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      Notch3 is required for arterial identity and maturation of vascular smooth muscle cells.

      Genes & development
      Actins, metabolism, Animals, Blood Flow Velocity, Blood Pressure, Cell Differentiation, Cells, Cultured, Desmin, Endothelial Cells, cytology, Homozygote, Humans, In Situ Hybridization, Lac Operon, physiology, Mice, Mice, Knockout, Mice, Transgenic, Microfilament Proteins, genetics, Muscle Proteins, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle, Proto-Oncogene Proteins, Receptors, Cell Surface, Receptors, Notch, Swine

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          Abstract

          Formation of a fully functional artery proceeds through a multistep process. Here we show that Notch3 is required to generate functional arteries in mice by regulating arterial differentiation and maturation of vascular smooth muscle cells (vSMC). In adult Notch3-/- mice distal arteries exhibit structural defects and arterial myogenic responses are defective. The postnatal maturation stage of vSMC is deficient in Notch3-/- mice. We further show that Notch3 is required for arterial specification of vSMC but not of endothelial cells. Our data reveal Notch3 to be the first cell-autonomous regulator of arterial differentiation and maturation of vSMC.

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