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Sökning: WFRF:(Cuervo Henar)

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1.
  • da Bandeira, Diana Sa, et al. (författare)
  • PDGFR beta(+) cells play a dual role as hematopoietic precursors and niche cells during mouse ontogeny
  • 2022
  • Ingår i: Cell Reports. - : CELL PRESS. - 2211-1247. ; 40:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Hematopoietic stem cell (HSC) generation in the aorta-gonad-mesonephros region requires HSC specification signals from the surrounding microenvironment. In zebrafish, PDGF-B/PDGFR beta signaling controls hematopoietic stem/progenitor cell (HSPC) generation and is required in the HSC specification niche. Little is known about murine HSPC specification in vivo and whether PDGF-B/PDGFR beta is involved. Here, we show that PDGFR beta is expressed in distinct perivascular stromal cell layers surrounding the mid-gestation dorsal aorta, and its deletion impairs hematopoiesis. We demonstrate that PDGFR beta(+) cells play a dual role in murine hematopoiesis. They act in the aortic niche to support HSPCs, and in addition, PDGFR beta(+) embryonic precursors give rise to a subset of HSPCs that persist into adulthood. These findings provide crucial information for the controlled production of HSPCs in vitro.
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2.
  • Van de Veire, Sara, et al. (författare)
  • Further pharmacological and genetic evidence for the efficacy of PlGF inhibition in cancer and eye disease
  • 2010
  • Ingår i: Cell. - : Elsevier BV. - 0092-8674 .- 1097-4172. ; 141:1, s. 178-190
  • Tidskriftsartikel (refereegranskat)abstract
    • Our findings that PlGF is a cancer target and anti-PlGF is useful for anticancer treatment have been challenged by Bais et al. Here we take advantage of carcinogen-induced and transgenic tumor models as well as ocular neovascularization to report further evidence in support of our original findings of PlGF as a promising target for anticancer therapies. We present evidence for the efficacy of additional anti-PlGF antibodies and their ability to phenocopy genetic deficiency or silencing of PlGF in cancer and ocular disease but also show that not all anti-PlGF antibodies are effective. We also provide additional evidence for the specificity of our anti-PlGF antibody and experiments to suggest that anti-PlGF treatment will not be effective for all tumors and why. Further, we show that PlGF blockage inhibits vessel abnormalization rather than density in certain tumors while enhancing VEGF-targeted inhibition in ocular disease. Our findings warrant further testing of anti-PlGF therapies.
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