Brigitte Pettmann

ORCID: 0000-0003-2059-5438
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About
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Research Areas
  • Nerve injury and regeneration
  • Neurogenetic and Muscular Disorders Research
  • Neurogenesis and neuroplasticity mechanisms
  • Amyotrophic Lateral Sclerosis Research
  • Cell death mechanisms and regulation
  • Mitochondrial Function and Pathology
  • RNA Research and Splicing
  • Neuroscience and Neuropharmacology Research
  • RNA modifications and cancer
  • S100 Proteins and Annexins
  • Fibroblast Growth Factor Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cancer, Hypoxia, and Metabolism
  • Axon Guidance and Neuronal Signaling
  • Cancer-related gene regulation
  • Amino Acid Enzymes and Metabolism
  • Virus-based gene therapy research
  • Tissue Engineering and Regenerative Medicine
  • RNA Interference and Gene Delivery
  • Nuclear Receptors and Signaling
  • GDF15 and Related Biomarkers
  • Cancer Research and Treatments
  • Endoplasmic Reticulum Stress and Disease
  • Neuroscience and Neural Engineering
  • Neural Networks and Applications

Inserm
2001-2014

Institut de Neurobiologie de la Méditerranée
2008-2014

Aix-Marseille Université
2010-2014

Institut de Biologie du Développement Marseille
1998-2006

Centre National de la Recherche Scientifique
1988-2006

Centre d’Immunologie de Marseille-Luminy
2003

Centre National pour la Recherche Scientifique et Technique (CNRST)
1990

Université de Strasbourg
1988-1989

University of California, San Diego
1988

Institut de Chimie
1979-1981

Embryonic and neonatal neurons require specific trophic supplements for their survival the induction of transmitter-synthesizing enzymes in vivo vitro. Acidic basic fibroblast growth factor (aFGF, bFGF) closely related astroglial factors AGF-1 AGF-2 were studied putative neurotrophic functions using dissociated, highly neuron-enriched cultures from chick rat peripheral ganglia central nervous system tissues. ciliary ganglion only that responded to bFGF by enhanced equivalent obtained with...

10.1073/pnas.84.15.5459 article EN Proceedings of the National Academy of Sciences 1987-08-01

About 50% of spinal motoneurons undergo programmed cell death (PCD) after target contact, but little is known about how this process initiated. Embryonic coexpress the receptor Fas and its ligand FasL at stage which PCD to begin. In absence trophic factors, many die in culture within 2 d. Most (75%) these were saved by Fas-Fc body, blocks interactions between FasL, or caspase-8 inhibitor tetrapeptide IETD. Therefore, activation endogenous underlies induced deprivation. presence neurotrophic...

10.1083/jcb.147.5.1049 article EN The Journal of Cell Biology 1999-11-29

Growth factor Cell culture Glial cell

10.1016/0014-5793(85)80851-6 article EN FEBS Letters 1985-09-09

ABSTRACT Apoptosis, or programmed cell death, involves a cascade of regulatory events leading to the activation specific proteases. However, key substrates for these proteases remain be identified. We previously demonstrated that levels five unidentified polypeptides were specifically increased in neurons from embryonic chicken ciliary ganglia undergoing apoptosis by trophic deprivation. Here we show microsequencing two they are fragments actin. One them represents cleavage actin at site...

10.1242/jcs.111.6.713 article EN Journal of Cell Science 1998-03-15

The cytokines ciliary neurotrophic factor (CNTF) and leukemia inhibitory (LIF) signal through a receptor complex formed between two transmembrane proteins, gp130 LIFRbeta. In addition, CNTF also uses ligand-binding component which is anchored to the cell membrane. case of cardiotrophin-1 (CT-1), LIFRbeta required in cardiomyocytes, but this has not been proven neurons, published data suggest that motoneurons may use different complex. We used Lifrbeta knockout mice assess requirement for...

10.1002/(sici)1097-4547(19990101)55:1<119::aid-jnr13>3.0.co;2-6 article EN Journal of Neuroscience Research 1999-01-01

Abstract We have developed a silicone nerve regeneration chamber that is partitioned into two compartments by strip of nitrocellulose paper. The modified two‐compartment allows the investigation effects on rat sciatic trophic or growth factors are initially bound to partition. In this study we compared untreated nitrocellulose, siliconized strip, and had been soaked in basic fibroblast factor (FGF) solution. FGF known angiogenic mitogen for endothelial cells, fibroblasts, Schwann cells. All...

10.1002/jnr.490200306 article EN Journal of Neuroscience Research 1988-07-01

The human SOD1G93A transgenic mouse has been used extensively since its development in 1994 as a model for amyotrophic lateral sclerosis (ALS). In that time, great many insights into the toxicity of mutant SOD1 have gained using this and other SOD models. They all demonstrate selective towards motor neurons some cases features pathology seen disease. These models two major drawbacks. Firstly generation robust preclinical data these highlighted an area concern. Secondly, amount time required...

10.1371/journal.pone.0023244 article EN cc-by PLoS ONE 2011-08-18

Cellular responses to protein misfolding are thought play key roles in triggering neurodegeneration. In the mutant superoxide dismutase (mSOD1) model of amyotrophic lateral sclerosis (ALS), subsets motoneurons selectively vulnerable degeneration. Fast fatigable activate an endoplasmic reticulum (ER) stress response that drives their early degeneration while a subset mSOD1 show exacerbated sensitivity activation motoneuron-specific Fas/NO pathway. However, links between two mechanisms and...

10.1523/jneurosci.5431-11.2012 article EN cc-by-nc-sa Journal of Neuroscience 2012-04-04

The two fibroblast growth factors called acidic and basic FGF (aFGF bFGF) show a strong homology (55%) of their amino acid sequence (Esch et al.: Proc. Nat. Acad. Sci. USA 85:6507-6511, 1985). effects these on the rate proliferation rat astroblasts expression glutamine synthetase activity in cells grown primary culture were investigated compared under various conditions. In all experimental conditions used, both triggered to same extent with similar dose dependence. mitogenic activities aFGF...

10.1002/glia.440010204 article EN Glia 1988-01-01

Programmed cell death of motoneurons in the developing spinal cord is thought to be regulated through availability target-derived neurotrophic factors. When deprived trophic support, embryonic vitro over-express FasL, a ligand activating Fas-mediated pathway. How factors regulate expression FasL presently unclear, but two regulators FOXO3a (FKHRL1) and JNK have been described play role other types. Thus, their potential function was investigated this study.We show here that as result removal...

10.1186/1471-2202-5-48 article EN cc-by BMC Neuroscience 2004-11-29

Abstract Spinal muscular atrophy (SMA) is among the most common recessive autosomal diseases and characterized by loss of spinal motor neurons. A gene termed ‘Survival Motor Neurons' (SMN) has been identified as SMA‐determining gene. Recent work indicates involvement SMN protein its associated SIP1 in spliceosomal snRNP biogenesis. However, function remains unknown. Here, we have studied subcellular localization rat cord more generally central nervous system (CNS), light fluorescence...

10.1046/j.1460-9568.1999.00428.x article EN European Journal of Neuroscience 1999-01-01

Abstract The presence of fibroblast growth factor (FGF) was investigated by immunocytochemistry in cultured neuronal cells derived from the peripheral (PNS) and central nervous system (CNS) chick rat embryos. Polyclonal antimouse FGF antibodies, which cross‐react with basic acidic FGF, were used peroxidase immunocytochemical staining method. immunoreactivity found neurons. Staining intensity brain increased during culture period, reached a maximum after 6–8 days, subsequently declined....

10.1002/jnr.490190204 article EN Journal of Neuroscience Research 1988-02-01

Embryonic motoneurons from mutant SOD1 (mSOD1) mouse models of amyotrophic lateral sclerosis (ALS), but not wild-type motoneurons, can be triggered to die by exposure nitric oxide (NO), leading activation a motoneuron-specific signaling pathway downstream the death receptor Fas/CD95. To identify effectors mSOD1-dependent cell death, we performed proteomic analysis. Treatment cultured mSOD1 with NO led 2.5-fold increase in levels collapsin response mediator protein 4a (CRMP4a) . In vivo ,...

10.1523/jneurosci.5411-09.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-01-13

Activation of the Fas death receptor leads to motoneurons in culture. To investigate role programmed cell and pathological situations, we used several mutant mice deficient for signaling made a novel transgenic FADD-DN (FAS-associated domain-dominant-negative) strain. In vitro, from all these were found be resistant activation show delay trophic deprivation-induced death. During normal development vivo, no changes motoneuron survival observed. However, number surviving was twofold higher...

10.1523/jneurosci.23-24-08526.2003 article EN Journal of Neuroscience 2003-09-17
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