Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NAD+ Modulates the Proliferation and Differentiation of Adult Neural Stem/Progenitor Cells via Akt Signaling Pathway

ABSTRACT: NAD+ Modulates the Proliferation and Differentiation of Adult Neural Stem/Progenitor Cells via Akt Signaling Pathway

PROVIDER: PRJNA824821 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18686502_1.fastq.gz	Fastqsanger.gz
	SRR18686502_2.fastq.gz	Fastqsanger.gz
	SRR18686503_1.fastq.gz	Fastqsanger.gz
	SRR18686503_2.fastq.gz	Fastqsanger.gz
	SRR18686504_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

NAD+ Modulates the Proliferation and Differentiation of Adult Neural Stem/Progenitor Cells via Akt Signaling Pathway

Project description:Collectively, our findings provide some insights into the roles and mechanisms in which NAD+ regulates aNSPCs and neuronal development.

2022-04-27 | GSE200494 | GEO

NAD+ Modulates the Proliferation and Differentiation of Adult Neural Stem/Progenitor Cells via Akt Signaling Pathway.

Project description:Nicotinamide adenine dinucleotide hydrate (NAD+) acts as the essential component of the tricarboxylic citric acid (TCA) cycle and has important functions in diverse biological processes. However, the roles of NAD+ in regulating adult neural stem/progenitor cells (aNSPCs) remain largely unknown. Here, we show that NAD+ exposure leads to the reduced proliferation and neuronal differentiation of aNSPCs and induces the apoptosis of aNSPCs. In addition, NAD+ exposure inhibits the morphological development of neurons. Mechanistically, RNA sequencing revealed that the transcriptome of aNSPCs is altered by NAD+ exposure. NAD+ exposure significantly decreases the expression of multiple genes related to ATP metabolism and the PI3k-Akt signaling pathway. Collectively, our findings provide some insights into the roles and mechanisms in which NAD+ regulates aNSPCs and neuronal development.

| S-EPMC9029130 | biostudies-literature

Xrn1 Modulates Mitochondrial NAD Levels through NAD-Capped RNA Decay

Project description:Xrn1 Modulates Mitochondrial NAD Levels through NAD-Capped RNA Decay

2021-06-10 | MSV000087605 | MassIVE

Piezo1 mediated mechanotransduction modulates macrophages proliferation during bone remodeling via PI3K-AKT-Ccnd1 axis

Project description:Piezo1 mediated mechanotransduction modulates macrophages proliferation during bone remodeling via PI3K-AKT-Ccnd1 axis

| PRJNA787241 | ENA

NAD+ depletion drives impaired endothelial cell proliferation and age-related vascular decline

Project description:Aging is accompanied by a decline in neovascularisation potential and increased susceptibility to ischemic injury. Here, we confirm the age-related impaired neovascularization following ischemic leg injury and impaired angiogenesis. The age-related deficits in angiogenesis arose primarily from diminished EC proliferation capacity, but not migration or VEGF sensitivity. Aged EC harvested from the mouse hindlimb displayed a pro-angiogenic gene expression phenotype, along with considerable changes in metabolic genes. Metabolomics analysis and 13C glucose tracing revealed that late passage HUVECs display impaired ATP production and altered glycolysis and TCA cycle intermediates, with significant shifts occurring at nicotinamide adenine dinucleotide (NAD⁺)-dependent steps along with NAD+ depletion, suggestive of compromised NAD⁺ metabolism. Supplementation with nicotinamide mononucleotide (NMN), a precursor of NAD⁺, enhances enhanced late-passage EC proliferation and sprouting angiogenesis from aged mice aortas. Taken together, our study illustrates the centrality of NAD+-dependent metabolism in the maintenance of EC proliferation capacity with age.

2024-11-25 | GSE270697 | GEO

Piezo1 mediated mechanotransduction modulates macrophages proliferation during bone remodeling via PI3K-AKT-Ccnd1 axis

Project description:Macrophages play a pivotal role in mechanical force-induced inflammatory bone remodeling. Yet, how macrophages perceive mechanical stimuli and thereby modulate biological behaviors remain elusive. The orthodontic tooth movement (OTM) model was established to access the role of Piezo1 in modulating macrophage response upon mechanical stimuli. The potential functions and molecule mechanisms of Piezo1 were explored by bone marrow-derived macrophages (BMDMs) using mechanical stretch system, western blotting, immunofluorescence, flow cytometry and RNA sequencing. We first found macrophage proliferative phenotype enhanced at the later stage of force application. The biological variation mediated by mechanical force could be suppressed by Piezo1 inhibition. Furthermore, Piezo1 activated PI3K-AKT signaling was closely associated with macrophage proliferation upon mechanical stimuli. Additionally, Ccnd1 was authenticated as a critical downstream factor of PI3K-AKT signaling and conditional ablation of Ccnd1 in macrophages inhibited macrophage proliferation in mechanical force-induced bone remodeling procedure.

2024-12-08 | GSE190470 | GEO

Protein abundance of AKT and ERK pathway components governs cell-type-specific regulation of proliferation

Project description:Signaling through the AKT and ERK pathways controls cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell-cycle progression, is poorly understood. Here we study different murine hematopoietic cell types, in which AKT and ERK signaling is triggered by erythropoietin (Epo). Although these cell types share the molecular network topology for pro-proliferative Epo signaling, they exhibit distinct proliferative responses. Iterating quantitative experiments and mathematical modeling, we identify two molecular sources for cell-type-specific proliferation. First, cell-type-specific protein abundance patterns cause differential signal flow along the AKT and ERK pathways. Second, downstream regulators of both pathways have differential effects on proliferation, suggesting that protein synthesis is rate-limiting for faster-cycling cells while slower cell-cycles are controlled at the G1-S progression. The integrated mathematical model of Epo-driven proliferation explains cell-type-specific effects of targeted AKT and ERK inhibitors and faithfully predicts based on the protein abundance anti-proliferative effects of inhibitors in primary human erythroid progenitor cells. Our findings suggest that the effectiveness of targeted cancer therapy might become predictable from protein abundance patterns.

2017-03-31 | MSV000080844 | MassIVE

The role of nicotinamide phosphoribosyltransferase (Nampt) in hippocampal neural stem/progenitor cells

Project description:Neural stem/progenitor cell (NSPC) proliferation and self-renewal, as well as insult-induced differentiation, decrease markedly with age, but the molecular mechanisms responsible for these declines remain unclear. Here we show that levels of NAD+ and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD+ biosynthesis, decrease with age in the hippocampus. Ablation of Nampt in adult NSPCs reduced their pool and proliferation in vivo. The decrease in the NSPC pool during aging can be rescued by enhancing hippocampal NAD+ levels. Nampt is the main source of NSPC NAD+ levels and required for G1/S progression of the NSPC cell cycle. Nampt is also critical for oligodendrocytic lineage fate decisions through a mechanism mediated redundantly by Sirt1 and Sirt2. Ablation of Nampt in the adult NSPCs in vivo reduced NSPC-mediated oligodendrogenesis upon injury. These phenotypes recapitulate defects in NSPCs during aging, implicating Nampt-mediated NAD+ biosynthesis as a mediator of these age-associated functional declines. Total RNA obtained from neurospheres derived from postnatal hippocampi subjected to 48 hours in vitro of incubation with Nampt-specific inhibitor FK866 (10 nM, 4 samples) or vehicle (DMSO, 1:1000, 4 samples).

2014-05-08 | E-GEOD-49784 | biostudies-arrayexpress

The Ednrb–Aim2–AKT axis regulates neural crest-derived melanoblast proliferation during early development

Project description:Ednrb is specifically required to develop neural crest (NC) stem cell-derived lineages. However, it is still unknown why Ednrb signaling is only needed for the early development of melanoblasts in the skin and eye. We show that Ednrb is required for the proliferation of melanoblasts during early mouse development. To understand the mechanism of melanoblast proliferation, we found that the gene absent in melanoma 2 (Aim2) is upregulated in Ednrb-deficient NC cells by RNA-sequencing analysis. Consequently, the knockdown or knockout of Aim2 partially rescued the proliferation of Ednrb-deficient melanoblasts. Conversely, the overexpression of Aim2 in melanoblasts suppressed their proliferation. We further show that Ednrb signaling could act through the microRNA miR-196b to block the suppression of melanoblast proliferation by Aim2 in primary NC cell cultures. These results reveal the Ednrb–Aim2–AKT axis in regulating melanocyte development and suggest that Ednrb signaling functions as a negative regulator of Aim2, which inhibits the proliferation of melanoblasts in early development. These findings uncover a previously unreported role for Aim2 outside the inflammasome, showing that it is a significant regulator controlling NC stem cell-derived lineage development.

2024-11-06 | GSE275956 | GEO

The Ednrb–Aim2–AKT axis regulates neural crest-derived melanoblast proliferation during early development

Project description:The Ednrb–Aim2–AKT axis regulates neural crest-derived melanoblast proliferation during early development

| PRJNA1153952 | ENA