PV and cholecystokinin GABAergic interneurons (13). In cholecystokinin cells, p11 regulates the surface levels of the 5-HT 1B serotonergic receptor to initiate the response to antidepressants, an effect mediated by disinhibition of PV cells (14).…”

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confidence: 99%

Reduced Kv3.1 Activity in Dentate Gyrus Parvalbumin Cells Induces Vulnerability to Depression

Medrihan¹,

Umschweif

Sinha

et al. 2020

Biological Psychiatry

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BACKGROUND: Parvalbumin (PV)-expressing interneurons are important for cognitive and emotional behaviors. These neurons express high levels of p11, a protein associated with depression and action of antidepressants. METHODS: We characterized the behavioral response to subthreshold stress in mice with conditional deletion of p11 in PV cells. Using chemogenetics, viral-mediated gene delivery, and a specific ion channel agonist, we studied the role of dentate gyrus PV cells in regulating anxiety-like behavior and resilience to stress. We used electrophysiology, imaging, and biochemical studies in mice and cells to elucidate the function and mechanism of p11 in dentate gyrus PV cells. RESULTS: p11 regulates the subcellular localization and cellular level of the potassium channel Kv3.1 in cells. Deletion of p11 from PV cells resulted in reduced hippocampal level of Kv3.1, attenuated capacity of high-frequency firing in dentate gyrus PV cells, and altered short-term plasticity at synapses on granule cells, as well as anxiety-like behavior and a pattern separation deficit. Chemogenetic inhibition or deletion of p11 in these cells induced vulnerability to depressive behavior, whereas upregulation of Kv3.1 in dentate gyrus PV cells or acute activation of Kv3.1 using a specific agonist induced resilience to depression. CONCLUSIONS: The activity of dentate gyrus PV cells plays a major role in the behavioral response to novelty and stress. Activation of the Kv3.1 channel in dentate gyrus PV cells may represent a target for the development of celltype specific, fast-acting antidepressants.

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confidence: 99%

Reduced Kv3.1 Activity in Dentate Gyrus Parvalbumin Cells Induces Vulnerability to Depression

Medrihan¹,

Umschweif

Sinha

et al. 2020

Biological Psychiatry

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“…Yet, we have seen some marker genes differentially expressed in only one of the clusters. For instance, radial glial markers s100a10 (Milosevic et al, 2017) and cx43 (Duval et al, 2002) are expressed in only one of the dRGC, mRGC and vRGC clusters (dRGC1, mRGC1, vRGC1; Dataset S1B). Since these genes are associated with a more progenitor state of the radial glia, we can speculate that s100a10+/cx43+ clusters could represent a radial glial state that is more progenitor-like.…”

Section: Resultsmentioning

confidence: 99%

Single cell analyses of the effects of Amyloid-beta42 and Interleukin-4 on neural stem/progenitor cell plasticity in adult zebrafish brain

Coşacak

Bhattarai

Zhang

et al. 2018

Preprint

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Neural stem cells (NSCs) constitute the reservoir for new cells and might be harnessed for stem cell-based regenerative therapies. Zebrafish has remarkable ability to regenerate its brain by inducing NSC plasticity upon Alzheimer’s pathology. We recently identified that NSCs enhance their proliferation and neurogenic outcome in an Amyloid-beta42-based (Aβ42) experimental Alzheimer’s disease model in zebrafish brain and Interleukin-4 (IL4) is a critical molecule for inducing NSC proliferation in AD conditions. However, the mechanisms by which Aβ42 and IL4 affect NSCs remained unknown. Using single cell transcriptomics, we determined distinct subtypes of NSCs and neurons in adult zebrafish brain, identified differentially expressed genes after Aβ42 and IL4 treatments, analyzed the gene ontology and pathways that are affected by Aβ42 and IL4, and investigated how cell-cell communication is altered through secreted molecules and their receptors. Our results constitute the most extensive resource in the Alzheimer’s disease model of adult zebrafish brain, are likely to provide unique insights into how Aβ42/IL4 affects NSC plasticity and yield in novel drug targets for mobilizing neural stem cells for endogenous neuro-regeneration.

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“…Several reports have shown that the depression disorder is regulated by the 5-HT1B receptor. Recently, it was documented that S100A10 is potentially able to be involved in the regulation of depression [76] through its distribution in the brain that is relative to the depression-like behavioral phenotype [76] or interacting with 5-HT1B receptor [77]. S100A10 distributes widely in the vertebrate body containing the brain in which the expression of S100A10 is subsistent in some neurons and nonneuronal cells as well as is discrepant within disparate regions.…”

Section: The Role Of S100a10 In Non-tumor Diseasesmentioning

confidence: 99%

Critical role and its underlying molecular events of the plasminogen receptor, S100A10 in malignant tumor and non-tumor diseases

Li¹,

Ma²,

Fei³

et al. 2020

J. Cancer

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S100A10 is a small molecular weight protein expressed in the cytoplasm of many cells and one of the members of the S100 protein family that binds calcium and forms the largest subgroup of EF-hand proteins. The regulatory processes of S100A10 are complicated. S100A10 participates in the regulation of a variety of tumor and non-tumor diseases through cascade reactions with multitudinous signaling molecules. In malignant tumors, such as acute promyelocytic leukemia (APL) and lung cancer, S100A10 is likely involved in their progression, including invasion and metastasis through the regulation of plasmin production and subsequent plasmin-dependent stimulation of other proteases, such as matrix metalloproteinase (MMP)-2 and -9. Both the plasmin and MMPs are capable of inducing degradation of the extracellular matrix (ECM) and basement membrane, which is a critical step for tumor progression. In non-tumor diseases, the distribution of S100A10 in the brain and its interaction with 5-hydroxytryptamine 1B (5-HT1B) receptor, an important mediator in the central nervous system that maintains a dynamic balance of the neurotransmitters, correlates with depression-like behavior. S100A10 also participates in inflammatory responses through the regulation of peripheral macrophage migration to the inflammatory sites, which depends on the generation of plasmin and other proteinases at the surface of macrophages. Considerable attention should be paid to understand the significant role of S100A10 in the modulation of malignant tumor and non-tumor diseases.

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Cell‐ and region‐specific expression of depression‐related protein p11 (S100a10) in the brain

Cited by 39 publications

References 94 publications

Reduced Kv3.1 Activity in Dentate Gyrus Parvalbumin Cells Induces Vulnerability to Depression

Reduced Kv3.1 Activity in Dentate Gyrus Parvalbumin Cells Induces Vulnerability to Depression

Single cell analyses of the effects of Amyloid-beta42 and Interleukin-4 on neural stem/progenitor cell plasticity in adult zebrafish brain

Critical role and its underlying molecular events of the plasminogen receptor, S100A10 in malignant tumor and non-tumor diseases

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