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  • 1
    Electronic Resource
    Electronic Resource
    Transforming growth factor-β superfamily members: roles in branching morphogenesis in the kidney (2001)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 6 (2001), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The process of nephrogenesis and the number of nephrons formed during kidney development are both highly dependent upon ureteric branching morphogenesis. Abnormalities in branching and growth of the ureter have been implicated in a range of urogenital/renal pathologies including cystic renal disease and some forms of renal agenesis. The issue of how the branching of the ureter is regulated is therefore an important one. There is a growing list of candidate molecules (growth factors, oncogenes, transcription factors and extracellular matrix components) which have been directly or indirectly implicated in the regulation of ureteric branching. Among these, members of the transforming growth factor-β (TGF-β) superfamily are well represented. This review summarizes our knowledge of the roles of TGF-β superfamily members in ureteric branching morphogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2001.00070.x
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  • 2
    Electronic Resource
    Electronic Resource
    GLOMERULAR CAPILLARY GROWTH AND CELLULAR HYPERPLASIA IN A MODEL OF FOCAL AND SEGMENTAL GLOMERULOSCLEROSIS (2000)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2000.005003a104.x
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  • 3
    Electronic Resource
    Electronic Resource
    ESTIMATING TOTAL GLOMERULAR NUMBER IN HUMAN KIDNEYS WITH A PHYSICAL DISECTOR/SMOOTH FRACTIONATOR COMBINATION (2000)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2000.abs118.x
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  • 4
    Electronic Resource
    Electronic Resource
    Studies on the effects of gentamicin on rat metanephric development in vitro (2000)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Reduced nephron endowment has been associated with increased risk of developing essential hypertension and chronic renal failure. Both in vivo and in vitro exposure of developing rat metanephroi to gentamicin has been reported to inhibit metanephric development resulting in reduced nephron endowment. The aim of the present study was to confirm that gentamicin results in reduced nephron endowment in vitro, and to extend understanding of the mechanisms responsible for this reduced endowment. Embryonic day 14 (E14) rat metanephroi were cultured for up to 4 days in serum-free medium with or without 50 μg/mL gentamicin. Metanephroi cultured in the presence of gentamicin were 25% smaller than control metanephroi after 2 days culture and 30% smaller after 4 days (P 〈 0.001). This decrease in total metanephric volume was reflected in reduced volumes of ureteric duct epithelium, mesenchyme/interstitium and nephron epithelia. The reduced volume of ureteric duct epithelium in gentamicin-treated metanephroi was associated with a 30% reduction in the number of ureteric duct branch points at 2 days. Metanephroi cultured with gentamicin contained 20% fewer glomeruli than control metanephroi (P 〈 0.005) at 4 days. These glomeruli were 30% smaller than control glomeruli (P 〈 0.05). Qualitative observations of Pax-2 immunostained mesenchymal condensates indicated no difference in condensate size, location or morphology. These results confirm that in vitro exposure of developing rat metanephroi to gentamicin results in reduced nephron endowment. The defect in nephrogenesis centres around the inhibition of ureteric duct branching.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2000.00512.x
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  • 5
    Electronic Resource
    Electronic Resource
    Glomerular stereology: Why, what and how to measure glomerular structure (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 2 (1996), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Quantitative methods are frequently used to analyse the structure of renal glomeruli. However, on most occasions, measurements are made on glomerular profiles (the two-dimensional samples of glomeruli seen in histological sections), and provide little or no information about the structure of whole, three-dimensional glomeruli. Stereology is the discipline concerned with the quantitative analysis of three-dimensional structures. With stereology one can estimate the total number of glomeruli in kidneys, as well as mean glomerular volume, the number of cells in glomeruli, and the length and surface area of glomerular capillaries. In addition to providing a means for detecting structural differences between glomeruli from different specimens, stereology provides quantitative structural information that can be correlated with quantitative physiological, biochemical and molecular data. Over the past decade we have witnessed the development of a new generation of unbiased, cost-efficient stereological methods that are ideally suited to analysing glomeruli. Some of these methods are introduced in this review, and then three recent studies from our laboratories that successfully utilized these methods are described. These studies concerned hypertension, kidney development, and the pathogenesis of focal and segmental glomerulosclerosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1996.tb00106.x
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  • 6
    Electronic Resource
    Electronic Resource
    Proceedings of the Symposium ‘Angiotensin AT1 Receptors: From Molecular Physiology to Therapeutics’: STRUCTURAL CHANGES IN THE RENAL VASCULATURE IN THE SPONTANEOUSLY HYPERTENSIVE RAT: NO EFFECT OF ANGIOTENSIN II BLOCKADE (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 〈list xml:id="l1" style="custom"〉1There is strong evidence for a renal basis to the development of hypertension in the spontaneously hypertensive rat (SHR). Alterations of the SHR renal vasculature, including the glomerulus, may be involved in the initiation and maintenance of hypertension in this animal model.2The arterial walls of pre-glomerular vessels of the SHR are hypertrophied compared with WKY vessels. Unlike other vascular beds in the SHR, this hypertrophy is independent of angiotensin II (AngII).3Glomerular number and volume are similar between SHR and the normotensive Wistar-Kyoto (WKY) rats. These results provide no support for the theory that a reduced filtration surface area within the kidneys of the SHR contributes to the elevated blood pressure in these animals.4Intrarenal hypertrophy may have similar haemodynamic consequences to clipping of the main renal artery, as in Goldblatt hypertension. Further analysis of the role of pre-glomerular arterial hypertrophy is warranted to determine its involvement in the initiation and maintenance of hypertension in the SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb03074.x
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  • 7
    Electronic Resource
    Electronic Resource
    Expression of transforming growth factor-β type II receptor mRNA in embryonic and adult rat kidney (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 1 (1995), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: The transforming growth factor-β (TGF-β) family of growth factors regulates cell proliferation, differentiation, extracellular matrix synthesis and angiogenesis in many developing tissues. Transforming growth factor-β1 was recently shown to affect the branching of ureteric epithelium and nephron formation in cultured rat metanephroi. As the TGF-β type II receptor is specific for the TGF-β family, the present study used in situ hybridization to localize mRNA for this receptor in metanephroi from Sprague-Dawley rat embryos. Transforming growth factor-β type II receptor mRNA was located in ureteric duct epithelium, undifferentiated mesenchymal cells in the nephrogenic zone, vesicles, comma-shaped bodies and S-shaped bodies. In some S-shaped bodies, TGF-β type II receptor mRNA was not expressed in the lower limb, which subsequently forms the renal corpuscle. Expression was not observed in capillary loop stage glomeruli and maturing glomeruli, or in proximal tubules and interstitial cells. In adult rat kidney, TGF-β type II receptor mRNA was expressed in cortical collecting ducts and distal tubules but not in glomeruli or proximal tubules. These findings demonstrate that the prominent expression of TGF-β type II receptor mRNA decreases as glomeruli and tubules develop. Expression then remains undetectable in adult glomeruli and proximal tubules. the developmentally-regulated expression of this receptor suggests a key role in glomerular and nephron development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1995.tb00054.x
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  • 8
    Electronic Resource
    Electronic Resource
    RENAL MEDULLA AND BRADYKININ DURING THE DEVELOPMENT OF HYPERTENSION IN SHR (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The long-term reduction in blood pressure following ACE inhibitor treatment in young spontaneously hypertensive rats (SHR) appears to depend on both the kidney and brady-kinin.2. The aim of this experiment was to examine the effects of ACE inhibition and bradykinin on renal morphology and blood pressure in SHR.3. Between 6 and 10 weeks of age male SHR received one of four treatments: water (n = 26), ramipril (1 mg/kg per day; n = 24), ramipril (1 mg/kg per day) plus Hoe 140 (0.5 mg/kg per day; n = 25) or Hoe 140 (0.5 mg/kg per day; n= 25).4. Renal medullary and cortical volumes were determined stereologically at 10 and 20 weeks of age.5. After 4 weeks of treatment, ramipril reduced the size of the renal medulla while Hoe 140 increased medullary volumes compared to control. Ten weeks after treatment was stopped the renal medulla of the ramipril group had returned to normal, however, there was a persistent increase in medullary volume of both Hoe 140 treated groups.6. Our results imply that bradykinin may influence the size of the renal medulla which may have important effects on the development of hypertension in SHR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02045.x
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  • 9
    Electronic Resource
    Electronic Resource
    Glomerular size and glomerulosclerosis in Australian Aborigines (2000)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2000.005003a96.x
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  • 10
    Electronic Resource
    Electronic Resource
    GLOMERULAR NUMBER AND SIZE IN BMP2 AND BMPR-IA HETEROZYGOUS MICE (2000)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2000.abs136.x
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