Roles of GluN2C in cerebral ischemia: GluN2C expressed in different cell types plays different role in ischemic damage

Ding, Yue; Wang, Le; Huo, Yuexiang; Sun, Yanping; Wang, Long; Sun, Yongjun

doi:10.1002/jnr.24574

Cited by 8 publications

(1 citation statement)

References 72 publications

(130 reference statements)

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“…Among NMDA receptor subunits, GluN2C is characterized with low sensitivity to magnesium block, low conductance, low calcium permeability and low opening probability. It was reported that neuronal GluN2C confer protective effects, whereas oligodendrocytic and astrocytic GluN2C mediates detrimental effects (reviewed in Ding et al, 2020). Therefore, the high expression of GRIN2C in the neuronal subcluster UnN3 might mediate protective effects.…”

Section: Integrated Sc/snrna-seq Dataset Offers Insights Into Parkins...mentioning

confidence: 99%

Cell–Cell Communication Alterations via Intercellular Signaling Pathways in Substantia Nigra of Parkinson’s Disease

Huang

Liu

et al. 2022

Front. Aging Neurosci.

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Parkinson’s disease (PD) is a neurodegenerative movement disorder characterized with dopaminergic neuron (DaN) loss within the substantia nigra (SN). Despite bulk studies focusing on intracellular mechanisms of PD inside DaNs, few studies have explored the pathogeneses outside DaNs, or between DaNs and other cells. Here, we set out to probe the implication of intercellular communication involving DaNs in the pathogeneses of PD at a systemic level with bioinformatics methods. We harvested three online published single-cell/single-nucleus transcriptomic sequencing (sc/snRNA-seq) datasets of human SN (GSE126838, GSE140231, and GSE157783) from the Gene Expression Omnibus (GEO) database, and integrated them with one of the latest integration algorithms called Harmony. We then applied CellChat, the latest cell–cell communication analytic algorithm, to our integrated dataset. We first found that the overall communication quantity was decreased while the overall communication strength was enhanced in PD sample compared with control sample. We then focused on the intercellular communication where DaNs are involved, and found that the communications between DaNs and other cell types via certain signaling pathways were selectively altered in PD, including some growth factors, neurotrophic factors, chemokines, etc. pathways. Our bioinformatics analysis showed that the alteration in intercellular communications involving DaNs might be a previously underestimated aspect of PD pathogeneses with novel translational potential.

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Section: Integrated Sc/snrna-seq Dataset Offers Insights Into Parkins...mentioning

confidence: 99%

Cell–Cell Communication Alterations via Intercellular Signaling Pathways in Substantia Nigra of Parkinson’s Disease

Huang

Liu

et al. 2022

Front. Aging Neurosci.

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Progresses in GluN2A-containing NMDA Receptors and their Selective Regulators

Niu

Yang

et al. 2022

Cell Mol Neurobiol

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Suppression of FPR2 expression inhibits inflammation in preeclampsia by improving the biological functions of trophoblast via NF-κB pathway

Zhai

et al. 2022

J Assist Reprod Genet

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Purpose The dysfunction of trophoblast during inflammation plays an important role in PE. Formyl peptide receptor 2 (FPR2) plays crucial roles in the development of inflammation-associated disease. This present study aimed to explore the effect of FPR2 on a trophoblast cellular model of preeclampsia. Methods The expression of FPR2 in placenta was detected by immunohistochemical staining and western blotting. Transfection of siRNA was used to knockdown FPR2 in HTR-8/SVneo cells. Inflammatory cytokines were detected by ELISA. CCK8, Transwell, wound healing, FACS and tube formation assays were performed to observe the abilities of cell proliferation, migration, invasion, apoptosis and angiogenesis. Western blotting was implemented to clarify that NF-κB signaling pathway was downstream of FPR2. Results The expression levels of FPR2 were higher in placental tissues of patients with PE. Knockdown of FPR2 expression by siFPR2 or inhibition of its activity by WRW4 decreased the release of proinflammatory cytokines in HTR8/SVneo cells treated with LPS. Knockdown of FPR2 expression or inhibition of its activity further reversed the LPS-induced attenuation of the proliferation, migration, invasion and angiogenesis and increase in apoptosis in HTR8/SVneo cells. Moreover, the NF-κB signaling pathway was activated in both placental tissues of patients with PE and LPS-treated HTR8/SVneo cells. However, the activation was attenuated when FPR2 was knocked down or inhibited. Conclusion Suppression of FPR2 expression alleviated the effects of inflammation induced by LPS on trophoblasts via the NF-κB signaling pathway, which provided a novel and potential strategy for the treatment of PE.

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Roles of GluN2C in cerebral ischemia: GluN2C expressed in different cell types plays different role in ischemic damage

Cited by 8 publications

References 72 publications

Cell–Cell Communication Alterations via Intercellular Signaling Pathways in Substantia Nigra of Parkinson’s Disease

Cell–Cell Communication Alterations via Intercellular Signaling Pathways in Substantia Nigra of Parkinson’s Disease

Progresses in GluN2A-containing NMDA Receptors and their Selective Regulators

Suppression of FPR2 expression inhibits inflammation in preeclampsia by improving the biological functions of trophoblast via NF-κB pathway

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