Involvement of JNK1 in Neuronal Polarization During Brain Development

Castro-Torres, Rubén Darío; Busquets, Oriol; Parcerisas, Antoni; Verdaguer, Ester; Olloquequi, Jordi; Ettcheto, Miren; Beas‐Zárate, Carlos; Folch, Jaume; Camins, Antoni; Auladell, Carme

doi:10.3390/cells9081897

Cited by 10 publications

(11 citation statements)

References 145 publications

(208 reference statements)

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“…The alterations detected in the dendritic projections of immature hippocampal neurons and mature cortical neurons of Mkk4 ∆/∆ and Mkk7 ∆/∆ mice support that the MKK4/MKK7-JNK signaling pathway has a role in the maintenance of the dendritic and axonal processes [35] in accordance with Bjorkblom et al, who found that JNK phosphorylation of MAP2 plays an important role in defining dendritic architecture in the brain [36].…”

Section: The Deletion Of Mkk4 and Mkk7 Gene Alters Immature Hippocampal Neuronssupporting

confidence: 87%

Dual Mkk4 and Mkk7 Gene Deletion in Adult Mouse Causes an Impairment of Hippocampal Immature Granule Cells

Castro-Torres

Olloquequi

Etchetto

et al. 2021

IJMS

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(1) Background: The c-Jun-NH2-terminal protein kinase (JNK) is a mitogen-activated protein kinase involved in regulating physiological processes in the central nervous system. However, the dual genetic deletion of Mkk4 and Mkk7 (upstream activators of JNK) in adult mice is not reported. The aim of this study was to induce the genetic deletion of Mkk4/Mkk7 in adult mice and analyze their effect in hippocampal neurogenesis. (2) Methods: To achieve this goal, Actin-CreERT2 (Cre+/−), Mkk4flox/flox, Mkk7flox/flox mice were created. The administration of tamoxifen in these 2-month-old mice induced the gene deletion (Actin-CreERT2 (Cre+/−), Mkk4∆/∆, Mkk7∆/∆ genotype), which was verified by PCR, Western blot, and immunohistochemistry techniques. (3) Results: The levels of MKK4/MKK7 at 7 and 14 days after tamoxifen administration were not eliminated totally in CNS, unlike what happens in the liver and heart. These data could be correlated with the high levels of these proteins in CNS. In the hippocampus, the deletion of Mkk4/Mkk7 induced a misalignment position of immature hippocampal neurons together with alterations in their dendritic architecture pattern and maturation process jointly to the diminution of JNK phosphorylation. (4) Conclusion: All these data supported that the MKK4/MKK7–JNK pathway has a role in adult neurogenic activity.

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Section: The Deletion Of Mkk4 and Mkk7 Gene Alters Immature Hippocampal Neuronssupporting

confidence: 87%

Dual Mkk4 and Mkk7 Gene Deletion in Adult Mouse Causes an Impairment of Hippocampal Immature Granule Cells

Castro-Torres

Olloquequi

Etchetto

et al. 2021

IJMS

Self Cite

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“…This network converges on the SIGNOR pathways for mitochondrial biogenesis and inflammation, and this is consistent with prior evidence linking mitochondrial dysfunction [ 44 , 45 , 46 , 47 , 48 , 49 ] and neuroinflammation [ 50 , 51 , 52 ] to ASD. The polarization and proliferation pathways are essential regulators of neural stem cell self-renewal and differentiation [ 53 , 54 , 55 ], while the apoptosis and cell death signalling pathways are implicated as mechanisms whereby microglia drive synaptic pruning, and the maturation and migration of neuronal progenitors [ 56 ]. In addition, this subset of proteins was significantly enriched for five ClinVar disease pathways associated with neuropathology, mitochondrial dysfunction or auto-immune disease ( Table 3 ).…”

Section: Discussionmentioning

confidence: 99%

Convergent Canonical Pathways in Autism Spectrum Disorder from Proteomic, Transcriptomic and DNA Methylation Data

Mahony

O’Ryan

2021

IJMS

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Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder with extensive genetic and aetiological heterogeneity. While the underlying molecular mechanisms involved remain unclear, significant progress has been facilitated by recent advances in high-throughput transcriptomic, epigenomic and proteomic technologies. Here, we review recently published ASD proteomic data and compare proteomic functional enrichment signatures with those of transcriptomic and epigenomic data. We identify canonical pathways that are consistently implicated in ASD molecular data and find an enrichment of pathways involved in mitochondrial metabolism and neurogenesis. We identify a subset of differentially expressed proteins that are supported by ASD transcriptomic and DNA methylation data. Furthermore, these differentially expressed proteins are enriched for disease phenotype pathways associated with ASD aetiology. These proteins converge on protein–protein interaction networks that regulate cell proliferation and differentiation, metabolism, and inflammation, which demonstrates a link between canonical pathways, biological processes and the ASD phenotype. This review highlights how proteomics can uncover potential molecular mechanisms to explain a link between mitochondrial dysfunction and neurodevelopmental pathology.

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“…While, studies also showed that blocking the JUN could prevent the degradation and apoptosis of chondrocytes [21], and the inhibition of JUN transcriptional activity protects against osteoarthritis cartilage destruction [22]. Moreover, studies also showed that JUN could participate in the regulation of antioxidant responses in neurons [23] and may have the potential of regulating the peripheral myelin development [24] and neuronal polarization during brain development [25].…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics Analysis of Some Novel Potential Biomarkers Associated With Osteoarthritis and Nervous System

Guo¹,

Qin²,

Chen³

et al. 2021

Preprint

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BackgroundOsteoarthritis (OA) is an age-related chronic inflammatory and degenerative changes that carries heavy burden for individuals and the society. The specific mechanism of OA still remains unclear today, which requires new methods and technologies to achieve some new breakthrough. Bioinformatics technology is a novel method to extract genetic information from many diseases. In this study, we aims at screening out some key genes to help to illuminate the pathogenesis of OA to help to diagnosis and cure it.Objective and MethodsBioinformatics technology was used to screen some key target genes that were closely related to OA and nervous system, and by using qRT-PCR to preliminary verify the results.ResultsIn this work, we analysis three gene expression profiles, GSE114007, GSE51588, and GSE55457, that downloaded from the Gene Expression Omnibus database (GEO). At last, a total of 878 DEGs were identified with dataset GSE114007 (P<0.05 and |logFC|>1.5), consisting of 495 up-regulated genes and 383 down-regulated genes between the osteoarthritis and normal cartilage tissues. And by combining with the screened results of GSE51588 and GSE55457, finally, three genes, HES1, JUN, and IRE2, which were closely correlated with the nervous system that may help to diagnosis and cure osteoarthritis in the future were identified, and the result of qRT-PCR preliminary confirmed our finding.ConclusionHES1, JUN, and IRE2 were three potential genes related to osteoarthritis and nervous system that may help to diagnosis and cure OA.

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Involvement of JNK1 in Neuronal Polarization During Brain Development

Cited by 10 publications

References 145 publications

Dual Mkk4 and Mkk7 Gene Deletion in Adult Mouse Causes an Impairment of Hippocampal Immature Granule Cells

Dual Mkk4 and Mkk7 Gene Deletion in Adult Mouse Causes an Impairment of Hippocampal Immature Granule Cells

Convergent Canonical Pathways in Autism Spectrum Disorder from Proteomic, Transcriptomic and DNA Methylation Data

Bioinformatics Analysis of Some Novel Potential Biomarkers Associated With Osteoarthritis and Nervous System

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