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      Kidney development: an overview.

      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Nephron. Experimental nephrology
      Publisher: S. Karger AG

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          Abstract

          Kidney diseases are worldwide public health problems with a high cost and increasing incidence. By revealing the genetic and cellular mechanism behind mammalian kidney development, better diagnostic methods and novel therapies can be expected to be developed. The mammalian kidney is a typical organ that develops on the basis of sequential and reciprocal cell and tissue interactions. Functional genetic analysis has identified that genes from different classes are involved in the construction of the kidney and the same genes are also connected to the development of diseases.

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          Six2 defines and regulates a multipotent self-renewing nephron progenitor population throughout mammalian kidney development.

          Akio Kobayashi, M Todd Valerius, Joshua Mugford … (2008)
          Nephrons, the basic functional units of the kidney, are generated repetitively during kidney organogenesis from a mesenchymal progenitor population. Which cells within this pool give rise to nephrons and how multiple nephron lineages form during this protracted developmental process are unclear. We demonstrate that the Six2-expressing cap mesenchyme represents a multipotent nephron progenitor population. Six2-expressing cells give rise to all cell types of the main body of the nephron during all stages of nephrogenesis. Pulse labeling of Six2-expressing nephron progenitors at the onset of kidney development suggests that the Six2-expressing population is maintained by self-renewal. Clonal analysis indicates that at least some Six2-expressing cells are multipotent, contributing to multiple domains of the nephron. Furthermore, Six2 functions cell autonomously to maintain a progenitor cell status, as cap mesenchyme cells lacking Six2 activity contribute to ectopic nephron tubules, a mechanism dependent on a Wnt9b inductive signal. Taken together, our observations suggest that Six2 activity cell-autonomously regulates a multipotent nephron progenitor population.
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            Wnt9b plays a central role in the regulation of mesenchymal to epithelial transitions underlying organogenesis of the mammalian urogenital system.

            Thomas Carroll, Joo-Seop Park, Shigemi Hayashi … (2005)
            The vertebrate urogenital system forms due to inductive interactions between the Wolffian duct, its derivative the ureteric bud, and their adjacent mesenchymes. These establish epithelial primordia within the mesonephric (embryonic) and metanephric (adult) kidneys and the Müllerian duct, the anlage of much of the female reproductive tract. We show that Wnt9b is expressed in the inductive epithelia and is essential for the development of mesonephric and metanephric tubules and caudal extension of the Müllerian duct. Wnt9b is required for the earliest inductive response in metanephric mesenchyme. Further, Wnt9b-expressing cells can functionally substitute for the ureteric bud in these interactions. Wnt9b acts upstream of another Wnt, Wnt4, in this process, and our data implicate canonical Wnt signaling as one of the major pathways in the organization of the mammalian urogenital system. Together these findings suggest that Wnt9b is a common organizing signal regulating diverse components of the mammalian urogenital system.
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              Glomerular number and size in autopsy kidneys: the relationship to birth weight.

              W Hoy, Karen B Farris, J Bertram … (2003)
              In the Southeast United States, African Americans have an estimated incidence of hypertension and end-stage renal disease (ESRD) that is five times greater than Caucasians. Higher rates of low birth weight (LBW) among African Americans is suggested to predispose African Americans to the higher risk, possibly by reducing the number of glomeruli that develop in the kidney. This study investigates the relationships between age, race, gender, total glomerular number (Nglom), mean glomerular volume (Vglom), body surface area (BSA), and birth weight. Stereologic estimates of Nglom and Vglom were obtained using the physical disector/fractionator combination for autopsy kidneys from 37 African Americans and 19 Caucasians. Nglom was normally distributed and ranged from 227,327 to 1,825,380, an 8.0-fold difference. A direct linear relationship was observed between Nglom and birth weight (r = 0.423, P = 0.0012) with a regression coefficient that predicted an increase of 257,426 glomeruli per kilogram increase in birth weight (alpha = 0.050:0.908). Among adults there was a 4.9-fold range in Vglom, and in adults, Vglom was strongly and inversely correlated with Nglom (r =-0.640, P = 0.000002). Adult Vglom showed no significant correlation with BSA for males (r = -0.0150, P = 0.936), although it did for females (r = 0.606, P = 0.022). No racial differences in average Nglom or Vglom were observed. Birth weight is a strong determinant of Nglom and thereby of glomerular size in the postnatal kidney. The findings support the hypothesis that LBW by impairing nephron development is a risk factor for hypertension and ESRD in adulthood.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nephron Exp. Nephrol.
                Title: Nephron. Experimental nephrology
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2129
                ISSN (Print): 1660-2129
                Publication date (Electronic): 2014
                Volume: 126
                Issue: 2
                Affiliations
                [1 ] Oulu Center for Cell-Matrix Research, Biocenter and Infotech Oulu, Laboratory of Developmental Biology, Intelligent Systems, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland.
                Article
                Publisher Item ID: 000360659
                DOI: 10.1159/000360659
                PubMed ID: 24854638
                SO-VID: e2f2da11-d965-4821-9120-6596f21cb1f9
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