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Description:
This scientific session will highlight the use of single cell omics and different newly developed imaging technologies to unravel the role of bone marrow niche under inflammation and aging. These stories highlight the importance of stress-induced changes in the composition and supportive role of the microenvironment for the communication with hematopoietic stem cells (HSCs) and the response and recovery of these stem cells upon stress.
Dr. Tiago Luis will discuss the role of the HSC niche in sensing specific demands in blood cell production and instructing HSCs to re-establish blood cell homeostasis. He will present a new feedback mechanism by which IL-1 secreted by activated platelets, activates the IL-1 signaling pathway in a specific subset of Lepr+IL-1R+ peri-sinusoidal cells. IL-1 signaling in this niche cell compartment is critical to the optimal activation of platelet-biased (Vwf+) HSCs. Dr. Luis will also discuss the dynamics of platelet-biased HSCs and their interactions with the surrounding bone marrow microenvironment, in homeostasis and post platelet depletion, analyzed by intravital imaging of highly pure Hoxb5+Vwf+ HSCs in the mouse calvarium.
Dr. Maria Carolina Florian will introduce how the bone marrow niche is remodeled upon aging focusing on the alterations of the vasculature and of the arteriolar vessels. She will show by 3D high resolution imaging that in aged mice the HSCs with the highest regenerative capacity have divided the less over time, are mostly polar for H4K16ac (epigenetic polarity) and are exclusively located next to bone marrow sinusoidal endothelial cells expressing the Notch ligand Jag2. Dr. Florian will also discuss data revealing that endothelial Jag2 regulates HSCs function upon aging through Notch signaling activation, which depends on HSC localization.
Dr. Daniel Lucas-Alcaraz will discuss new strategies to emerge stepwise hematopoiesis across the skeleton. He will provide an overview of the anatomy of normal and stress blood cell production highlighting novel patterns of progenitor movement and behavior and demonstrating that terminal differentiation for each blood lineage occurs in distinct, specialized, vascular niches. He will link hematopoietic plasticity to lineage- and insult-specific changes in the output of the production sites for each lineage.
Dr. Tiago Luis will discuss the role of the HSC niche in sensing specific demands in blood cell production and instructing HSCs to re-establish blood cell homeostasis. He will present a new feedback mechanism by which IL-1 secreted by activated platelets, activates the IL-1 signaling pathway in a specific subset of Lepr+IL-1R+ peri-sinusoidal cells. IL-1 signaling in this niche cell compartment is critical to the optimal activation of platelet-biased (Vwf+) HSCs. Dr. Luis will also discuss the dynamics of platelet-biased HSCs and their interactions with the surrounding bone marrow microenvironment, in homeostasis and post platelet depletion, analyzed by intravital imaging of highly pure Hoxb5+Vwf+ HSCs in the mouse calvarium.
Dr. Maria Carolina Florian will introduce how the bone marrow niche is remodeled upon aging focusing on the alterations of the vasculature and of the arteriolar vessels. She will show by 3D high resolution imaging that in aged mice the HSCs with the highest regenerative capacity have divided the less over time, are mostly polar for H4K16ac (epigenetic polarity) and are exclusively located next to bone marrow sinusoidal endothelial cells expressing the Notch ligand Jag2. Dr. Florian will also discuss data revealing that endothelial Jag2 regulates HSCs function upon aging through Notch signaling activation, which depends on HSC localization.
Dr. Daniel Lucas-Alcaraz will discuss new strategies to emerge stepwise hematopoiesis across the skeleton. He will provide an overview of the anatomy of normal and stress blood cell production highlighting novel patterns of progenitor movement and behavior and demonstrating that terminal differentiation for each blood lineage occurs in distinct, specialized, vascular niches. He will link hematopoietic plasticity to lineage- and insult-specific changes in the output of the production sites for each lineage.