Overexpression of protocadherin 7 inhibits neuronal survival by downregulating BIRC5 in vitro

Xiao, Huajuan; Sun, Zheng; Wan, Jun; Hou, Sheng T.; Xiong, Yi

doi:10.1016/j.yexcr.2018.03.016

Cited by 11 publications

(10 citation statements)

References 37 publications

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“…The enhanced thrombus recanalization and organization in miR-126-Exo group could be attributed to the inhibition of Pcdh7 expression. Consistently, previous reports [ 29 , 30 ] have indicated that Pcdh7 is reversely correlated with angiogenesis, which could explain that angiogenesis is promoted by miR-126 mimics.…”

Section: Discussionsupporting

confidence: 91%

RETRACTED ARTICLE: Endothelial progenitor cell-derived exosomes, loaded with miR-126, promoted deep vein thrombosis resolution and recanalization

Sun

Zhang

et al. 2018

Stem Cell Res Ther

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BackgroundDeep vein thrombosis (DVT) is caused by blood clotting in the deep veins. Thrombosis resolution and recanalization can be accelerated by endothelial progenitor cells. In this report, we investigated the effects of miR-126-loaded EPC-derived exosomes (miR-126-Exo) on EPCs function and venous thrombus resolution.MethodsIn vitro promotional effect of miR-126-Exo on the migration and tube incorporation ability of EPCs was investigated via transwell assay and tube formation assay. In addition, a mouse venous thrombosis model was constructed and treated with miR-126-Exo to clarify the therapeutic effect of miR-126-Exo by histological analysis. Lastly, this study predicted a target gene of miR-126 using target prediction algorithms and confirmed it by luciferase activity assay, RT-qPCR, and Western blot.ResultsTranswell assay and tube formation assay indicated that miR-126-Exo could enhance the migration and tube incorporation ability of EPCs. Moreover, in vivo study manifested enhanced thrombus organization and recanalization after miR-126-Exo treatment. Meanwhile, we identified that Protocadherin 7 as a target gene of miR-126.ConclusionsTo sum up, our results demonstrated that EPC-derived exosomes loaded with miR-126 significantly promoted thrombus resolution in an animal model of venous thrombosis, indicating exosomes as a promising potential vehicle carrying therapeutic molecules for DVT therapy.

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Section: Discussionsupporting

confidence: 91%

RETRACTED ARTICLE: Endothelial progenitor cell-derived exosomes, loaded with miR-126, promoted deep vein thrombosis resolution and recanalization

Sun

Zhang

et al. 2018

Stem Cell Res Ther

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“…receptor [41]. Overexpression of protocadherin 7 inhibits neuronal survival [42]. As corroborating data to support findings from their GWAS analyses, Li et al reanalyzed two independent gene expression datasets and found decreased expression levels of PCDH7 in postmortem tissue of the dorsolateral prefrontal cortex in patients with schizophrenia [17].…”

Section: Pcdh7mentioning

confidence: 78%

A Systematic Review of Genome-Wide Association Studies of Antipsychotic Response

Allen

Bishop

2019

Pharmacogenomics

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Clinical symptom response to antipsychotic medications is highly variable. Genome-wide association studies (GWAS) provide a 'hypothesis-free' method of interrogating the genome for biomarkers of antipsychotic response. We performed a systematic review of GWAS findings for antipsychotic efficacy or effectiveness. 14 studies met our inclusion criteria, ten of which examined antipsychotic response using quantitative rating scales to measure symptom improvement. 15 genome-wide significant loci were identified, seven of which were replicated in other antipsychotic GWAS publications: CNTNAP5, GRID2, GRM7, 8q24 (KCNK9), PCDH7, SLC1A1 and TNIK. Notably, four replicated loci are involved in glutamatergic pathways. Additional validation and evaluation of the biological significance of these markers is warranted. These markers should also be evaluated for clinical utility, especially in the context of other validated pharmacogenomic variants (e.g., CYP450 genes). These findings may generate new avenues for development of novel antipsychotic treatments.

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“…Excessive Pcdh7 causes primary cortical neuron apoptosis via downregulation of the apoptotic inhibitor survivin (BIRC5), and effect that is mediated by the cytoplasmic CM2 domain of Pcdh7 (Xiao et al, 2018).…”

Section: Dosage Of Pcdhs In Relation To Apoptosis In the Brainmentioning

confidence: 99%

Protocadherins at the Crossroad of Signaling Pathways

Pancho

Aerts

Mitsogiannis

et al. 2020

Front. Mol. Neurosci.

102

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Protocadherins (Pcdhs) are cell adhesion molecules that belong to the cadherin superfamily, and are subdivided into clustered (cPcdhs) and non-clustered Pcdhs (ncPcdhs) in vertebrates. In this review, we summarize their discovery, expression mechanisms, and roles in neuronal development and cancer, thereby highlighting the context-dependent nature of their actions. We furthermore provide an extensive overview of current structural knowledge, and its implications concerning extracellular interactions between cPcdhs, ncPcdhs, and classical cadherins. Next, we survey the known molecular action mechanisms of Pcdhs, emphasizing the regulatory functions of proteolytic processing and domain shedding. In addition, we outline the importance of Pcdh intracellular domains in the regulation of downstream signaling cascades, and we describe putative Pcdh interactions with intracellular molecules including components of the WAVE complex, the Wnt pathway, and apoptotic cascades. Our overview combines molecular interaction data from different contexts, such as neural development and cancer. This comprehensive approach reveals potential common Pcdh signaling hubs, and points out future directions for research. Functional studies of such key factors within the context of neural development might yield innovative insights into the molecular etiology of Pcdh-related neurodevelopmental disorders.

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Overexpression of protocadherin 7 inhibits neuronal survival by downregulating BIRC5 in vitro

Cited by 11 publications

References 37 publications

RETRACTED ARTICLE: Endothelial progenitor cell-derived exosomes, loaded with miR-126, promoted deep vein thrombosis resolution and recanalization

RETRACTED ARTICLE: Endothelial progenitor cell-derived exosomes, loaded with miR-126, promoted deep vein thrombosis resolution and recanalization

A Systematic Review of Genome-Wide Association Studies of Antipsychotic Response

Protocadherins at the Crossroad of Signaling Pathways

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