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Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita mutation.

Wu X, Davis RC, McMillen TS, Schaeffer V, Zhou Z, Qi H, Mazandarani PN, Alialy R, Hudkins KL, Lusis AJ, LeBoeuf RC - Physiol Rep (2014)

Bottom Line: Urine albumin-to-creatinine ratios (ACRs), volume and cystatin C as well as blood urea nitrogen and lipoprotein levels varied significantly among the diabetic strains.ACRs correlated with cystatin C (P = 0.0286), a measure of hyperfiltration and an interstitial tubular marker associated with DN onset in humans suggesting that tubule damage as well as podocyte-stress contributed to reduced kidney function assessed by ACR.However, glomerular hypertrophy and collagen IV content were found to vary significantly among strains suggesting a genetic basis for early onset features of DN.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

No MeSH data available.


Related in: MedlinePlus

Impact of genetic background on diabetic kidney pathology as measured by (A) Glomerular area (μm2) and (B) Percent glomerular area staining for collagen IV. Genetic background variation is determined by the maternal strain, indicated on the horizontal axis. Strains are in rank order based on the average level observed in diabetic mice. (C) Example of collagen IV immunostaining for two mouse strains, CBA and FVB, with one control shown lacking treatment with primary antibody. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐5A, and 5B at the end of the manuscript.
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fig05: Impact of genetic background on diabetic kidney pathology as measured by (A) Glomerular area (μm2) and (B) Percent glomerular area staining for collagen IV. Genetic background variation is determined by the maternal strain, indicated on the horizontal axis. Strains are in rank order based on the average level observed in diabetic mice. (C) Example of collagen IV immunostaining for two mouse strains, CBA and FVB, with one control shown lacking treatment with primary antibody. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐5A, and 5B at the end of the manuscript.

Mentions: A primary marker of kidney damage and dysfunction is glomerular hypertrophy. Among the nondiabetic strains, areas ranged from 1931 to 4163 μm2 (Fig. 5A). With diabetes, six strains showed no change while most of the remaining strains showed modest increases of ~25% and C3H/HeJ showed a 2‐fold increase. Thus, there appear to be genetic factors contributing to glomerular area in both nondiabetic and diabetic mice. Glomerular hypertrophy did not correlate with ACR or with kidney weight, another trait associated with glomerular hypertrophy. In addition, based on visual inspection of H&E stained kidney sections, no major changes in gross structure of the tubulointerstitium were seen for any of the strains.


Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita mutation.

Wu X, Davis RC, McMillen TS, Schaeffer V, Zhou Z, Qi H, Mazandarani PN, Alialy R, Hudkins KL, Lusis AJ, LeBoeuf RC - Physiol Rep (2014)

Impact of genetic background on diabetic kidney pathology as measured by (A) Glomerular area (μm2) and (B) Percent glomerular area staining for collagen IV. Genetic background variation is determined by the maternal strain, indicated on the horizontal axis. Strains are in rank order based on the average level observed in diabetic mice. (C) Example of collagen IV immunostaining for two mouse strains, CBA and FVB, with one control shown lacking treatment with primary antibody. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐5A, and 5B at the end of the manuscript.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255814&req=5

fig05: Impact of genetic background on diabetic kidney pathology as measured by (A) Glomerular area (μm2) and (B) Percent glomerular area staining for collagen IV. Genetic background variation is determined by the maternal strain, indicated on the horizontal axis. Strains are in rank order based on the average level observed in diabetic mice. (C) Example of collagen IV immunostaining for two mouse strains, CBA and FVB, with one control shown lacking treatment with primary antibody. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐5A, and 5B at the end of the manuscript.
Mentions: A primary marker of kidney damage and dysfunction is glomerular hypertrophy. Among the nondiabetic strains, areas ranged from 1931 to 4163 μm2 (Fig. 5A). With diabetes, six strains showed no change while most of the remaining strains showed modest increases of ~25% and C3H/HeJ showed a 2‐fold increase. Thus, there appear to be genetic factors contributing to glomerular area in both nondiabetic and diabetic mice. Glomerular hypertrophy did not correlate with ACR or with kidney weight, another trait associated with glomerular hypertrophy. In addition, based on visual inspection of H&E stained kidney sections, no major changes in gross structure of the tubulointerstitium were seen for any of the strains.

Bottom Line: Urine albumin-to-creatinine ratios (ACRs), volume and cystatin C as well as blood urea nitrogen and lipoprotein levels varied significantly among the diabetic strains.ACRs correlated with cystatin C (P = 0.0286), a measure of hyperfiltration and an interstitial tubular marker associated with DN onset in humans suggesting that tubule damage as well as podocyte-stress contributed to reduced kidney function assessed by ACR.However, glomerular hypertrophy and collagen IV content were found to vary significantly among strains suggesting a genetic basis for early onset features of DN.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

No MeSH data available.


Related in: MedlinePlus