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Expression profiles of primary cortical neurons after knocking down Tdp-43 and Cugbp1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE46148 | GEO | 2013/04/18

SECONDARY ACCESSION(S): PRJNA197365

REPOSITORIES: GEO

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Expression profiles of primary cortical neurons after knocking down Tdp-43 and Cugbp1

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-18 | E-GEOD-46148 | biostudies-arrayexpress

Expression profiles of primary cortical neurons after knocking down Tdp-43

2013-04-18 | GSE46146 | GEO

Expression profiles of primary cortical neurons after knocking down Tdp-43

Project description:To clarify the functional properties of Tdp-43, we established the differentially expressed alternative exons in Tdp-43-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary motor neuron infected with lentivirus expressing shRNA against mouse Tdp-43 or control. RNA was harvested 11 days after transfection.

2013-04-18 | E-GEOD-46146 | biostudies-arrayexpress

Expression profiles of primary cortical neurons after knocking down Cugbp1

2013-04-18 | GSE46147 | GEO

Expression profiles of primary cortical neurons after knocking down Cugbp1

Project description:To clarify the functional properties of Cugbp1, we established the differentially expressed alternative exons in Cugbp1-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary motor neuron infected with lentivirus expressing shRNA against mouse Cugbp1 or control. RNA was harvested 11 days after transfection.

2013-04-18 | E-GEOD-46147 | biostudies-arrayexpress

Expression profiles of primary cortical neurons after knocking down Fus

Project description:To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary cortical neuron infected with lentivirus expressing shRNA against mouse Fus or control. RNA was harvested 11 days after transfection.

2012-07-23 | E-GEOD-36153 | biostudies-arrayexpress

Expression profiles of primary cortical neurons after knocking down Fus

2012-07-24 | GSE36153 | GEO

Expression profiles of primary motor neurons after knocking down Fus

Project description:To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary motor neurons by using exon-sensitive microarray technology. To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary glial cells by using exon-sensitive microarray technology. To clarify the functional properties of FUS, we established the differentially expressed alternative exons in FUS-silenced primary cerebellar neurons by using exon-sensitive microarray technology.

2012-11-21 | GSE42421 | GEO

TDP-43 induces p53-mediated cell death of cortical progenitors and immature neurons.

Project description:TAR DNA-binding protein 43 (TDP-43) is a key player in neurodegenerative diseases including frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). Accumulation of TDP-43 is associated with neuronal death in the brain. How increased and disease-causing mutant forms of TDP-43 induce cell death remains unclear. Here we addressed the role of TDP-43 during neural development and show that reduced TDP-43 causes defects in neural stem/progenitor cell proliferation but not cell death. However, overexpression of wild type and TDP-43A315T proteins induce p53-dependent apoptosis of neural stem/progenitors and human induced pluripotent cell (iPS)-derived immature cortical neurons. We show that TDP-43 induces expression of the proapoptotic BH3-only genes Bbc3 and Bax, and that p53 inhibition rescues TDP-43 induced cell death of embryonic mouse, and human cortical neurons, including those derived from TDP-43G298S ALS patient iPS cells. Hence, an increase in wild type and mutant TDP-43 induces p53-dependent cell death in neural progenitors developing neurons and this can be rescued. These findings may have important implications for accumulated or mutant TDP-43 induced neurodegenerative diseases.

| S-EPMC5970242 | biostudies-literature

Progranulin reduces insoluble TDP-43 levels, slows down axonal degeneration and prolongs survival in mutant TDP-43 mice.

Project description:BACKGROUND:TAR DNA binding protein 43 (TDP-43) is the main disease protein in most patients with amyotrophic lateral sclerosis (ALS) and about 50% of patients with frontotemporal dementia (FTD). TDP-43 pathology is not restricted to patients with missense mutations in TARDBP, the gene encoding TDP-43, but also occurs in ALS/FTD patients without known genetic cause or in patients with various other ALS/FTD gene mutations. Mutations in progranulin (GRN), which result in a reduction of ~?50% of progranulin protein (PGRN) levels, cause FTD with TDP-43 pathology. How loss of PGRN leads to TDP-43 pathology and whether or not PGRN expression protects against TDP-43-induced neurodegeneration is not yet clear. METHODS:We studied the effect of PGRN on the neurodegenerative phenotype in TDP-43(A315T) mice. RESULTS:PGRN reduced the levels of insoluble TDP-43 and histology of the spinal cord revealed a protective effect of PGRN on the loss of large axon fibers in the lateral horn, the most severely affected fiber pool in this mouse model. Overexpression of PGRN significantly slowed down disease progression, extending the median survival by approximately 130 days. A transcriptome analysis did not point towards a single pathway affected by PGRN, but rather towards a pleiotropic effect on different pathways. CONCLUSION:Our findings reveal an important role of PGRN in attenuating mutant TDP-43-induced neurodegeneration.

| S-EPMC6192075 | biostudies-literature

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