NDLI: Calcineurin Aß regulates NADPH oxidase (Nox) expression and activity via nuclear factor of activated T cells (NFAT) in response to high glucose.

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Calcineurin Aß regulates NADPH oxidase (Nox) expression and activity via nuclear factor of activated T cells (NFAT) in response to high glucose.

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Calcineurin Aß regulates NADPH oxidase (Nox) expression and activity via nuclear factor of activated T cells (NFAT) in response to high glucose.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Williams, Clintoria R. Gooch, Jennifer L.
Description	Author Affiliation: Williams CR ( From the Atlanta Veterans Administration Medical Center, Atlanta, Georgia 30033 and.)
Abstract	Hypertrophy is an adaptive response that enables organs to appropriately meet increased functional demands. Previously, we reported that calcineurin (Cn) is required for glomerular and whole kidney hypertrophy in diabetic rodents (Gooch, J. L., Barnes, J. L., Garcia, S., and Abboud, H. E. (2003). Calcineurin is activated in diabetes and is required for glomerular hypertrophy and ECM accumulation. Am. J. Physiol. Renal Physiol. 284, F144-F154; Reddy, R. N., Knotts, T. L., Roberts, B. R., Molkentin, J. D., Price, S. R., and Gooch, J. L. (2011). Calcineurin Aß is required for hypertrophy but not matrix expansion in the diabetic kidney. J. Cell Mol. Med. 15, 414-422). Because studies have also implicated the reactive oxygen species-generating enzymes NADPH oxidases (Nox) in diabetic kidney responses, we tested the hypothesis that Nox and Cn cooperate in a common signaling pathway. First, we examined the role of the two main isoforms of Cn in hypertrophic signaling. Using primary kidney cells lacking a catalytic subunit of Cn (CnA (-/-) or CnAß(-/-)), we found that high glucose selectively activates CnAß, whereas CnA is constitutively active. Furthermore, CnAß but not CnA mediates hypertrophy. Next, we found that chronic reactive oxygen species generation in response to high glucose is attenuated in CnAß(-/-) cells, suggesting that Cn is upstream of Nox. Consistent with this, loss of CnAß reduces basal expression and blocks high glucose induction of Nox2 and Nox4. Inhibition of nuclear factor of activated T cells (NFAT), a CnAß-regulated transcription factor, decreases Nox2 and Nox4 expression, whereas NFAT overexpression increases Nox2 and Nox4, indicating that the CnAß/NFAT pathway modulates Nox. These data reveal that the CnAß/NFAT pathway regulates Nox and plays an important role in high glucose-mediated hypertrophic responses in the kidney.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	8
Volume Number	289
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2014-02-21
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Calcineurin Metabolism Glucose Pharmacology Membrane Glycoproteins NADPH Oxidase NFATC Transcription Factors Animals Enzyme Activation Drug Effects Fibroblasts Enzymology Pathology Hypertrophy Kidney Mice Models, Biological Genetics Reactive Oxygen Species Transcription, Genetic Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S. Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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