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Elimination of the four extracellular matrix molecules tenascin-C, tenascin-R, brevican and neurocan modifies the expression of key molecules of synapse formation and transmission

ABSTRACT: Elimination of the four extracellular matrix molecules tenascin-C, tenascin-R, brevican and neurocan modifies the expression of key molecules of synapse formation and transmission

PROVIDER: PRJNA524355 | ENA |

REPOSITORIES: ENA

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Elimination of the four extracellular matrix molecules tenascin-C, tenascin-R, brevican and neurocan modifies the expression of key molecules of synapse formation and transmission

Project description:The extracellular matrix (ECM) molecules tenascin-C (Tnc), tenascin-R (Tnr), brevican (Bcan) and neurocan (Ncan) are completely knocked out in the quadruple knockout mouse. This removal of these central ECM molecules lead to an altered gene expression in the hippocampus of postnatal day (P) 21 old quadruple knockout mice. Among others, the expression of genes involved in the process of synapse formation associated with synaptic transmission were significantly changed in the quadruple knockout hippocampus compared to the wildtype hippocampus. We found e.g. an upregulated expression of Gamma-aminobutyric acid receptor subunit theta (Gabrq), Glutamate decarboxylase (Gad2) and semaphorin 4c (Sema4c), which are known contributors at synapses. Interestingly, some extracellular molecules e.g. like glypican 3 (Gpc3), calreticulin (Calr) and three different types of collagens (Col1a2, Col4a3 and Col27a1) showed also a modified expression. These data indicate the importance of the four ECM molecules for an intact gene expression in the murine hippocampus.

2019-10-08 | GSE127216 | GEO

Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling

Project description:Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling

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Comparison of tenascin-C proficient versus tenascin-C deficient Mouse Embryonic Fibroblasts (MEFs)

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Senescent cell elimination modifies features of Alzheimer’s disease in 3xTg-AD mice

Project description:Senescent cell elimination modifies features of Alzheimer’s disease in 3xTg-AD mice

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Tenascin-C modifies expression levels and territories of key patterning genes during spinal cord astrocyte specification [mus musculus]

Project description:We demonstrate for the first time that the extracellular matrix glycoprotein Tenascin-C regulates the expression of key patterning genes during late embryonic spinal cord development, leading to a timely maturation of gliogenic neural precursor cells. We first show that Tenascin-C is expressed by gliogenic neural precursor cells during late embryonic development. The loss of Tenascin-C leads to a sustained generation and delayed migration of Fibroblast growth factor receptor 3 expressing immature astrocytes in vivo. Furthermore, we could demonstrate an upregulation of Nk2 transcription factor related locus 2 (Nkx2.2) and its downstream target Sulfatase 1 in vivo. A dorsal expansion of Nkx2.2-positive cells within the ventral spinal cord indicates a potential progenitor cell domain shift. Moreover, Sulfatase 1 is known to regulate growth factor signalling by cleaving sulphate residues from heparan sulphate proteoglycans. Consistent with this possibility we observed changes in both Fibroblast growth factor 2 and Epidermal growth factor responsiveness of spinal cord neural precursor cells. Taken together our data clearly show that Tenascin-C promotes the astroglial lineage progression during spinal cord development.

2011-10-20 | GSE33091 | GEO

Tenascin-C modifies expression levels and territories of key patterning genes during spinal cord astrocyte specification [mus musculus]

2011-10-19 | E-GEOD-33091 | biostudies-arrayexpress

Complement C1q-dependent synapse elimination by astrocytes in a mouse model of Alzheimer's disease

Project description:Synapse loss and glial activation are hallmarks of Alzheimer's disease (AD). In Tau P301S transgenic mice, the complement pathway contributes to neuronal damage through microglial elimination of synapses. Here, we used unbiased proteomic profiling of postsynaptic density (PSD) fractions from Tau P301S mice in C1q-WT versus C1q knockout backgrounds to identify C1q-dependent changes at synapses. Integrative multi-omics analysis revealed that astrocyte- and microglia- specific proteins are increased in Tau P301S synapse fractions with age and in a C1q-dependent manner. The same set of glial proteins (including C1q, C4, Gpnmb, and S100a4) is elevated in human AD synaptic fractions, and C4 levels are raised in cerebrospinal fluid (CSF) from AD patients. Besides microglia, we show that astrocytes contribute substantially to excitatory and inhibitory synapse engulfment in Tau P301S hippocampus. Based on staining of synapse markers within lysosomes, astrocytes showed preference for excitatory synapses whereas microglia preferred to engulf inhibitory synapse markers. Genetic deletion of C1q reduced astrocytic eating of excitatory and inhibitory synapses in Tau P301S mice, and rescued synapse density. Together, our data indicate that astrocytes contact and phagocytose synapses in a C1q- dependent manner and thereby contribute to synapse loss and neurodegeneration in AD.

2021-11-03 | MSV000088313 | MassIVE

Comparison of tenascin-C proficient versus tenascin-C deficient Mouse Embryonic Fibroblasts (MEFs)

Project description:In order to investigate what signalling pathways are turned on by tenascin-C, we generated Mouse Embryonic Fibroblasts (MEFs) deficient for tenascin-C and compared their gene expression profile to MEFs proficient for tenascin-C. TNC-KO MEFs as well as WT MEFs in which tenascin-C was knocked-down (following stable transfection of a short hairpin RNA) were compared to WT MEFs (expressing strong endogenous levels of tenascin-C).

2011-02-22 | E-GEOD-23547 | biostudies-arrayexpress

S-SCAM is essential for synapse formation

Project description:Synapse formation is critical for the wiring of neural circuits in the developing brain. The synaptic scaffolding protein S-SCAM/MAGI-2 has important roles in the assembly of signaling complexes at postsynaptic densities. However, the role of S-SCAM in establishing the entire synapse is not known. Here, we report significant effects of RNAi-induced S-SCAM knockdown on the number of synapses in early stages of network development in vitro. In vivo knockdown during the first three postnatal weeks reduced the number of dendritic spines in the rat brain neocortex. Knockdown of S-SCAM in cultured hippocampal neurons severely reduced the clustering of both pre- and postsynaptic components. This included synaptic vesicle proteins, pre- and postsynaptic scaffolding proteins, and cell adhesion molecules, suggesting that entire synapses fail to form. Correspondingly, functional and morphological characteristics of developing neurons were affected by reducing S-SCAM protein levels: neurons displayed severely impaired synaptic transmission and reduced dendritic arborization. A next generation sequencing approach showed normal expression of housekeeping genes, but changes of expression levels in 39 synaptic signaling molecules in cultured neurons. These results indicate that S-SCAM mediates the recruitment of all key classes of synaptic molecules during synapse assembly and is critical for the development of neural circuits in the developing brain.

2023-10-02 | GSE228093 | GEO

Elimination of the four extracellular matrix molecules tenascin-C, tenascin-R, brevican and neurocan alters the ratio of excitatory and inhibitory synapses.

Project description:The synaptic transmission in the mammalian brain is not limited to the interplay between the pre- and the postsynapse of neurons, but involves also astrocytes as well as extracellular matrix (ECM) molecules. Glycoproteins, proteoglycans and hyaluronic acid of the ECM pervade the pericellular environment and condense to special superstructures termed perineuronal nets (PNN) that surround a subpopulation of CNS neurons. The present study focuses on the analysis of PNNs in a quadruple knockout mouse deficient for the ECM molecules tenascin-C (TnC), tenascin-R (TnR), neurocan and brevican. Here, we analysed the proportion of excitatory and inhibitory synapses and performed electrophysiological recordings of the spontaneous neuronal network activity of hippocampal neurons in vitro. While we found an increase in the number of excitatory synaptic molecules in the quadruple knockout cultures, the number of inhibitory synaptic molecules was significantly reduced. This observation was complemented with an enhancement of the neuronal network activity level. The in vivo analysis of PNNs in the hippocampus of the quadruple knockout mouse revealed a reduction of PNN size and complexity in the CA2 region. In addition, a microarray analysis of the postnatal day (P) 21 hippocampus was performed unravelling an altered gene expression in the quadruple knockout hippocampus.

| S-EPMC6763627 | biostudies-literature

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