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The neurotrophic factor neuritin impacts T cell electrical and metabolic state for the balance of tolerance and immunity.

ABSTRACT: The neurotrophic factor neuritin impacts T cell electrical and metabolic state for the balance of tolerance and immunity.

PROVIDER: PRJNA929537 | ENA |

REPOSITORIES: ENA

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The neurotrophic factor neuritin impacts T cell electrical and metabolic state for the balance of tolerance and immunity.

Project description:In order to understand the role of Nrn1, we compared the gene expression profile of Nrn1_KO and WT iTreg cells or Th0 cells.

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Impacts of ciliary neurotrophic factor on the retinal transcriptome in a mouse model of photoreceptor degeneration

Project description:Ciliary neurotrophic factor (CNTF) has been tested in clinical trials for human retinal degeneration due to its potent neuroprotective effects in various animal models. To decipher CNTF-triggered molecular events in the degenerating retina, high-throughput RNA sequencing analyses were performed using the Rds/Prph2 (P216L) transgenic mouse as a preclinical model for retinitis pigmentosa. Retinal transcriptome data was obtained for untreated wild type retinas, Rds retinas treated with a lentivirus expressing CNTF from postnatal day 25 to 35, and Rds retinas similarly treated with a control lentivirus expressing GFP. Comparisons of transcriptome data detect significant changes between wild type and Rds retinas. In addition, RNA-seq data reveal elevation of transcripts in the innate immune system and growth factor signaling, as well as altered neuronal transmission and metabolism in CNTF-treated Rds retinas. These results demonstrate the influence of exogenous CNTF on the retinal transcriptome landscape and illuminate likely CNTF impacts in degenerating human retinas.

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Impacts of ciliary neurotrophic factor on the retinal transcriptome in a mouse model of photoreceptor degeneration

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2015-11-05 | E-GEOD-74669 | biostudies-arrayexpress

Cancer-cell intrinsic electrical activity drives small-cell lung cancer progression

Project description:Elevated or ectopic expression of neuronal receptors and ion channels promotes tumor progression in many cancer types; neuroendocrine (NE) transformation of various adenocarcinomas has also been associated with increased aggressiveness. Whether the defining neuronal feature, namely electrical excitability, exists in cancer cells and whether this impacts cancer progression remains mostly unexplored. Small cell lung cancer (SCLC) is an archetypical example of highly aggressive NE cancers and is comprised of two major distinct subtypes of cancer cells: NE cells and non-NE cells. Here, we show that the NE cells are excitable, like neurons, while non-NE cells cannot fire action potentials, like astrocytes and other non-excitable cells. Action potential firing in NE cells directly promotes SCLC malignancy; however, the high ATP demand of electrical activity also leads to an unusual dependency on oxidative phosphorylation (OXPHOS) in NE cells. This finding contrasts with most cancer cells reported in the literature, which are non-excitable and heavily rely on aerobic glycolysis. Additionally, we find that non-NE cells metabolically support NE cells to supply their high ATP demand, promoting their excitability and malignancy, a process akin to the astrocyte-neuron metabolite shuttle. Lastly, we observe drastic changes in the innervation landscape during SCLC progression, which coincide with increased intratumoral heterogeneity (ITH) and elevated neuronal protein expression in SCLC cells, suggesting an induction of a tumor autonomous vicious cycle driven by cancer cell-intrinsic electrical activity, which confers long-term tumorigenic capability and metastatic potential.

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Neurotrophic factors and their receptors are altered by the mere partial IGF-1 deficiency

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