Regulation of Single Hematopoietic Stem Cells by Intake of Vitamin A
Quiescence preserves the self-renewal capacity and the long-term function of hematopoietic stem cells (HSCs). The regulators of this dormant state include intrinsic pathways and soluble components in the bone marrow niche. Dysregu...
ver más
¿Tienes un proyecto y buscas un partner? Gracias a nuestro motor inteligente podemos recomendarte los mejores socios y ponerte en contacto con ellos. Te lo explicamos en este video
Proyectos interesantes
TFs-HSCs
The identification of the Combinatorial Transcription Factor...
212K€
Cerrado
M5C RNA
Cytosine 5 methylated RNAs as stem cell regulators in normal...
1M€
Cerrado
GSCs maintenance
Post transcriptional regulation of Germline Stem Cells GSCs...
250K€
Cerrado
SAF2012-40107
REGULACION EPIGENETICA DEL ESTADO DE CEULA MADRE
164K€
Cerrado
StemLinc
Identification and characterization of long non-coding RNAs...
165K€
Cerrado
SAF2016-75613-R
ESPECIFICACION DE CELULA MADRE HEMATOPOYETICA Y LEUCEMICA
436K€
Cerrado
Información proyecto VitASTEM
Duración del proyecto: 78 meses
Fecha Inicio: 2017-10-04
Fecha Fin: 2024-04-30
Fecha límite de participación
Sin fecha límite de participación.
Descripción del proyecto
Quiescence preserves the self-renewal capacity and the long-term function of hematopoietic stem cells (HSCs). The regulators of this dormant state include intrinsic pathways and soluble components in the bone marrow niche. Dysregulation of this process is poorly defined and might cause aberrant hematopoiesis. In my previous work, we defined the molecular landscape of HSCs by applying state of the art DNA-methylome, RNA-seq and proteome analyses, and found vitamin A/retinoic acid (RA)-induced signaling predominantly enriched in HSCs (Cabezas-Wallscheid et al., Cell Stem Cell 2014). Intriguingly, we observed that mice fed with a vitamin A-free diet exhibited a robust loss of HSCs (Cabezas-Wallscheid et al., Cell 2017). Treatment of mice with a RA agonist preserved HSC quiescence in stress-activated conditions, indicating that the balance between HSC maintenance and differentiation is tightly regulated by vitamin A signaling.
However, we are only beginning to understand the mechanisms how vitamin A regulates HSC fate. Since treatment of vitamin A deficiency currently shows extremely low therapeutic success, novel insights into the role of HSCs in the development of the disease will be of enormous therapeutic value.