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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

Genetic background does not result in marked changes to tubulointerstitium. Representative tubulointerstitial areas stained with markers for macrophages (F4/80) (A,B) and cellular proliferation (Ki67) (C,D) for FVB and AxB19 mouse strains. Overall tubulointerstitial architecture shows lack of dilation and associated proliferation of tubular epithelial cells. FVB mice show only occasional positivity for macrophages. Although immunostaining for macrophages is somewhat more frequent for AXB19, across six strains examined (AXB19, A/J, KK/HI, C57BL/6, C3H/He, FVB), there was no correlation between the numbers of macrophages and ACR values (data not shown). Thus, macrophage number is unlikely to contribute to diabetic pathology among these mice.
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fig06: Genetic background does not result in marked changes to tubulointerstitium. Representative tubulointerstitial areas stained with markers for macrophages (F4/80) (A,B) and cellular proliferation (Ki67) (C,D) for FVB and AxB19 mouse strains. Overall tubulointerstitial architecture shows lack of dilation and associated proliferation of tubular epithelial cells. FVB mice show only occasional positivity for macrophages. Although immunostaining for macrophages is somewhat more frequent for AXB19, across six strains examined (AXB19, A/J, KK/HI, C57BL/6, C3H/He, FVB), there was no correlation between the numbers of macrophages and ACR values (data not shown). Thus, macrophage number is unlikely to contribute to diabetic pathology among these mice.

Mentions: We also examined the tubulointerstitium architecture for several mouse strains with high and low ACR values (Fig. 6). Significant tubular changes were not seen. No signs of tubular dilation, extensive tubular proliferation of epithelial cells, or macrophage invasion were found. Thus, diabetes under conditions rendered here did not provoke extensive interstitial tubule pathology.


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)

Genetic background does not result in marked changes to tubulointerstitium. Representative tubulointerstitial areas stained with markers for macrophages (F4/80) (A,B) and cellular proliferation (Ki67) (C,D) for FVB and AxB19 mouse strains. Overall tubulointerstitial architecture shows lack of dilation and associated proliferation of tubular epithelial cells. FVB mice show only occasional positivity for macrophages. Although immunostaining for macrophages is somewhat more frequent for AXB19, across six strains examined (AXB19, A/J, KK/HI, C57BL/6, C3H/He, FVB), there was no correlation between the numbers of macrophages and ACR values (data not shown). Thus, macrophage number is unlikely to contribute to diabetic pathology among these mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig06: Genetic background does not result in marked changes to tubulointerstitium. Representative tubulointerstitial areas stained with markers for macrophages (F4/80) (A,B) and cellular proliferation (Ki67) (C,D) for FVB and AxB19 mouse strains. Overall tubulointerstitial architecture shows lack of dilation and associated proliferation of tubular epithelial cells. FVB mice show only occasional positivity for macrophages. Although immunostaining for macrophages is somewhat more frequent for AXB19, across six strains examined (AXB19, A/J, KK/HI, C57BL/6, C3H/He, FVB), there was no correlation between the numbers of macrophages and ACR values (data not shown). Thus, macrophage number is unlikely to contribute to diabetic pathology among these mice.
Mentions: We also examined the tubulointerstitium architecture for several mouse strains with high and low ACR values (Fig. 6). Significant tubular changes were not seen. No signs of tubular dilation, extensive tubular proliferation of epithelial cells, or macrophage invasion were found. Thus, diabetes under conditions rendered here did not provoke extensive interstitial tubule pathology.

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