Neurobiology of Disease Neurotoxic Activation of Microglia Is Promoted by a Nox1- Dependent NADPH Oxidase

نویسندگان

  • Cyril Chéret
  • Annie Gervais
  • Aurélia Lelli
  • Catherine Colin
  • Lahouari Amar
  • Philippe Ravassard
  • Jacques Mallet
  • Ana Cumano
  • Karl-Heinz Krause
  • Michel Mallat
چکیده

Cyril Chéret,1,2 Annie Gervais,1,2 Aurélia Lelli,1,2 Catherine Colin,1,2 Lahouari Amar,2,3 Philippe Ravassard,2,3 Jacques Mallet,2,3 Ana Cumano,4 Karl-Heinz Krause,5 and Michel Mallat1,2 1Inserm, Unité Mixte de Recherche (UMR) 711, Institut Fédératif de Recherche 70, 75013 Paris, France, 2Université Pierre et Marie Curie Paris 06, 75005 Paris, France, 3Centre National de la Recherche Scientifique, UMR 7091, 75013 Paris, France, 4Inserm, U668, Institut Pasteur, 75724 Paris Cedex 15, France, and 5Biology of Ageing Laboratories, University of Geneva, 1211 Geneva, Switzerland

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

Neurotoxic activation of microglia is promoted by a nox1-dependent NADPH oxidase.

Reactive oxygen species (ROS) modulate intracellular signaling but are also responsible for neuronal damage in pathological states. Microglia, the resident CNS macrophages, are prominent sources of ROS through expression of the phagocyte oxidase which catalytic subunit Nox2 generates superoxide ion (O2(.-)). Here we show that microglia also express Nox1 and other components of nonphagocyte NADP...

متن کامل

Expression of ALS-linked SOD1 mutant increases the neurotoxic potential of microglia via TLR2

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease, in which activated microglia overexpressing ALS-linked SOD1 mutants (mSOD1) are known to contribute to neuronal death. However, it is unclear how mSOD1 expression affects micoglial activation and subsequently damage neurons. In this study, we created mSOD1overexpressing BV-2 microglial cell lines. Following TLR2, but not...

متن کامل

SOD1 mutant increases microglial neurotoxicity - 1 - Expression of ALS-linked SOD1 mutant increases the neurotoxic potential of microglia via TLR2

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease, in which activated microglia overexpressing ALS-linked SOD1 mutants (mSOD1) are known to contribute to neuronal death. However, it is unclear how mSOD1 expression affects micoglial activation and subsequently damage neurons. In this study, we created mSOD1overexpressing BV-2 microglial cell lines. Following TLR2, but not...

متن کامل

Phosphorylation of Nox1 regulates association with NoxA1 activation domain.

RATIONALE Activation of Nox1 initiates redox-dependent signaling events crucial in the pathogenesis of vascular disease. Selective targeting of Nox1 is an attractive potential therapy, but requires a better understanding of the molecular modifications controlling its activation. OBJECTIVE To determine whether posttranslational modifications of Nox1 regulate its activity in vascular cells. M...

متن کامل

Essential role of ATF-1 in induction of NOX1, a catalytic subunit of NADPH oxidase: involvement of mitochondrial respiratory chain.

NADPH oxidase is the major source of superoxide production in cardiovascular tissues. We and others reported that PG (prostaglandin) F2alpha, PDGF (platelet-derived growth factor) and angiotensin II cause hypertrophy of vascular smooth muscle cells by induction of NOX1 (NADPH oxidase 1), a catalytic subunit of NADPH oxidase. We found DPI (diphenylene iodonium), an inhibitor of flavoproteins, in...

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 2008