NOX4 Antibodies in Diabetic Nephropathy Research

Mon, 01/09/2012 - 11:33

Diabetic nephropathy (DN) is one of the leading complications resulting from chronic diabetes. It manifests as progressive renal failure caused by mesangial cell hyperplasia and fibrosis, and is one of the leading causes of terminal kidney disease (1). While the etiology is complex, an imbalance between pro- and anti-oxidant pathways in the kidney leading to an excess accumulation of reactive oxygen species (ROS) is believed to contribute in large part to the development of DN. The primary source of ROS in the context of DN are NAD(P)H oxidases, a family of enzymes that facilitate respiratory bursts in phagocytic cells and participate in ROS-mediated signaling in a variety of other cell types (2). In the renal environment, ROS such as superoxide anion and hydrogen peroxide are generated as intermediates in redox reactions but are quickly neutralized by enzymes such as superoxide dismutase and catalase.

Immunocytochemistry/Immunofluorescence: NOX4 Antibody

Recent antibody studies have indicated that high glucose levels up-regulate NAD(P)H oxidases, altering oxidant homeostasis and contributing to vascular dysfunction observed in DN.  Sechi, et al. demonstrated that anti-oxidant enzyme activity was increased in the kidneys of streptozotocine-induced diabetic rats (3), and numerous other studies associate a rise in ROS with susceptibility to DN secondary to diabetes. Podocytes are especially vulnerable to the effects of high glucose levels; Piwkowska et al confirmed the pivotal role of the NAD(P)H oxidase, Nox4, in promoting damage characteristic of DN (4). This is not surprising, as Nox4 antibody research have suggested NOX4 is a master regulator of oxidative stress in previous studies, and is known to be constitutively expressed in the kidney (4,5). In addition to podocytes, mesangial cells show the pathological features of DN and elevated NOX4 activity subsequent to hyperglycemia (4). Considerable data has been amassed solidifying the potential of NOX4 as a therapeutic target for DN, and interesting evidence has emerged suggesting that herbal remedies may help treat DN by interfering with NOX4 (6).

Novus offers high quality NOX4 antibodies, guaranteed for most species and immunological applications. NOX4 antibodies are supplied in a variety of DyLight fluorescent conjugates and excellent staining data is available for each. Please contact our technical support department with any questions or for additional information.

  1. Ren G, Huynh C, Bijian K, Cybulsky A.  2008.  Role of apoptosis signal-regulating kinase 1 in complement-mediated glomerular epithelial cell injury.  Mol Immunol.  45:2236-2246.
  2. Touyz R, Briones A.  2011.  Reactive oxygen species and vascular biology: implications in human hypertension.  Hypertension Research  34, 5-14.
  3. Sechi L, Ceriello A, Griffin CA, Catena C, Anstad P, Schambelan M, Bartoli E.  1997.  Renal antioxidant enzyme mRNA levels are increased in rats with experimental diabetes mellitus.  Diabetologia  40:23-29.
  4. Piwkowska T, Rogacka D, Audzeyenka I, Jankowski M, Angielski S.  2011.  High Glucose Concentration Affects the Oxidant-Antioxidant Balance in Cultured Mouse Podocytes.  J Biol Chem  112:1661-1672.
  5. Jeong S, Kim S, Kwon T, YuK, Kim S.  2011.  Schizandrin prevents damage of murine mesangial cells via blocking NAD(P)H oxidase-induced ROS signaling in high glucose.  Food and Chemical Toxicology  (article in press).
  6. Morgensen C.  2003.  Microalbuminuria and hypertension with focus on type 1 and type 2 diabetes.  J Intern Med  254:45-66.
  7. Yi F, Zhang A, Li N, Muh R, Fillet M, Renert A, Li P.  Inhibition of ceramide-redox signaling pathway blocks glomerular injury in hyperhomocysteinemic rats. Kidney Int  70, 88-96. 2006.

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