| 1. |
- Billing, Matilda, et al.
(författare)
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Signaling via Smad2 and Smad3 is dispensable for adult murine hematopoietic stem cell function in vivo
- 2017
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Ingår i: Experimental Hematology. - : Elsevier BV. - 0301-472X.
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Tidskriftsartikel (refereegranskat)abstract
- Transforming growth factor-β (TGFβ) is a member of a large family of polypeptide growth factors. TGFβ signals mainly through the intracellular proteins Smad2 and Smad3, which are highly similar in amino acid sequence identity. A number of studies have shown that these proteins, dependent on context, have distinct roles in the TGFβ signaling pathway. TGFβ is one of the most potent inhibitors of hematopoietic stem and progenitor cell proliferation in vitro, but its role in hematopoiesis in vivo is still being determined. To circumvent possible redundancies at the receptor level and to address specifically the role of the Smad circuitry downstream of TGFβ and activin in hematopoiesis, we studied the effect of genetically deleting both Smad2 and Smad3 in adult murine hematopoietic cells. Indeed, TGFβ signaling is impaired in vitro in primitive bone marrow (BM) cells of Smad2 and Smad3 single knockout models. However, blood parameters appear normal under steady state and in the transplantation setting. Interestingly, upon deletion of both Smad2 and Smad3 in vivo, mice quickly develop a lethal inflammatory disease, suggesting that activin/TGFβ signaling is crucial for immune cell homeostasis in the adult context. Furthermore, concurrent deletion of Smad2 and Smad3 in BM cells in immune-deficient nude mice did not result in any significant alterations of the hematopoietic system. Our findings suggest that Smad2 and Smad3 function to mediate crucial aspects of the immunoregulatory properties of TGFβ, but are dispensable for any effect that TGFβ has on primitive hematopoietic cells in vivo.
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| 2. |
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| 3. |
- Dahl, Maria, et al.
(författare)
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Bone marrow transplantation without myeloablative conditioning in a mouse model for Diamond-Blackfan anemia corrects the disease phenotype
- 2021
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Ingår i: Experimental Hematology. - : Elsevier BV. - 0301-472X. ; 99, s. 2-53
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Tidskriftsartikel (refereegranskat)abstract
- Diamond-Blackfan anemia (DBA) is a congenital erythroid hypoplasia caused by a functional haploinsufficiency of genes coding for ribosomal proteins. Among these genes, the ribosomal protein S19 (RPS19) gene is the most frequently mutated. Previously, a mouse model deficient in RPS19 was developed by our laboratory, which recapitulates the hematopoietic disease phenotype by manifesting pathologic features and clinical symptoms of DBA. Characterization of this model revealed that chronic RPS19 deficiency leads to exhaustion of hematopoietic stem cells and subsequent bone marrow (BM) failure. In this study, we evaluated a nonmyeloablative conditioning protocol for BM transplants in RPS19-deficient mice by transplanting wild-type BM cells to RPS19-deficient recipients given no conditioning or sublethal doses of irradiation before transplant. We describe full correction of the hematopoietic phenotype in mice given sublethal doses of irradiation, as well as in animals completely devoid of any preceding irradiation. In comparison, wild-type animals receiving the same preconditioning regimen and number of transplanted cells exhibited significantly lower engraftment levels. Thus, robust engraftment and repopulation of transplanted cells can be achieved in reduced-intensity conditioned RPS19-deficient recipients. As gene therapy studies with autologous gene-corrected hematopoietic stem cells are emerging, we propose the results described here can guide determination of the level of conditioning for such a protocol in RPS19-deficient DBA. On the basis of our findings, a relatively mild conditioning strategy would plausibly be sufficient to achieve sufficient levels of engraftment and clinical success.
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| 4. |
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| 5. |
- Dahl, Matilda, 1978-
(författare)
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Granskningssamhället och det nya Europa : när de Baltiska staterna sattes på prov
- 2012
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Bok (övrigt vetenskapligt/konstnärligt)abstract
- I den här skriften analyseras det framväxande granskningssamhället, med utgångspunkt i hur de baltiska staterna synades inför EU-inträdet. Då länderna skulle bli en del av det nya Europa öppnade de sig för granskning av bl.a. EU-kommissionen, EBRD och Transparency International. Men frågan är om granskning verkligen är en så neutral praktik som det ges sken av?Genom att jämföra granskning av stater med revision av företag visar författaren på att granskningssamhället inte bara skapar ordning, utan ensärskild ordning. Granskningsförfaranden blir slagkraftiga styrningsmekanismer mot bestämda mål, just eftersom de oftast framställs och uppfattas som värderingsfria och neutrala teknologier. rapporter, siffror och rankningar reflekterar verkligheten samtidigt som de är med och konstruerar den.
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| 6. |
- Dahl, Matilda
(författare)
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Går det att granska finansmarknaden?
- 2014
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Ingår i: Veckans affärer. - Stockholm : Specialtidningsförlaget. - 0506-4406.
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Tidskriftsartikel (populärvet., debatt m.m.)
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| 7. |
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| 8. |
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| 9. |
- Dahl, Matilda, 1978-
(författare)
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Je suis Gemeinschaft
- 2020
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Ingår i: Om undran inför företagsekonomin. - : Santérus Academic Press Sweden. - 9789173591560
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 10. |
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