The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Catalase deficiency accelerates diabetic renal injury through peroxisomal dysfunction.
Inah Hwang; Jiyoun Lee; Joo Young Huh; Jehyun Park; Hi Bahl Lee; Ye-Shih Ho; Hunjoo Ha (Profiled Author: Ye-Shih Ho)
Department of Bioinspired Science, Division of Life and Pharmaceutical Sciences, Center for Cell Signaling and Drug Discovery Research, College of Pharmacy, Ewha Womans University, Seoul, Korea.
Mitochondrial reactive oxygen species (ROS) play an important role in diabetes complications, including diabetic nephropathy (DN). Plasma free fatty acids (FFAs) as well as glucose are increased in diabetes, and peroxisomes and mitochondria participate in FFA oxidation in an interconnected fashion. Therefore, we investigated whether deficiency of catalase, a major peroxisomal antioxidant, accelerates DN through peroxisomal dysfunction and abnormal renal FFA metabolism. Diabetes was induced by multiple injections of low-dose streptozotocin into catalase knock-out (CKO) and wild-type (WT) C57BL/6 mice. Murine mesangial cells (MMCs) transfected with catalase small interfering RNA followed by catalase overexpression were used to further elucidate the role of endogenous catalase. Despite equivalent hyperglycemia, parameters of DN, along with markers of oxidative stress, were more accelerated in diabetic CKO mice than in diabetic WT mice up to 10 weeks of diabetes. CKO mice and MMCs showed impaired peroxisomal/mitochondrial biogenesis and FFA oxidation. Catalase deficiency increased mitochondrial ROS and fibronectin expression in response to FFAs, which were effectively restored by catalase overexpression or N-acetylcysteine. These data provide unprecedented evidence that FFA-induced peroxisomal dysfunction exacerbates DN and that endogenous catalase plays an important role in protecting the kidney from diabetic stress through maintaining peroxisomal and mitochondrial fitness.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Terlecky, Stanley R
1 September 2000 - 31 July 2006
NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
Total Funding: $ 1,095,399
Stanley R Terlecky; Jay I KoepkeAdvanced drug delivery reviews 2007;59(8):739-47.
Christopher S Wood; Jay I Koepke; Hua Teng; Krissy K Boucher; Sharon Katz; Patrick Chang; Laura J Terlecky; Irene Papanayotou; Paul A Walton; Stanley R TerleckyTraffic (Copenhagen, Denmark) 2006;7(1):97-107.
Stanley R Terlecky; Jay I Koepke; Paul A WaltonBiochimica et biophysica acta 2006;1763(12):1749-54.
Appears in this Publication
Author of this Publication