Zinc Uptake and Storage During the Formation of the Cerebral Cortex in Mice

Hasna, Jessy; Bohic, Sylvain; Lemoine, Sophie; Blugeon, Corinne; Bouron, Alexandre

doi:10.1007/s12035-019-1581-7

Cited by 11 publications

(17 citation statements)

References 53 publications

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“…Table 1 provides the list of the 60 mouse genes selected [26][27][28][29][30] . The transcriptomic data were extracted from a recent RNAseq study 22 . The expression pattern of putative lipid sensing GPCRs was analyzed at 3 embryonic ages: E11, E13 and E17.…”

Section: Resultsmentioning

confidence: 99%

“…mRNA expression of putative lipid sensing GPCRs in the embryonic murine cortex. The data used to plot this graph were extracted from a previous whole-genome transcriptomic analysis 22 . A total of 60 genes encoding for putative lipid sensing GPCRs were selected (see Table 1).…”

Section: Discussionmentioning

confidence: 99%

“…To reach that goal, we took advantage of a recent transcriptomic analysis of the whole murine genome by RNA-seq. 22 . This allowed us to consider the mRNA expression of 60 putative lipid sensing GPCRs [26][27][28][29][30] .…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of store-operated calcium channels by N-arachidonoyl glycine (NAGly): no evidence for the involvement of lipid-sensing G protein coupled receptors

Deveci

Hasna

Bouron

2020

Sci Rep

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n-arachidonoyl glycine (nAGly) is an endogenous lipid deriving from the endocannabinoid anandamide (AEA). Identified as a ligand of several G-protein coupled receptors (GPCRs), it can however exert biological responses independently of GPCRs. NAGly was recently shown to depress store-operated ca 2+ entry (SOCE) but its mechanism of action remains elusive. The major aim of this study was to gain a better knowledge on the NAGly-dependent impairment of SOCE in neurons of the central nervous system (CNS) from mice. First, we examined the expression of genes encoding for putative lipid sensing GPCRs using transcriptomic data publicly available. This analysis showed that the most abundant GPCRs transcripts present in the cerebral cortices of embryonic brains were coding for lysophosphatidic acid (LPA) and sphingosine-1 phosphate (S1P) receptors. Next, the presence of functional receptors was assessed with live-cell calcium imaging experiments. In primary cortical cells S1P and LPA mobilize ca 2+ from internal stores via a mechanism sensitive to the S1P and LPA receptor antagonists Ex26, H2L5186303, or Ki16425. However, none of these compounds prevented or attenuated the NAGlydependent impairment of Soce. We found no evidence for the requirement of lipid sensing GpcRs in this inhibitory process, indicating that NAGly is an endogenous modulator interfering with the core machinery of Soce. Moreover, these data also raise the intriguing possibility that the depression of SOCE could play a role in the central effects of NAGly.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibition of store-operated calcium channels by N-arachidonoyl glycine (NAGly): no evidence for the involvement of lipid-sensing G protein coupled receptors

Deveci

Hasna

Bouron

2020

Sci Rep

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“…The mean +/− standard error of mean (SEM) is shown from n = 3 distinct biological samples. All the data presented were extracted from a genome-wide transcriptome sequencing (RNA-Seq) analysis (Hasna et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…The aim of this report was to provide a detailed picture of the expression of genes encoding the putative plasma membrane and organellar Ca 2+ -transporting proteins during embryonic cortical formation and development. The work is based on a recent genome-wide transcriptome sequencing (RNA-Seq) analysis estimating gene expression [ 12 ]. Tissues were collected at four ages: embryonic days 11 (E11), 13 (E13), and 17 (E17), and post-natal day 1 (PN1) corresponding to four crucial stages: when the neural progenitor cells begin to differentiate into neurons (E11), the peak (E13) and end of neurogenesis (E17), followed by the beginning of the maturation process and circuit assembly (PN1).…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic Profiling of Ca2+ Transport Systems during the Formation of the Cerebral Cortex in Mice

Bouron

2020

Cells

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Cytosolic calcium (Ca2+) transients control key neural processes, including neurogenesis, migration, the polarization and growth of neurons, and the establishment and maintenance of synaptic connections. They are thus involved in the development and formation of the neural system. In this study, a publicly available whole transcriptome sequencing (RNA-Seq) dataset was used to examine the expression of genes coding for putative plasma membrane and organellar Ca2+-transporting proteins (channels, pumps, exchangers, and transporters) during the formation of the cerebral cortex in mice. Four ages were considered: embryonic days 11 (E11), 13 (E13), and 17 (E17), and post-natal day 1 (PN1). This transcriptomic profiling was also combined with live-cell Ca2+ imaging recordings to assess the presence of functional Ca2+ transport systems in E13 neurons. The most important Ca2+ routes of the cortical wall at the onset of corticogenesis (E11–E13) were TACAN, GluK5, nAChR β2, Cav3.1, Orai3, transient receptor potential cation channel subfamily M member 7 (TRPM7) non-mitochondrial Na+/Ca2+ exchanger 2 (NCX2), and the connexins CX43/CX45/CX37. Hence, transient receptor potential cation channel mucolipin subfamily member 1 (TRPML1), transmembrane protein 165 (TMEM165), and Ca2+ “leak” channels are prominent intracellular Ca2+ pathways. The Ca2+ pumps sarco/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) and plasma membrane Ca2+ ATPase 1 (PMCA1) control the resting basal Ca2+ levels. At the end of neurogenesis (E17 and onward), a more numerous and diverse population of Ca2+ uptake systems was observed. In addition to the actors listed above, prominent Ca2+-conducting systems of the cortical wall emerged, including acid-sensing ion channel 1 (ASIC1), Orai2, P2X2, and GluN1. Altogether, this study provides a detailed view of the pattern of expression of the main actors participating in the import, export, and release of Ca2+. This work can serve as a framework for further functional and mechanistic studies on Ca2+ signaling during cerebral cortex formation.

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