Journal de la Société de Biologie (J Soc Biol )

Publisher: Société de biologie (Paris, France); Agence francophone pour l'enseignement supérieur et la recherche; France. Délégation générale à la langue française, EDP Sciences

Description

Le Journal de la Société de Biologie publie des mises au point de haut niveau en langue française, consacrées à des sujets d'actualité en biologie. Écrits par des spécialistes, les articles groupés par theme font un tour complet des questions traitées. Vous y trouverez également un état des avancées les plus récentes et la bibliographie correspondante.

  • Impact factor
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  • 5-year impact
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  • Cited half-life
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  • Immediacy index
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  • Eigenfactor
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  • Website
    Journal de la Société de Biologie website
  • ISSN
    1295-0661
  • OCLC
    41537709
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

EDP Sciences

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's personal website or institutional website or OAI compliant website
    • Some journals require an embargo for deposit in funder's designated repositories (see journal)
    • Publisher's version/PDF may be used (see journal)
    • Must link to publisher version
    • Publisher copyright and source must be acknowledged
    • On a non-profit server
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The vertebrate neuron axon has long been considered as devoid of the protein synthesis machinery. During the early nineties however, the cytochemical visualization of identified mRNAs within certain rodent neuron axons challenged this dogma of cellular neurobiology. The aim of this paper is to illustrate, taking mainly the mouse olfactory system as an example, conceptual and methodological approaches developed in particular in my group, that aim at identifying the function of these axonal mRNAs.
    Journal de la Société de Biologie 02/2009; 203(1):65-73.
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    ABSTRACT: The formation of blood cells and vascular networks occurs simultaneously during development, and both lineages remain in close association in all adult tissues. The functional setting of both systems within the embryo and their renewal during adult life are highly complex processes, and require the involvement of numerous molecular actors, the activities of which are often overlapping. Here, I review the activity of TAL-1, a basic-helix-loop-helix transcription factor, which plays a key role in the formation and functioning of both blood and endothelial systems, with a particular emphasis on recent data that associate TAL-1 with angiogenesis.
    Journal de la Société de Biologie 02/2009; 203(2):143-53.
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    ABSTRACT: The endothelium, lining the inner side of all vessel types, is constituted of a monolayer of endothelial cells with cobblestone morphology. Endothelial cell-cell contacts contain numerous transmembrane adhesive proteins that are either clustered in junctional structures or located along the intercellular cleft. These proteins promote cell-cell adhesion and control vascular permeability to fluids and molecules, as well as transmigration of various types of leukocytes. In addition, recent findings showed that constituents of the junctions might be part of the vascular invasion machinery by activating cell protrusions. Such activities may thus be considered as markers of pathological angiogenesis or targets of antiangiogenic therapy.
    Journal de la Société de Biologie 02/2009; 203(2):119-23.
  • Journal de la Société de Biologie 02/2009; 203(2):209.
  • Journal de la Société de Biologie 02/2009; 203(1):5-1.
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    ABSTRACT: The mammalian circadian clock, whose central component is located in the suprachiasmatic nucleus of the hypothalamus (SCN), orchestrates rhythmic events in metabolism, physiology and behavior. Adaptation of the organism to its environment requires precise adjustment of the clock to the 24 h astronomical time, primarily by the light/dark cycle. Photic synchronization acts on both the molecular loops which trigger circadian oscillations and the phasing of the multiple SCN cellular oscillators whose coordination permits elaboration of the rhythmic message that will be distributed throughout the organism. It is concomitant with structural plastic events characterized by day/night rearrangements of the SCN neuronal-glial network. The two main sources of SCN efferents, namely the VIP (vasoactive intestinal peptide)-synthesizing neurons which are major integrators of photic signals and the AVP (arginine-vasopressin)-synthesizing neurons which are known to importantly contribute to conveying rhythmic messages to brain targets, are involved in these mechanisms. Over the light/dark cycle, they indeed undergo ultrastructural changes in the extent of their membrane coverage by glial, axon terminal and/or somato-dendritic elements. These structural rearrangements appear to be dependent on light entrainment, as the rhythmic expression in SCN of glial fibrillary acidic protein (GFAP), a marker for brain astrocytes whose changing expression has proved to be a reliable index of neuronal-glial plasticity, is disrupted under constant darkness. Glucocorticoid hormones, which are known as important endocrine outputs of the clock, are required to maintain amplitude of the SCN GFAP rhythm to normal values, indicating that they modulate astrocytic plasticity within the SCN and, therefore, nycthemeral changes of the configuration of its neuronal-glial network. The view that such plastic events may subserve synchronization of the clock to the light-dark cycle is reinforced by other data showing that the daily fluctuations of circulating glucocorticoids actually are involved in modulation of light effects, contributing to the resistance of the circadian timing system to variations of the photoperiod. It is thus proposed that the capacity of the clock to integrate cyclic variations of the environment rely on the inherent capacity of the SCN to undergo neuronal-glial plasticity.
    Journal de la Société de Biologie 02/2009; 203(1):49-63.
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    ABSTRACT: VEGF represents a model of gene expression regulation. RAS/RAF/MEK/ERK and PI3 Kinase pathways, activated in response to growth factors stimulation or by oncogenes, contribute to its expression by activating transcription factors or inactivating proteins implicated in degradation of its mRNA. These factors (Sp1/Sp3, HIF-1 and TTP) constitute molecular markers of tumor aggressiveness. VEGF is overexpressed in solid or hematologic tumors. Thus, numerous compounds regulating angiogenesis by targeting VEGF have been developed. However, their effects are not as spectacular as expected. The existence of anti-angiogenic isoforms of VEGF could be a cause of their less potent activity. These different points are discussed in this review article.
    Journal de la Société de Biologie 02/2009; 203(2):181-92.
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    ABSTRACT: The endothelium is a tissue with a distinct identity due to the specific expression of molecular markers by endothelial cells. Further, the endothelium displays a structural heterogeneity illustrated by the expression of specific markers in arteries and in veins. Here, we present a review of the transcriptional and epigenetic mechanisms regulating the expression of the main markers of endothelial cells in man and mouse, demonstrating that there is no common and unique mechanism of specific expression of genes in these cells.
    Journal de la Société de Biologie 02/2009; 203(2):125-41.
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    ABSTRACT: Intra-aortic haematopoiesis is a transient phenomenon, characterised by the emergence of Hematopoietic Stem Cells (HSC) from the ventral aortic endothelium through an endothelial cell (EC) to HSC lineage switch. HSC differentiation is followed by the colonization of definitive haematopoietic organs. Since intra-aortic haematopoiesis is born from EC of the aortic floor, we wondered how vascular integrity was maintained during hematopoietic production. We have used interspecific quail to chick grafts to study the aortic morphogenesis during hematopoiesis. We have demonstrated that: 1) before haematopoiesis, the aortic endothelium, originally entirely from splanchnic origin, was colonized by somitic EC, creating a new roof and sides derived from the somite, whereas the floor was contributed by splanchnopleural-derived EC. 2) As haematopoiesis proceeded, somite-derived EC colonized the aortic floor, where they settled underneath the HSC clusters. 3) After haematopoiesis, splanchnopleural ECs have disappeared from the aortic floor and have been replaced by somite-derived EC. At this stage, the whole aortic endothelium originated from somitic cells. 4) We have identified that the somite contributed to the vascular smooth muscle cells (VSMC). 5) Using grafts of either single quail dermomyotome or sclerotome in the chick, we showed that EC originated from the dermomyotome whereas the vascular smooth muscle cells originated from the sclerotome. Taken together, our results bring about new insights on aorta morphogenesis and the time-restricted production of HSCs.
    Journal de la Société de Biologie 02/2009; 203(2):155-60.
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    ABSTRACT: This talk, given as an introduction to a symposium organised to honor André Calas, calls forth his personality, recalls the major events in his career and summarizes the evolution of his research.
    Journal de la Société de Biologie 02/2009; 203(1):7-18.
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    ABSTRACT: Closing this symposium, André Calas remembers his teachers, his past and present collaborators, his students, his teaching and research itineraries and enlarges on the problems of public policy concerning these areas in France.
    Journal de la Société de Biologie 02/2009; 203(1):113-6.
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    ABSTRACT: The GABA(B) receptors belong to the family of class C metabotropic receptors. They are inhibitory receptors forming obligatory heterodimers. Their analgesic role in the dorsal horn of the spinal cord is well established since more than 25 years ago. However, Baclofen, the reference agonist of the GABA(B) receptor, proved to have little efficiency in clinics in neuropathic patients. It seems therefore useful to decipher GABA(B) functions in the nociceptive circuitry, and their regulation in conditions of chronic pain. In the present review, we will focus first on the distribution of the GABA(B) subtypes. Then, we will consider their pre- and post-synaptic functions in the dorsal horn of naïve rats. Finally, we will document the mechanisms that may lead to receptor impairment in neuropathic conditions.
    Journal de la Société de Biologie 02/2009; 203(1):87-97.
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    ABSTRACT: Developmental genetics of congenital heart diseases have evolved from analysis of embryonic hearts towards molecular genetics of cardiac morphogenesis with a dynamic view of cardiac development. Ablation techniques, transgenic animal models and clonal analysis of the developing heart led to identification of different cardiac lineages and their respective roles. The mechanistic approach for great arteries anomalies has led to emerging concepts such as common embryological origin of anatomically different cardiac defects, phenotypic continuum of left heart obstructive defects, or developmental algorithms for cardiac isomerisms. Recent experiments that demonstrated the myocardial rotation of the outflow tract in mouse embryos led to a better understanding of the origin of transposition of the large arteries. This has also raised the hypothesis of a new group of congenital heart anomalies defined as laterality defects limited to a segment of the embryonic heart. These results confirm that genetic heterogeneity of congenital heart defects is related to the heterogeneity of the mechanisms that finally produce the same phenotype.
    Journal de la Société de Biologie 02/2009; 203(2):161-5.
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    ABSTRACT: The surgeon must know the importance of angiogenesis in wound healing. He must also use anti-angiogenics to change the clinical situations and make curative a potentially ineffective surgery. However, these strategies require daily biological indicators able to quantify the tissue activity, that we do not possess yet, nor have we any indicator to predict tumour sensitivity to anti-angiogenics.
    Journal de la Société de Biologie 02/2009; 203(2):193-5.
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    ABSTRACT: Reproduction in mammals is directly controlled by GnRH neurons. These neurons are regulated by many external and internal factors, among which sexual steroids, in particular oestradiol, play an important part. However the mechanisms through which these steroids regulate GnRH secretion are largely unappreciated, and the neurochemical identity of central neurons liable to transmit the steroidal information to GnRH neurons is not completely clarified. Many functional neuroanatomy studies have been carried out on the ovine model, which is particularly favorable to understand the neuroendocrine mechanisms controlling reproduction. These studies have brought about the identification of some of the potential actors in this regulation. The present review reports the major results concerning two recently discovered neuropeptides, galanin and kisspeptin, which appear to be major actors in integration of signals regulating reproduction, among which steroids. These results have revealed the major interaction sites between neurons expressing these neuropeptides and GnRH neurons.
    Journal de la Société de Biologie 02/2009; 203(1):19-28.
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    ABSTRACT: Injection of endothelial progenitor cells (EPC) expanded ex vivo has been shown to increase neovascularization in preclinical models of ischemia and in adult patients, but the precise origin and identity of the cell population responsible for these clinical benefits are controversial. Given the potential usefulness of EPC as a cell therapy product, their thorough characterization is of major importance. This review describes the two cell populations currently called EPC and the means to find differential phenotypic markers. We have shown that BMP2/4 are specific markers of late EPC and play a key role in EPC commitment and outgrowth during neovascularization. Several authors have attempted to expand EPC ex vivo in order to obtain a homogeneous cell therapy product. One possible mean of expanding EPC ex vivo is to activate the thrombin receptor PAR-1 with the specific peptide SFLLRN. Indeed, PAR-1 activation increases angiogenic properties of EPC through activation of SDF-1, angiopoietin and IL-8 pathways. This review summarizes the characterization of EPC and different methods of ex vivo expansion.
    Journal de la Société de Biologie 02/2009; 203(2):197-207.
  • Journal de la Société de Biologie 02/2009; 203(2):117.
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    ABSTRACT: The various components of the endocannabinoid system were discovered in the last twenty years. The cannabinoid system has attracted pharmacologists interest for its potential as therapeutic targets for several diseases ranging from obesity to Parkinson's disease and from multiple sclerosis to pain. Research initially focused on cannabinoid receptor 1 (CB1), but, due to psychotropic side effects related to its activation, the attempts to develop an agonist drug for this receptor has been so far unsuccessful. Recently the possibility to target CB2 has emerged as an alternative for the treatment of pain. The main advantage of targeting CB2 resides in the possibility to elicit the analgesic effect without the psychotropic side effects. Evidence of the analgesic effect of CB2 selective agonists has been obtained in various models of both inflammatory and neuropathic chronic pain. To explain the mechanism at the basis of this analgesic effect different hypotheses have been proposed: effect on inflammatory cells, reduction of basal NGF tone, induction of beta-endorphin release from keratinocytes, direct action on nociceptors. Evidence in support of this last hypothesis comes from down regulation of capsaicin-induced CGRP release in spinal cord slices and Dorsal Root Ganglia (DRG) neurons in culture after treatment with CB2 selective agonists. CB2 agonists are probably acting through several mechanisms and thus CB2 represents an interesting and promising target in the chronic pain field. Further clarification of the mechanisms at the basis of CB2 analgesic effect would surely be an intriguing and stimulating area of research for the years to come.
    Journal de la Société de Biologie 02/2009; 203(1):99-106.
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    ABSTRACT: In contrast to monoaminergic (MA-ergic) neurons possessing the whole set of the enzymes for MA synthesis from the precursor amino-acid, some, mostly peptidergic, neurons co-express only one of the enzymes of monoamine synthesis. They are widely distributed in the brain, being particularly numerous in ontogenesis and, in adulthood, under certain physiological conditions. Most monoenzymatic neurons possess one of the enzymes for dopamine (DA) synthesis, tyrosine hydroxylase (TH) or aromatic L-amino acid decarboxylase (AADC). TH and AADC are enzymatically active in a substantial number of monoenzymatic neurons, where they are capable of converting L-tyrosine to L-3,4-dihydroxy-phenylalanine (L-DOPA) and L-DOPA to dopamine (DA) (or 5-hydroxy-tryptophan, 5-HTP to serotonin), respectively. According to our data L-DOPA synthesized in monoenzymatic TH-neurons is released and taken up by monoenzymatic AADC-neurons for DA synthesis. Moreover, L-DOPA captured by dopaminergic neurons and serotoninergic neurons serves to stimulate dopamine synthesis in the former and to start DA synthesis in the latter. Cooperative synthesis of MAs is considered as a compensatory reaction under a failure of MA-ergic neurons, e.g. in neurodegenerative diseases like hyperprolactinemia and Parkinson's disease, which are developed primarily because of degeneration of DA-ergic neurons of the tuberoinfundibular system and the nigrostriatal system, respectively. Noteworthy, the neurotoxin-induced increase of prolactin secretion returns with time to a normal level due to the stimulation of DA synthesis by the tuberoinfundibular most probably monoenzymatic neurons. The same compensatory mechanism is supposed to be used under the failure of the nigrostriatal DA-ergic system that is manifested by an increased number of monoenzymatic neurons in the striatum of animals with neurotoxin-induced parkinsonism and in humans with Parkinson's disease. Expression of the enzymes of MA synthesis in non-monoaminergic neurons is controlled by intercellular signals such as classical neurotransmitters (catecholamines), etc. Thus, a substantial number of brain neurons express partly the monoaminergic phenotype, namely individual complementary enzymes of MA synthesis, serving to produce MAs in cooperation, which is considered as a compensatory reaction under the failure of MA-ergic neurons.
    Journal de la Société de Biologie 02/2009; 203(1):75-85.
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    ABSTRACT: There is considerable evidence that the human brain maintains the ability to reorganize itself throughout life, an ability known as neuroplasticity. Initially demonstrated in physiological situations, neuroplasticity includes, and relies on, a number of adaptive mechanisms that include not only phenotypic modifications of neurons or synaptic reorganisation but also major modifications of brain circuitry after insults. Recently, the presence of neurogenic zones in the adult brain has unveiled a new aspect of brain plasticity that, together with emerging stem cell therapy, opens the possibility to take advantage of these natural reminders of the developmental period to repair lesioned tissues, a concept known as "therapeutic plasticity".
    Journal de la Société de Biologie 02/2009; 203(1):107-11.