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Friday, 10 October 2008

Hector Leonardo AguilaZamoljeni smo da vam prenesemo da vas Hrvatsko imunološko društvo s velikim zadovoljstvom poziva na predavanje Hectora Leonarda Aguile, PhD University of Connecticut Health Center Department of Immunology. Farmington, CT. USA pod nazivom "Bone Development and Hematopoietic Microenvironment".
Isto činimo na obostrano zadovoljstvo jer smatramo da među našim kolegama te posebno studentima vlada mišljenje da je dolazak na ova i ovakva predavanja prevelik gubitak vremena. Nažalost, ne radi se o usamljenim glasovima što nas čini posebno tužnim. Naime, nekad dvorane pune studenata "željnih" znanja danas zjape gotovo prazne, a vrlo često se radi o itekako kvalitetnim predavanjima i predavačima.
Sada, pa i u buduće STUDMEF će s posebnim veseljem objavljivati i promovirati porvratak na predavanja te u skoroj budućnosti i sam svojim akcijama nastojati aktivno sudjelovati u njima.
Stoga, dođite u utorak, 14. listopada, 2008. u 13:00 sati na Hrvatski institut za istraživanje mozga u Seminarskoj dvorani, 1. kat Šalata 12, Zagreb gdje ćete moći poslušati nešto o slijedećem:

Summary:
Hematopoiesis is regulated by interactions between developing hematopoietic progenitors and microenvironmental signals. In the bone marrow cells of the osteoblastic lineage have been proposed to be one of the main components supporting hematopoiesis. We have been using transgenic mouse models in which reporter genes are expressed under the control of osteoblast lineage promoters. Using one of these systems (Col2.3ΔTK) in which osteoblasts can be selectively ablated after treatment with the drug gancyclovir (Gcv) we reported a dependence between early osteoblasts and hematopoiesis as these mice loss their bone marrow hematopoietic potential upon osteoblast ablation. The effect involves a rapid loss of cells whose primary development depend on the bone marrow microenvironment. These include B cell progenitors, NK cells, myeloid progenitors and ultimately early progenitors including hematopoietic stem cells. We postulate that osteoblast depletion or alterations in bone remodeling homeostasis could be used as a way to modify hematopoietic niches. To test this hypothesis we ablated osteoblasts in transgenic mice in the C57BL/6 (B6) background by treating them with Gcv for 10 days
followed by injection of a limited number of hematopoietic stem cells from B6 transgenic mice bearing a GFP transgene driven by the H-2Kb MHC Class I promoter. These transplanted mice developed hematopoietic chimerism, scored by hematopoietic cells expressing GFP, to degrees equivalent to the observed in lethally irradiated control recipient mice. The chimerism is multilineage, including donor cells of myeloid and lymphoid origin. Moreover, sequential transplants of bone marrow from these primary chimeras to lethally irradiated recipients, congenic for the CD45.1 molecule, indicates that the initial transplant engrafted longterm hematopoietic stem cells. This was scored by the presence of GFP CD45.2 positive multilineage hematopoietic cells in the host animals. In another set of experiments we prevented osteoblastogenesis in utero, through the injection of Gcv in pregnant wild type females mated with transgenic males. After injection of Gcv at the onset of osteoblast development (10-15 days of embryonic life) a fraction of the progeny was born with an immature skeleton, that progressively generate mineralized bone after birth. These mice present anomalies in the dose of hematopoietic progenitors in the bone marrow, with active hematopoiesis in periphery. Interestingly, as osteoblastogenesis initiate, hematopoiesis in the bone marrow began to establish. These combined results emphasize the fundamental role of osteoblastogenesis on not only maintaining hematopoiesis in the bone marrow, but also on defining the origin of hematopoietic niches. These results show that controlled alterations in bone remodeling could be used as a regime to facilitate hematopoietic engraftment after bone marrow transplantation and provide a model to study the initiation of hematopoietic niches in the bone marrow post migration of progenitors from extramedular sites.
Summary:
Hematopoiesis is regulated by interactions between developing hematopoietic progenitors and microenvironmental signals. In the bone marrow cells of the osteoblastic lineage have been proposed to be one of the main components supporting hematopoiesis. We have been using transgenic mouse models in which reporter genes are expressed under the control of osteoblast lineage promoters. Using one of these systems (Col2.3ΔTK) in which osteoblasts can be selectively ablated after treatment with the drug gancyclovir (Gcv) we reported a dependence between early osteoblasts and hematopoiesis as these mice loss their bone marrow hematopoietic potential upon osteoblast ablation. The effect involves a rapid loss of cells whose primary development depend on the bone marrow microenvironment. These include B cell progenitors, NK cells, myeloid progenitors and ultimately early progenitors including hematopoietic stem cells. We postulate that osteoblast depletion or alterations in bone remodeling homeostasis could be used as a way to modify hematopoietic niches. To test this hypothesis we ablated osteoblasts in transgenic mice in the C57BL/6 (B6) background by treating them with Gcv for 10 days
followed by injection of a limited number of hematopoietic stem cells from B6 transgenic mice bearing a GFP transgene driven by the H-2Kb MHC Class I promoter. These transplanted mice developed hematopoietic chimerism, scored by hematopoietic cells expressing GFP, to degrees equivalent to the observed in lethally irradiated control recipient mice. The chimerism is multilineage, including donor cells of myeloid and lymphoid origin. Moreover, sequential transplants of bone marrow from these primary chimeras to lethally irradiated recipients, congenic for the CD45.1 molecule, indicates that the initial transplant engrafted longterm hematopoietic stem cells. This was scored by the presence of GFP CD45.2 positive multilineage hematopoietic cells in the host animals. In another set of experiments we prevented osteoblastogenesis in utero, through the injection of Gcv in pregnant wild type females mated with transgenic males. After injection of Gcv at the onset of osteoblast development (10-15 days of embryonic life) a fraction of the progeny was born with an immature skeleton, that progressively generate mineralized bone after birth. These mice present anomalies in the dose of hematopoietic progenitors in the bone marrow, with active hematopoiesis in periphery. Interestingly, as osteoblastogenesis initiate, hematopoiesis in the bone marrow began to establish. These combined results emphasize the fundamental role of osteoblastogenesis on not only maintaining hematopoiesis in the bone marrow, but also on defining the origin of hematopoietic niches. These results show that controlled alterations in bone remodeling could be used as a regime to facilitate hematopoietic engraftment after bone marrow transplantation and provide a model to study the initiation of hematopoietic niches in the bone marrow post migration of progenitors from extramedular sites.



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