Brain Degenerative Diseases P01-01 Control of Neurite Growth by S-nitroglutathione Reductase via Denitrosylation of Hdac2

نویسندگان

  • K Wu
  • W Su
  • B Wen
  • Y Zhang
  • T Wang
  • L Zhang
  • P Wang
  • J Wang
  • L Liu
  • C Chen
  • DI Finkelstein
  • MJ Fox
چکیده

Neurite growth control is central to the development and plasticity of neural circuits. By controlling intracellular level of S-nitrosoglutathione (GSNO), S-nitrosoglutathione reductase (GSNOR) has been implicated in many biological processes. However, as the sole brain alcohol dehydrogenase, its role in the nerve system is still largely a mystery. Here we report that GSNOR is significantly downregulated during developing mouse brain and the neurite growth was negatively regulated by GSNOR. Our data further show this negative regulation is mediated by denitrosylation of histone deacetylase 2 (HDAC2). Our findings define a novel role of GSNOR in neurite development via interacting with the NO signaling and provide a new molecular insight into the control of neurite growth and neurogenesis.

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

Improving Brain Magnetic Resonance Image (MRI) Segmentation via a Novel Algorithm based on Genetic and Regional Growth

Background: Regarding the importance of right diagnosis in medical applications, various methods have been exploited for processing medical images solar. The method of segmentation is used to analyze anal to miscall structures in medical imaging.Objective: This study describes a new method for brain Magnetic Resonance Image (MRI) segmentation via a novel algorithm based on genetic and regiona...

متن کامل

Requirement of Retinoic Acid Receptor β for Genipin Derivative-Induced Optic Nerve Regeneration in Adult Rat Retina

Like other CNS neurons, mature retinal ganglion cells (RGCs) are unable to regenerate their axons after nerve injury due to a diminished intrinsic regenerative capacity. One of the reasons why they lose the capacity for axon regeneration seems to be associated with a dramatic shift in RGCs' program of gene expression by epigenetic modulation. We recently reported that (1R)-isoPropyloxygenipin (...

متن کامل

Retraction: Denitrosylation of HDAC2 by targeting Nrf2 restores glucocorticosteroid sensitivity in macrophages from COPD patients.

Chronic obstructive pulmonary disease (COPD), which is caused primarily by cigarette smoking, is a major health problem worldwide. The progressive decline in lung function that occurs in COPD is a result of persistent inflammation of the airways and destruction of the lung parenchyma. Despite the key role of inflammation in the pathogenesis of COPD, treatment with corticosteroids - normally hig...

متن کامل

Squid ink polysaccharide reduces cyclophosphamide-induced testicular damage via Nrf2/ARE activation pathway in mice

Objective(s):Cyclophosphamide (CP) toxicity on testis was hampered by squid ink polysaccharide (SIP) via restoration of antioxidant ability in our previous investigations. This study investigated roles of Nrf2/ARE signal pathway in testis of treated mice. Materials and Methods: Male Kunming mice were employed to undergo treatment with SIP and/or CP. Protein levels of Nrf2, keap-1, histone deac...

متن کامل

Regulation of Neuronal Traits by a Novel Transcriptional Complex

The transcriptional repressor, REST, helps restrict neuronal traits to neurons by blocking their expression in nonneuronal cells. To examine the repercussions of REST expression in neurons, we generated a neuronal cell line that expresses REST conditionally. REST expression inhibited differentiation by nerve growth factor, suppressing both sodium current and neurite growth. A novel corepressor ...

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 2013