The relationship between nephron number, kidney size and body weight in two inbred mouse strains

Murawski, Inga J.; Maina, Rita W.; Gupta, Indra R.

doi:10.4161/org.6.3.12125

Cited by 37 publications

(40 citation statements)

References 26 publications

(51 reference statements)

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“…The results of previous studies that examined sex differences in the C57BL/6J mouse model, with regards to nephron endowment, are inconclusive (12,18). In the present study, nephron number in adulthood was not different between the sexes; however, nephron density was greater in females (highly significant at 10 mo), which may be explained by their reduced kidney size compared with males and also implies a proportionately greater increase in tubular mass in males.…”

Section: Hyperoxia Does Not Appear To Affect Nephrogenesiscontrasting

confidence: 46%

Neonatal hyperoxia: effects on nephrogenesis and long-term glomerular structure

Sutherland

O’Reilly

Kenna

et al. 2013

American Journal of Physiology-Renal Physiology

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Preterm neonates are born while nephrogenesis is ongoing and are commonly exposed to factors in the extrauterine environment that may impair renal development. Supplemental oxygen therapy exposes the preterm infant to a hyperoxic environment that may induce oxidative stress. Our aim was to determine the immediate and long-term effects of exposure to hyperoxia, during the period of postnatal nephrogenesis, on renal development. Newborn mice (C57BL/6J) were kept in a normoxic (room air, 21% oxygen) or a controlled hyperoxic (65% oxygen) environment from birth to postnatal day 7 ( P7d). From P7d, animals were maintained in room air until early adulthood at postnatal day 56 ( P56d) or middle age (10 mo; P10mo). Pups were assessed for glomerular maturity and renal corpuscle cross-sectional area at P7d (control n = 14; hyperoxic n = 14). Nephron number and renal corpuscle size were determined stereologically at P56d (control n = 14; hyperoxic n = 14) and P10mo (control n = 10; hyperoxic n = 10). At P7d, there was no effect of hyperoxia on glomerular size or maturity. In early adulthood ( P56d), body weights, relative kidney weights and volumes, and nephron number were not different between groups, but the renal corpuscles were significantly enlarged. This was no longer evident at P10mo, with relative kidney weights and volumes, nephron number, and renal corpuscle size not different between groups. Furthermore, hyperoxia exposure did not significantly accelerate glomerulosclerosis in middle age. Hence, our findings show no overt long-term deleterious effects of early life hyperoxia on glomerular structure.

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Section: Hyperoxia Does Not Appear To Affect Nephrogenesiscontrasting

confidence: 46%

Neonatal hyperoxia: effects on nephrogenesis and long-term glomerular structure

Sutherland

O’Reilly

Kenna

et al. 2013

American Journal of Physiology-Renal Physiology

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“…Although humans have almost a 10-fold variation in nephron number, the average is about 900,000 nephrons per kidney (35). By contrast, mice have about 20,000 nephrons per kidney (36). The average resting glomerular filtration rate (GFR) in humans is 125 mL/min, whereas in mice it is roughly 0.25 mL/min (37).…”

Section: Discussionmentioning

confidence: 99%

Differentiated kidney epithelial cells repair injured proximal tubule

Kusaba

Lalli

Kramann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

410

381

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Significance When epithelial cells in the proximal portion of the nephron are damaged they rapidly proliferate to repair the damage to the kidney. Whether a stem cell is responsible for this proliferative response or not is controversial. Although a scattered population of cells can be found in the human proximal tubule that seem to have stem-cell characteristics, they could also represent isolated damaged cells that have dedifferentiated and lost their epithelial characteristics. We resolve these conflicting models using genetic lineage analysis to demonstrate that fully differentiated proximal tubule cells not only proliferate after injury, but they also upregulate apparent stem-cell markers. This study shows that epithelial dedifferentiation is responsible for repair of mouse proximal tubule, rather than an adult stem-cell population.

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“…Total nephron counts were obtained by counting every tenth section as we have done previously. 21 Each kidney was sectioned in its entirety and serial sections of 7 mm thickness were obtained and stained with hematoxylin and eosin. The sections were analyzed using Image J (v1.36b).…”

Section: Methodsmentioning

confidence: 99%

Claudin-7, -16, and -19 during mouse kidney development

et al. 2014

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Abbreviations: E, embryonic day; P, postnatal; FHHNC, familial hypomagnesaemia with hypercalciuria and nephrocalcinosis; nd, nephric duct; ub, ureteric bud; MET, mesenchymal to epithelial transition.Members of the claudin family of tight junction proteins are critical for establishing epithelial barriers and for the regulation of paracellular transport. To understand their roles during kidney development, we first performed RT-PCR analyses and determined that 23 claudin family members were expressed in embryonic day (E) 13.5 mouse kidneys. Based on their developmental expression and phenotypes in mouse models, we hypothesized that 3 claudin members could affect nephron formation during kidney development. Using whole mount in situ hybridization and immunohistochemistry, we demonstrated that Claudin-7 (Cldn7) was expressed in the nephric duct, the emerging ureteric bud, and in tubules derived from ureteric bud branching morphogenesis. In contrast, Claudin-16 (Cldn16) and Claudin-19 (Cldn19) were expressed at later stages of kidney development in immature renal tubules that become the Loop of Henle. To determine if a loss of these claudins would perturb kidney development, we examined newborn kidneys from mutant mouse models lacking Cldn7 or Cldn16. In both models, we noted no evidence for any congenital renal malformation and quantification of nephron number did not reveal a decrease in nephron number when compared to wildtype littermates. In summary, Cldn7, Cldn16, and Cldn19 are expressed in different epithelial lineages during kidney development. Mice lacking Cldn7 or Cldn16 do not have defects in de novo nephron formation, and this suggests that these claudins primarily function to regulate paracellular transport in the mature nephron.

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The relationship between nephron number, kidney size and body weight in two inbred mouse strains

Cited by 37 publications

References 26 publications

Neonatal hyperoxia: effects on nephrogenesis and long-term glomerular structure

Neonatal hyperoxia: effects on nephrogenesis and long-term glomerular structure

Differentiated kidney epithelial cells repair injured proximal tubule

Claudin-7, -16, and -19 during mouse kidney development

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