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      The Renal Glomerulus and Vasculature in ‘Aggregation’ Chimeric Mice

      a , b


      S. Karger AG

      Glomerulus, Endothelium, Mouse, Aggregation chimera

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          In glomerular development, the glomerular epithelium is derived from the lower loop of the S-shaped renal vesicle. However, it is unclear whether the capillary endothelium is derived directly by vasculogenesis (e.g. differentiated directly from local metanephric mesenchyme) or whether they are derived by angiogenesis (i.e. derived from pre-existing vasculature in the metanephros). This question has been addressed in other laboratories using surgically created chimeric kidney model systems. In the present study, chimeric kidneys were developed by aggregating the cells from 4- to 8-cell embryos from Mus musculus with ones from Mus caroli and implanting the aggregated embryos into pseudopregnant hosts [Goldowitz D: Neuron 1989;3:705–713]. Species specific DNA clones were used in conjunction with in situ hybridization to identify the species origin of cells. Interspecies aggregate chimeras had varying proportions of renal cells derived from Mus caroli and Mus musculus; however, regions were identified in which the renal tubular and Bowman’s capsule or parietal epithelia were from one species while vessel endothelium and cells in the interstitium were from the other species. In those regions, glomeruli always contained an admixture of cells from both species however; many of the glomerular endothelial cells appear to be from the same species as the vessel endothelium and interstitial cells. These findings support the hypothesis that angiogenesis may contribute cells that help form the glomerular capillary endothelium. Most intrarenal arteries contained cells from both species. However a few vessels were found in which the endothelium was derived from one species while the smooth muscle cells were from the other species. This finding suggests that intrarenal arterial development has two cells of origin: the endothelial tube develops and is surrounded by mesenchymal cells that form the tunica media. The aggregation chimeric mouse kidney may become a useful model system for studying in situ aspects of the complex processes involved in kidney development.

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          Developmental Biology of the Vascular Smooth Muscle Cell: Building a Multilayered Vessel Wall

          The assembly of the vessel wall from its cellular and extracellular matrix components is a critical process in the development and maturation of the cardiovascular system. However, fundamental questions concerning the origin of vessel wall cells and the mechanisms that regulate their development and differentiation remain unanswered. The initial step of vessel wall morphogenesis is formation of a primary vascular network, comprised of nascent endothelial cell tubes, via the processes of vasculogenesis and angiogenesis. Subsequently, primordial vascular smooth muscle cells (VSMCs) are recruited to the endothelium to form a multilayered vessel wall. During the course of development and maturation, the VSMC plays diverse roles: it is a biosynthetic, proliferative, and contractile component of the vessel wall. Although the field of vascular development has blossomed in the past decade, the molecules and mechanisms that regulate this developmental pathway are not well defined. The focus of this review is on those facets of VSMC development important for transforming a nascent endothelial tube into a multilayered structure. We discuss the primordial VSMC with particular attention to its purported origins, the components of the extracellular milieu that contribute to its development, and the contribution of embryonic hemodynamics to vessel wall assembly.
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            Alleles of APC modulate the frequency and classes of mutations that lead to colon polyps.

            Most inherited mutant alleles of the adenomatosis polyposis coli gene (APC) cause the appearance of large numbers of colon polyps, the familial polyposis syndrome. (These mutant alleles are designated APCp alleles.) A subset of APC mutations, the attenuated or APC(AP) alleles, predispose to only a few colon polyps. This leads to the hypothesis that if mutation of the inherited normal allele is rate limiting in polyp development, the increased number of polyps associated with the APCp allele indicates that the frequency of mutations that can lead to polyp formation is higher among APCp carriers than among APC(AP) carriers. We have previously suggested that the APC protein might modulate the frequency of mutations, such as loss of heterozygosity (LOH), necessary for colon polyp formation. We thus reasoned that tumours from patients who carry an APC(AP) allele might show a reduced frequency of LOH compared with tumours from patients who carry an APCp allele. Loss of AAPC mutant alleles is designated as LOH(AP). Screening of tumours from APC(AP) carriers revealed a reduction of LOH compared with that of an unselected group of polyposis patients. In fact, no loss of the inherited APC(N) allele was observed, although sequencing showed that the inherited APC(N) allele had frequently undergone point mutations and small deletions in the tumours. A low frequency loss of the inherited APC(AP) allele was seen. These findings support the suggestion that the APC(AP) allele has residual gene activity and that this activity modulates the spectrum and frequency of mutations that lead to adenoma formation.

              Author and article information

              S. Karger AG
              March 2002
              25 February 2002
              : 90
              : 3
              : 267-272
              aDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Ind. and bDepartment of Anatomy and Neurobiology, University of Tennessee College of Medicine, Memphis, Tenn., USA
              49062 Nephron 2002;90:267–272
              © 2002 S. Karger AG, Basel

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              Page count
              Figures: 4, References: 17, Pages: 6
              Self URI (application/pdf):
              Original Paper

              Cardiovascular Medicine, Nephrology

              Aggregation chimera, Mouse, Endothelium, Glomerulus


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