Expression of Cux‐1 and Cux‐2 in the developing somatosensory cortex of normal and barrel‐defective mice

Ferrere, Arnaud; Vitalis, Tania; Gingras, Hélène; Gaspar, Patricia; Cases, Olivier

doi:10.1002/ar.a.20284

Cited by 48 publications

(42 citation statements)

References 25 publications

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“…CUX1 is a well-defined molecular marker of upper-layer neurons (cortical layers II-IV). 30 We detected reduced CT in deep cortical layers in the Injury compared with the Sham animals ( Figure 1b). This observation confirmed previous reports that at P2 deep cortical layers are particularly susceptible to hypoxic-ischemic brain injury.…”

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confidence: 82%

PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling

et al. 2015

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A synthetic peptide (sPIF) analogous to the mammalian embryo-derived PreImplantation Factor (PIF) enables neuroprotection in rodent models of experimental autoimmune encephalomyelitis and perinatal brain injury. The protective effects have been attributed, in part, to sPIF's ability to inhibit the biogenesis of microRNA let-7, which is released from injured cells during central nervous system (CNS) damage and induces neuronal death. Here, we uncover another novel mechanism of sPIF-mediated neuroprotection. Using a clinically relevant rat newborn brain injury model, we demonstrate that sPIF, when subcutaneously administrated, is able to reduce cell death, reverse neuronal loss and restore proper cortical architecture. We show, both in vivo and in vitro, that sPIF activates cyclic AMP dependent protein kinase (PKA) and calcium-dependent protein kinase (PKC) signaling, leading to increased phosphorylation of major neuroprotective substrates GAP-43, BAD and CREB. Phosphorylated CREB in turn facilitates expression of Gap43, Bdnf and Bcl2 known to have important roles in regulating neuronal growth, survival and remodeling. As is the case in sPIF-mediated let-7 repression, we provide evidence that sPIF-mediated PKA/PKC activation is dependent on TLR4 expression. Thus, we propose that sPIF imparts neuroprotection via multiple mechanisms at multiple levels downstream of TLR4. Given the recent FDA fast-track approval of sPIF for clinical trials, its potential clinical application for treating other CNS diseases can be envisioned.

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confidence: 82%

PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling

et al. 2015

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“…4 A, B) and Cux-1 staining (Fig. 4G,H ), both of which are expressed in cortical layers II through IV (McEvilly et al, 2002;Ferrere et al, 2006) as well as reelin (Fig. 4 E, F ) and calretinin (Fig.…”

Section: Specific Diminishment Of Superficial Cortical Layers In Shcfmentioning

confidence: 96%

Neural-Specific Inactivation of ShcA Results in Increased Embryonic Neural Progenitor Apoptosis and Microencephaly

et al. 2006

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Brain size is precisely regulated during development and involves coordination of neural progenitor cell proliferation, differentiation, and survival. The adapter protein ShcA transmits signals from receptor tyrosine kinases via MAPK (mitogen-activated protein kinase)/ ERK (extracellular signal-regulated kinase) and PI3K (phosphatidylinositol 3-kinase)/Akt signaling pathways. In the CNS, ShcA expression is high during embryonic development but diminishes as cells differentiate and switches to ShcB/Sck/Sli and ShcC/N-Shc/Rai. To directly test ShcA function in brain development, we used Cre/lox technology to express a dominant-negative form of ShcA (ShcFFF) in nestin-expressing neural progenitors. ShcFFF-expressing mice display microencephaly with brain weights reduced to 50% of littermate controls throughout postnatal and adult life. The cerebrum appeared most severely affected, but the gross architecture of the brain is normal. Body weight was mildly affected with a delay in reaching mature weight. At a mechanistic level, the ShcFFF microencephaly phenotype appears to be primarily attributable to elevated apoptosis levels throughout the brain from embryonic day 10.5 (E10.5) to E12, which declined by E14.5. Apoptosis remained at normal basal levels throughout postnatal development. Proliferation indices were not significantly altered in the embryonic neuroepithelium or within the postnatal subventricular zone. In another approach with the same nestin-Cre transgene, conditional deletion of ShcA in mice with a homozygous floxed shc1 locus also showed a similar microencephaly phenotype. Together, these data suggest a critical role for ShcA in neural progenitor survival signaling and in regulating brain size.

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“…It is well accepted that the subventricular zone (SZ) plays an important role during the period of neocortical neurogenesis, by containing stem and progenitor cells that generate neuroblasts throughout life. Interestingly, a large proportion of the cortical neurons (from the layer II/III) are born in the SZ [Miller, 1989;Tarabykin et al, 2001;Nieto et al, 2004;Noctor et al, 2004;Zimmer et al, 2004;Englund et al, 2005;Ferrere et al, 2006;Martinez-Cerdeno et al, 2006].…”

Section: State Of Research and Mouse Modelsmentioning

confidence: 99%

<i>FOXG1</i>-Related Disorders: From Clinical Description to Molecular Genetics

Florian

Bahi‐Buisson²,

Bienvenu³

2011

Mol Syndromol

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Rett syndrome (RTT) is a severe neurodevelopmental disease that affects approximately 1 in 10,000 live female births and is often caused by mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2). Mutations in loci other than MECP2 have also been found in individuals that have been labeled as atypical RTT. Among them, a mutation in the gene forkhead box G1 (FOXG1) has been involved in the molecular aetiology of the congenital variant of RTT. The FOXG1 gene encodes a winged-helix transcriptional repressor essential for the development of the ventral telencephalon in embryonic forebrain. Later, FOXG1 continues to be expressed in neurogenetic zones of the postnatal brain. Although RTT affects quasi-exclusively girls, FOXG1 mutations have also been identified in male patients. As far as we know, about 12 point mutations and 13 cases with FOXG1 molecular abnormalities (including translocation, duplication and large deletion on the chromosome 14q12) have been described in the literature. Affected individuals with FOXG1 mutations have shown dysmorphic features and Rett-like clinical course, including normal perinatal period, postnatal microcephaly, seizures and severe mental retardation. Interestingly, the existing animal models of FOXG1 deficiency showed similar phenotype, suggesting that animal models may be a fascinating model to understand this human disease. Here, we describe the impacts of FOXG1 mutations and their associated phenotypes in human and mouse models.

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Expression of Cux‐1 and Cux‐2 in the developing somatosensory cortex of normal and barrel‐defective mice

Cited by 48 publications

References 25 publications

PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling

PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling

Neural-Specific Inactivation of ShcA Results in Increased Embryonic Neural Progenitor Apoptosis and Microencephaly

<i>FOXG1</i>-Related Disorders: From Clinical Description to Molecular Genetics

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