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Nox-4 deletion reduces oxidative stress and injury by PKC-α-associated mechanisms in diabetic nephropathy.

Thallas-Bonke V, Jha JC, Gray SP, Barit D, Haller H, Schmidt HH, Coughlan MT, Cooper ME, Forbes JM, Jandeleit-Dahm KA - Physiol Rep (2014)

Bottom Line: Nox4 deletion attenuated diabetes-associated increases in albuminuria, glomerulosclerosis, and extracellular matrix accumulation.Lack of Nox4 resulted in a decrease in diabetes-induced renal cortical ROS derived from the mitochondria and the cytosol, urinary isoprostanes, and PKC activity.Downregulation of the PKC pathway was observed in tandem with reduced expression of vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β1 and restoration of the podocyte slit pore protein nephrin.

View Article: PubMed Central - PubMed

Affiliation: Diabetes Complications Division, Baker IDI Heart & Diabetes Institute, JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Melbourne, Victoria, Australia Department of Medicine, Austin and Northern Clinical Schools, University of Melbourne, Melbourne, Victoria, Australia.

No MeSH data available.


Related in: MedlinePlus

(A) Analysis of Nox4 mRNA levels in the renal cortex of control wild‐type and knockout mice. B) Genotyping by PCR of genomic DNA extracted from mouse tails of wild‐type and Nox4 knockout mice.
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fig01: (A) Analysis of Nox4 mRNA levels in the renal cortex of control wild‐type and knockout mice. B) Genotyping by PCR of genomic DNA extracted from mouse tails of wild‐type and Nox4 knockout mice.

Mentions: Deletion of Nox4 was confirmed by the analysis of Nox4 mRNA levels in the renal cortex of kidneys and by genotyping by PCR of genomic DNA extracted from mouse tails (Fig. 1).


Nox-4 deletion reduces oxidative stress and injury by PKC-α-associated mechanisms in diabetic nephropathy.

Thallas-Bonke V, Jha JC, Gray SP, Barit D, Haller H, Schmidt HH, Coughlan MT, Cooper ME, Forbes JM, Jandeleit-Dahm KA - Physiol Rep (2014)

(A) Analysis of Nox4 mRNA levels in the renal cortex of control wild‐type and knockout mice. B) Genotyping by PCR of genomic DNA extracted from mouse tails of wild‐type and Nox4 knockout mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255803&req=5

fig01: (A) Analysis of Nox4 mRNA levels in the renal cortex of control wild‐type and knockout mice. B) Genotyping by PCR of genomic DNA extracted from mouse tails of wild‐type and Nox4 knockout mice.
Mentions: Deletion of Nox4 was confirmed by the analysis of Nox4 mRNA levels in the renal cortex of kidneys and by genotyping by PCR of genomic DNA extracted from mouse tails (Fig. 1).

Bottom Line: Nox4 deletion attenuated diabetes-associated increases in albuminuria, glomerulosclerosis, and extracellular matrix accumulation.Lack of Nox4 resulted in a decrease in diabetes-induced renal cortical ROS derived from the mitochondria and the cytosol, urinary isoprostanes, and PKC activity.Downregulation of the PKC pathway was observed in tandem with reduced expression of vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β1 and restoration of the podocyte slit pore protein nephrin.

View Article: PubMed Central - PubMed

Affiliation: Diabetes Complications Division, Baker IDI Heart & Diabetes Institute, JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Melbourne, Victoria, Australia Department of Medicine, Austin and Northern Clinical Schools, University of Melbourne, Melbourne, Victoria, Australia.

No MeSH data available.


Related in: MedlinePlus