Mitochondrial Redox Control of Angiogenesis revised submission, 12/23/2004 MITOCHONDRIAL H2O2 REGULATES THE ANGIOGENIC PHENOTYPE VIA PTEN OXIDATION

نویسندگان

  • Kip M. Connor
  • Sita Subbaram
  • Kevin J. Regan
  • Kristin K. Nelson
  • Joseph E. Mazurkiewicz
  • Peter J. Bartholomew
  • Andrew E. Aplin
  • Yu-Tzu Tai
  • Julio Aguirre-Ghiso
  • Sonia C. Flores
  • J. Andres Melendez
چکیده

Centers for Immunology & Microbial Disease, Neuropharmacology & Neuroscience and Cell biology and Cancer Research, Albany Medical College, 47 New Scotland Ave., Albany, NY 12208. Harvard Medical School,M551, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115. Structural and Cell Biology Department of Biomedical Sciences School of Public Health, University at Albany, One University Place, Rensselaer, NY 12144. Webb-Waring Institute for Cancer, Aging and Antioxidant Research, University of Colorado Health Sciences Center, Denver, Colorado 80262. Running Title: Mitochondrial Redox Control of Angiogenesis.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Mitochondrial H2O2 regulates the angiogenic phenotype via PTEN oxidation.

Recent studies have demonstrated that the tumor suppressor PTEN (phosphatase and tensin homolog deleted from chromosome 10), the antagonist of the phosphosphoinositol-3-kinase (PI3K) signaling cascade, is susceptible to H2O2-dependent oxidative inactivation. This study describes the use of redox-engineered cell lines to identify PTEN as sensitive to oxidative inactivation by mitochondrial H2O2....

متن کامل

ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis.

Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) and mitochondria play a critical role in growth factor-induced switch from a quiescent to an angiogenic phenotype in endothelial cells (ECs). However, how highly diffusible ROS produced from different sources can coordinate to stimulate VEGF signaling and drive the angiogenic process remains unknown. Using the cytosol- and mitochond...

متن کامل

Lysosomal Oxidative Stress Cytotoxicity Induced By Para-phenylenediamine Redox Cycling In Hepatocytes

It has already been reported that muscle necrosis induced by various phenylenediamine derivatives are correlated with their autoxidation rate. Now in a more detailed investigation of the cytotoxic mechanism using a model system of isolated hepatocytes and ring-methylated structural isomer durenediamine (DD) we have shown that under aerobic conditions, phenylenediamine induced cytotoxicity and R...

متن کامل

Lysosomal Oxidative Stress Cytotoxicity Induced By Para-phenylenediamine Redox Cycling In Hepatocytes

It has already been reported that muscle necrosis induced by various phenylenediamine derivatives are correlated with their autoxidation rate. Now in a more detailed investigation of the cytotoxic mechanism using a model system of isolated hepatocytes and ring-methylated structural isomer durenediamine (DD) we have shown that under aerobic conditions, phenylenediamine induced cytotoxicity and R...

متن کامل

Loss of bcl-2 during the senescence exacerbates the impaired angiogenic functions in endothelial cells by deteriorating the mitochondrial redox state.

Ageing is an important risk factor for ischemic cardiovascular diseases, although its underlying molecular mechanisms remain to be elucidated. Here, we report a crucial role of Bcl-2 in the impaired angiogenic functions in senescent endothelial cells (ECs) by modulating the mitochondrial redox state. Cellular senescence impaired angiogenic functions in ECs without attenuating the mitogen-activa...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2004