P Evrard

French Institute of Health and Medical Research, Lutetia Parisorum, Île-de-France, France

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Publications (180)551.85 Total impact

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    ABSTRACT: Microglial cells penetrate into and scatter throughout the human cortical grey and white matter according to a specific spatiotemporal pattern during the first 2 trimesters of gestation. Routes of entry were quantitatively and qualitatively different from those identified in the diencephalon. Starting at 4.5 gestational weeks, amoeboid microglial cells, characterized by different antibodies as Iba1, CD68, CD45, and MHC-II, entered the cerebral wall from the ventricular lumen and the leptomeninges. Migration was mainly radial and tangential toward the immature white matter, subplate layer, and cortical plate, whereas pial cells populated the prospective layer I. The intraparenchymal vascular route of entry was detectable only from 12 gestational weeks. Interestingly, microglial cells accumulated in restricted laminar bands particularly at 19 to 24 gestational weeks among the corona radiata fibers rostrally, extending caudally in the immature white matter to reach the visual radiations. This accumulation of proliferating MIB1-positive microglia (as shown by MIB1-Iba1 double immunolabeling) was located at the site of white matter injury in premature neonates. The spatiotemporal organization of microglia in the immature white and grey matter suggests that these cells may play active roles in developmental processes and in injury to the developing brain.
    Journal of Neuropathology and Experimental Neurology 06/2007; 66(5):372-82. · 4.35 Impact Factor
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    ABSTRACT: The role for growth restriction in the multifactorial pathophysiology of developing white-matter damage remains debated. We studied rat pups with prenatal growth restriction (GR) induced by unilateral ligation of the uterine artery. Pups with severe GR exhibited white-matter damage that persisted to adulthood [Olivier, P., Baud, O., Evrard, P., Gressens, P.,Verney, C., 2005. Prenatal ischemia and white matter damage in rats. J. Neuropathol. Exp. Neurol. 64, 998-1006]. Moderate GR was associated with diffuse white-matter lesions, microglial activation, and astrogliosis. Loss of pre-oligodendrocytes on postnatal day 7 was followed by a delay in myelination. Following a cortical excitotoxic insult on postnatal day 5, the size of the induced white-matter lesion was smaller in pups with moderate GR and larger in pups with severe GR, compared to normal pups. The increased pre-oligodendrocyte proliferation seen in the white matter of pups with moderate GR subjected to this "double-hit" injury may constitute a heretofore-undescribed neuroprotective mechanism of immature white matter.
    Neurobiology of Disease 05/2007; 26(1):253-63. · 5.62 Impact Factor
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    ABSTRACT: We describe the topographical distribution of microglial subpopulations during development of the human diencephalon and telencephalon. Brains from embryos and fetuses age 5-23.5 gestational weeks (gw) were subjected to single- and double-immunolabeling for lectin RCA-1 (Ricinus Communis Agglutinin 1), Iba1 (a microglial marker), CD68 (specific of macrophages), CD45 (marker for mononucleate cells of hematopoietic lineage), CD34 (expressed on endothelial cells), and MIB1 and Ki67 (markers for cell proliferation). At 5.5 gw the first intracerebral microglial cells were seen close to the meninges and choroid plexus near the di-telencephalic fissure. They were amoeboid and positive for Iba1, CD45, and RCA-1, whereas cells in the deep parenchyma expressed Iba1/CD68/RCA-1 and constituted clusters. In the developing diencephalon, microglial clusters were located in junctional regions of the white matter anlagen, most notably at the junctions of the internal capsule with the thalamic projections, the external capsule, and the cerebral peduncle. In the cortical anlagen, Iba1+/RCA-1/CD68+/CD45+ cells accumulated at 10-12 gw, constituting a tangential band at the junction between the cortical plate and the subplate. Between 10 and 16 gw microglial clusters increased markedly in size and cellular density. Contact between Iba1+ microglia and CD34+ blood vessels was clearly visible from 10-12 gw onward, first in microglial clusters of the white matter anlagen and subsequently throughout the parenchyma. From the middle of the second trimester onward microglial cells colonized the entire cerebral parenchyma, developed a ramified morphology, and downregulated their surface antigens, but remained more numerous in the white matter.
    The Journal of Comparative Neurology 01/2007; 499(4):565-82. · 3.66 Impact Factor
  • Annals of the New York Academy of Sciences 12/2006; 814(1):152 - 160. · 4.38 Impact Factor
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    ABSTRACT: To define the contribution of prenatal investigation and evaluate the prognosis of isolated mild ventriculomegaly (IMV). Retrospective study. University hospital between January 1992 and December 2002. One hundred and sixty-seven cases of prenatal unilateral or bilateral IMV without any associated anomaly at the time of initial diagnosis. Complementary investigations were performed: amniocentesis with karyotyping, screening for viruses and acetylcholinesterase electrophoresis, magnetic resonance imaging (MRI), and ultrasonography every 3-4 weeks. Results of prenatal investigations, pregnancy outcome, and postnatal psychomotor development. IMV was diagnosed around 26.5 weeks. Amniocentesis revealed four chromosomal anomalies and two cytomegalovirus infections. MRI diagnosed brain-associated anomalies in 15 cases and ultrasonographic monitoring highlighted malformations not initially diagnosed in 28 cases. Termination of pregnancy (TOP) was considered in 21 pregnancies (12.6%). Indications were aneuploidy, fetal infectious disease or associated malformations. In women for whom a TOP was considered, consanguinity, fetus of female sex and frontal horn enlargement were statistically more frequent, ventriculomegaly was more often bilateral and asymmetrical, atrial width, and the rate of progressive ventricular enlargement were significantly higher. One hundred and one children with prenatal IMV were assessed between 19 and 127 months (mean age 54.68 +/- 2.87 months). Twelve children had neurological disease or psychomotor delay and 89 children had a normal psychomotor development. Poor neurological outcome was more often associated with atrial width greater than or equal to 12 mm, asymmetrical bilateral enlargement, and progression of the ventriculomegaly. The detection of IMV raises the question of the child's psychomotor development and justifies meticulous prenatal investigation. In addition to associated anomalies, three criteria are often associated with an unfavourable outcome: atrial width greater than 12 mm, progression of the enlargement, and asymmetrical and bilateral ventriculomegaly.
    BJOG An International Journal of Obstetrics & Gynaecology 10/2006; 113(9):1072-9. · 3.76 Impact Factor
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    ABSTRACT: Ischemia/reperfusion injury to the developing brain is a major cause of neurologic abnormalities in preterm infants. To investigate the underlying mechanisms, we modified a previously described rat model of unilateral uterine-artery ligation on the 17th embryonic day (E17). Growth retardation was taken as an index of in utero ischemia, and pups born with a birth weight more than 2 standard deviations below that of controls were compared with the same-litter, normal-growth control pups born from the nonligated horn. Prenatal ischemia probably associated with hypoxia and followed by reperfusion at birth induced white matter damage at a developmental stage corresponding to extreme prematurity in humans. On P0 (day of birth), growth-retarded pups exhibited lesions in the cingular white matter and internal capsule with increased counts of activated microglial cells for 2 weeks compared with controls. Astrogliosis was detected in the injured white matter. On P3, increased apoptotic cell death was seen in O4-positive preoligodendrocytes, which were abnormally scarce on P7. Defective myelination, as assessed by myelin-binding-protein labeling, was detected until adulthood. The diffuse white matter damage in growth-retarded rats replicated the main features of white matter damage in human preterm infants.
    Journal of Neuropathology and Experimental Neurology 12/2005; 64(11):998-1006. · 4.35 Impact Factor
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    Philippe Evrard
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    ABSTRACT: Deux choses sont simples: raconter le passé et prédire l'avenir. Y voir clair au jour le jour est une autre entreprise.1
    Developmental Medicine & Child Neurology 11/2005; 47(10):651. · 2.68 Impact Factor
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    ABSTRACT: Aicardi-Goutieres syndrome, first described in 1984, is a progressive infantile familial encephalopathy featuring cerebral calcifications, mainly of the basal ganglia, cerebral white matter abnormalities and cerebrospinal fluid lymphocytosis. Most of the patients present with severe developmental retardation, microcephaly, abnormal eye movements, pyramidal tract signs, and prominent dystonic movements. An elevated level of interferon-alpha in the CSF is a constant feature, particularly during the first stages of the disease course. One locus has been mapped on chromosome 3p21 in about half of the families so far studied. and results. We report two new French cases and discuss the limits of the clinical syndrome, the differential diagnosis and issues raised by the pathophysiological mechanisms involved. The major concern is to separate this condition from intrauterine infections because of the genetic and therapeutic consequences. A number of other questions remain unanswered. For example, we still do not know today at what age the absence of features like CSF lymphocytosis, and possibly absence of calcifications, rules out the diagnosis of the condition. The origin of the vasculitis lesions is not known, but seems to be related to dysregulation of interferon production and secretion. Currently about 75 patients have been reported, even though many more probably exist. The study of this syndrome can contribute to the understanding of some mechanisms of CNS calcification and in a broader perspective to that of chronic encephalopathies with dysregulation of immune mechanisms.
    Revue Neurologique 05/2005; 161(4):445-50. · 0.51 Impact Factor
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    ABSTRACT: Sudden infant death syndrome remains a leading cause of post-neonatal mortality in developed countries. Its etiopathogenic mechanisms are unknown. In this neuropathologic study, we noticed that the weights of the brains of infants who died from sudden infant death syndrome (n = 97) were invariably heavier in comparison with those of a group of age-matched controls (n = 23) issuing from the same local population. Brain edema was not a major element, and there were no significant microscopic or macroscopic cerebral anomalies in the brains from either of the study groups. Head circumference did not show a parallel increase in infants with sudden infant death syndrome. The excessive brain weight might reflect abnormal cerebral development and could be detrimental to vital neural control. In a previous study, we disclosed cytokine overexpression in the brains of these victims. Whether increased brain weight is linked to cytokine up-regulation remains, however, a moot case and merits further exploration.
    Journal of Child Neurology 04/2005; 20(3):244-6. · 1.39 Impact Factor
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    ABSTRACT: In the management of autoimmune myasthenia, thymectomy is recognized as effective surgical therapy. The necessity of complete radical thymectomy to achieve maximal improvement has been emphasized. Video-assisted thoracoscopic surgery has been successfully used for thymectomy in adults, and more recently in children, and has been described as achieving the same radicality and functional improvement as median sternotomy or as transcervical thymectomy. The aim of this work is to report our first thoracoscopic experience in this indication. Patients with myasthenia gravis on anticholinesterase drugs and/or steroids are discussed for surgery in case of clinical deterioration despite increasing doses of medication or in case of no improvement. We decided to perform thoracoscopic thymectomies by a left-sided approach. Preoperative localization of thymic tissue is done by a thoracic CT exam. Patients are placed on their right side with a thoracic tilt under the thorax. Four thoracoscopic ports are used, a 10-mm for the camera and three 5-mm operating ports. The left lung was collapsed by selective intubation (double-lumen endotrachial intubation). Two boys, 7.5 and 14 years old, were addressed by the department of neurology for radical thymectomy. They presented an ocular myasthenia gravis for 2 years and a mild general myasthenia gravis for 7 years. The operative times were 120 and 240 min. There was no intraoperative or postoperative complication. Duration of thoracic drainage was 2 days. The children were discharged on the third postoperative day. For the second procedure, an ultrasound exam during surgery was necessary to localize the thymus exactly, thus enabling its complete resection without the need for a conversion. The follow-up is 19 and 7 months with a clinical improvement enabling the diminution of medication for both children, the end of ptosis for the first child, and the general improvement of muscle strength for the second. Thoracoscopic thymectomy in children with juvenile myasthenia gravis seems to offer a complete surgical resection, as do open techniques. In case of difficulties in finding the thymus, an ultrasound exam is feasible to enable complete resection. The left-sided thoracoscopic approach gives a good mediastinal and cervical exposition. Furthermore, being less painful in the postoperative period, it presents a less pronounced impairment of pulmonary function, and it presents good cosmetic effect.
    Surgical Endoscopy 02/2005; 19(1):140-2. · 3.43 Impact Factor
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    ABSTRACT: Periventricular leukomalacia is a major neuropathological substrate underlying most of the neurologic morbidity in cerebral palsy. Etiopathogenesis of periventricular leukomalacia is believed to be multifactorial, involving hypoxic-ischemic insults and inflammatory processes. While emphasis was previously placed on hypoxia/ischemia, epidemiological, clinical, experimental and other studies conducted over the last decade have provided evidence for an important role of infective/inflammatory conditions and immune mediators in the pathogenesis of periventricular leukomalacia. Tumor necrosis factor alpha (TNF-a), interleukin-1 beta (IL-1b) and interleukin-2 (IL-2) are overexpressed in affected brains, and receptors for these cytokines are present on many inflammatory and neural cells in the white matter. These findings may be part of a wider network of cytokines, chemokines and other inflammatory factors. There is also evidence for interaction between infective/inflammatory conditions and ischemia/hypoxia as etiopathogenic factors in periventricular leukomalacia/cerebral palsy, as the former may enhance the effects of the latter. These developments in the understanding of the immune responses associated with perinatal brain damage, and the characterization of the implicated cellular and molecular mechanisms may have important implications for neuroprotection strategies aiming at prevention of periventricular leukomalacia and cerebral palsy.
    Current Pediatric Reviews. 01/2005; 1(1).
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    ABSTRACT: Injectable dexamethasone (DXM) is widely used during the postnatal period in premature infants. However, this treatment has been associated with an increased incidence of neuromotor disorders. Few studies have directly addressed the impact of DXM therapy on neuronal differentiation. We used a murine model of postnatal steroid therapy in which mouse pups aged 3 and 4 postnatal days (P) received intraperitoneal injections of 1 mg . kg(-1) . 12 h(-1) of an injectable preparation that contained DXM and sulfites (DXM), pure DXM, or sulfites. The animals were weighed before they were killed on P5, P10, or P21, and their brains were investigated by immunohistochemistry with markers for neuronal differentiation. DXM administration was associated with a 20-30% reduction in body and brain weight gains and in cortical thickness on P5 and P10. gamma-Amino-butyric acid+ (GABA+) interneuron density was significantly increased (+50%) in the cerebral cortex of the animals given injectable DXM on P5 to P21 compared with controls (p < 0.01). In parallel, the density of cortical neurons expressing two interneuron markers (calbindin 28-kD and calretinin) increased significantly. These alterations occurred with injectable DXM but not with pure DXM or sulfites alone. In contrast, none of the study treatments modified the expression of other markers for neuronal transmission or axon myelination. In the animals that were given injectable DXM, cleaved caspase 3 antibody showed increased neuronal cell death, but calbindin antibody did not. In conclusion, in a murine model of postnatal steroid therapy, injectable DXM induced a selective increase in GABAergic neurons in the cerebral cortex.
    Pediatric Research 01/2005; 57(1):149-56. · 2.67 Impact Factor
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    ABSTRACT: Introduction Aicardi-Goutières syndrome, first described in 1984, is a progressive infantile familial encephalopathy featuring cerebral calcifications, mainly of the basal ganglia, cerebral white matter abnormalities and cerebrospinal fluid lymphocytosis. Most of the patients present with severe developmental retardation, microcephaly, abnormal eye movements, pyramidal tract signs, and prominent dystonic movements. An elevated level of interferon-alpha in the CSF is a constant feature, particularly during the first stages of the disease course. One locus has been mapped on chromosome 3p21 in about half of the families so far studied. Patients and results We report two new French cases and discuss the limits of the clinical syndrome, the differential diagnosis and issues raised by the pathophysiological mechanisms involved. The major concern is to separate this condition from intrauterine infections because of the genetic and therapeutic consequences. A number of other questions remain unanswered. For example, we still do not know today at what age the absence of features like CSF lymphocytosis, and possibly absence of calcifications, rules out the diagnosis of the condition. The origin of the vasculitis lesions is not known, but seems to be related to dysregulation of interferon production and secretion. Conclusion Currently about 75 patients have been reported, even though many more probably exist. The study of this syndrome can contribute to the understanding of some mechanisms of CNS calcification and in a broader perspective to that of chronic encephalopathies with dysregulation of immune mechanisms.
    Revue Neurologique - REV NEUROL. 01/2005; 161(4):445-450.
  • Nadia Sahir, Philippe Evrard, Pierre Gressens
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    ABSTRACT: Caffeine affects early in vivo murine brain development by accelerating the evagination of the primitive neuroepithelium into telencephalic vesicles. In this model, caffeine induces the expression of the regulatory subunit alpha of protein kinase A (PKA RI alpha) and of Sonic hedgehog (Shh). The understanding of the molecular mechanisms linking caffeine and neural gene expression would benefit from a reproducible in vitro model. Accordingly, the present study aimed to determine whether caffeine modulated the expression of these genes in primary neuronal and astroglial cultures derived from developing murine neocortex. Using real-time PCR, the results showed that caffeine induced robust overexpression of Shh mRNA in both cell types without significantly modifying PKA RI alpha gene expression.
    Journal of Molecular Neuroscience 02/2004; 24(2):201-5. · 2.89 Impact Factor
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    ABSTRACT: Lactate and the other monocarboxylates are a major energy source for the developing brain. We investigated the immunocytochemical expression of two monocarboxylate transporters, MCT1 and MCT2, in the human visual cortex between 13 and 26 post-ovulatory weeks. We used immunoperoxidase and immunofluorescence techniques to determine whether these transporters co-localized with markers for blood vessels (CD34), neurons (microtubule-associated protein 2 [MAP2], SMI 311), radial glia (vimentin), or astrocytes (glial fibrillary acidic protein [GFAP], S100beta protein). MCT1 immunoreactivity was visible in blood vessel walls as early as the 13th week of gestation mainly in the cortical plate and subplate. At this stage, less than 10% of vessels in the ventricular layer expressed MCT1, whereas all blood vessels walls showed this immunoreactivity at the 26th gestational week. Starting at the 19th week of gestation, sparse MCT1 positive cell bodies were detected, some of them co-localized with MAP2 immunoreactivity. MCT2 immunoreactivity was noted in astrocytic cell bodies from week 19 and spread subsequently to the astrocyte end-feet in contact with blood vessels. MCTs immunoreactivities were most marked in the subplate and deep cortical plate, where the most differentiated neurons were located. Our findings suggest that monocarboxylate trafficking between vessels (MCT1), astrocytes (MCT2) and some postmitotic neurons (MCT1) could develop gradually toward 20 gestational weeks (g.w.). These data suggest that lactate or other monocarboxylates could represent a significant energy source for the human visual cortex at this early stage.
    Developmental Brain Research 02/2004; 148(1):69-76. · 1.78 Impact Factor
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    ABSTRACT: In the premature infant, periventricular leukomalacia, usually related to hypoxicischemic white matter damage, is the main cause of neurological impairment. We hypothesized that protracted prenatal hypoxia might induce white matter damage during the perinatal period. Pregnant Sprague-Dawley rats were placed in a chamber supplied with hypoxic gas (10% O2-90% N2) from embryonic day 5 (E5) to E20. Neonatal rat brains were investigated by histology, immunocytochemistry, western blotting, in situ hybridization, DNA fragmentation analysis, and in vivo magnetic resonance imaging (MRI). Body weight of pups subjected to prenatal hypoxia was 10 to 30% lower from P0 to P14 than in controls. Specific white matter cysts were detected between P0 and P7 in pups subjected to prenatal hypoxia, in addition to abnormal extra-cellular matrix, increased lipid peroxidation, white matter cell death detected by TUNEL, and increased activated macrophage counts in white matter. Subsequently, gliotic scars and delayed myelination primarily involving immature oligodendrocytes were seen. In vivo MRI with T1, T2, and diffusion sequences disclosed similar findings immediately after birth, showing strong correlations with histological abnormalities. We speculate that protracted prenatal hypoxia in rat induces white matter damage occurring through local inflammatory response and oxidative stress linked to re-oxygenation during the perinatal period.
    Brain Pathology 02/2004; 14(1):1-10. · 4.74 Impact Factor
  • Revue Neurologique 01/2004; 24:146-147. · 0.51 Impact Factor
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    ABSTRACT: Functional peroxisome deficiency, as encountered in Zellweger syndrome, causes a specific impairment of neuronal migration. Although the molecular mechanisms underlying the neuronal migration defect are at present unknown, the excess of very long chain fatty acids in brain, a consequence of peroxisomalbeta-oxidation deficiency, has often been hypothesized to play a major role. The purpose of the present study was to investigate the contribution of peroxisomal dysfunction in brain as opposed to peroxisomal dysfunction in extraneuronal tissues to the migration defect. Peroxisomes were selectively reconstituted either in brain or liver of Pex5 knock-out mice, a model for Zellweger syndrome, by tissue-selective overexpression of Pex5p. We found that both rescue strains exhibited a significant correction of the neuronal migration defect despite an incomplete reconstitution of peroxisomal function in the targeted tissue. Animals with a simultaneous rescue of peroxisomes in both tissues displayed a pattern of neuronal migration indistinguishable from that of wild-type animals on the basis of cresyl violet staining and 5',3'-bromo-2'-deoxyuridine birth-dating analysis. These data suggest that peroxisomal metabolism in brain but also in extraneuronal tissues affects the normal development of the mouse neocortex. In liver-rescued mice, the improvement of the neuronal migration was not accompanied by changes in very long chain fatty acid, docosahexaenoic acid, or plasmalogen levels in brain, indicating that other metabolic factors can influence the neuronal migration process.
    Journal of Neuroscience 11/2003; 23(30):9732-41. · 6.91 Impact Factor
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    ABSTRACT: In addition to glucose, monocarboxylates including lactate represent a major source of energy for the brain, especially during development. We studied the immunocytochemical expression of the monocarboxylate transporters MCT1 and MCT2 in the rat brain between embryonic day (E) 16 and postnatal day (P) 14. At E16-18, MCT1-like immunoreactivity was found throughout the cortical anlage, being particularly marked medially in the hippocampal anlage next to the ventricle. In a complementary pattern, MCT2-like immunoreactivity was expressed along the medial and ventral border of the ventricle in the medial septum and habenula before birth. The hypothalamic area exhibited MCT2 and MCT1 positive areas from E18 on. These transient labelings revealed four main sites of monocarboxylate and/or glucose exchange: the brain parenchyma, the epithelial cells, the ependymocytes, and the glia limitans. During the first postnatal week, MCT1 immunoreactivity extended massively to the vessel walls and moderately to the developing astrocytes in the cortex. In contrast, MCT2 immunoreactivity was faint in blood vessels but massive in developing astrocytes from P3 to P7. Neither MCT2 nor MCT1 colocalized with neuronal, microglial, or oligodendrocytic markers during the first postnatal week. At P14, a part of the scattered punctate MCT2 staining could be associated with astrocytes and postsynaptic dendritic labeling. The transient pattern of expression of MCTs throughout the perinatal period suggests a potential relationship with the maturation of the blood-brain barrier.
    The Journal of Comparative Neurology 11/2003; 465(3):445-54. · 3.66 Impact Factor
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    ABSTRACT: Rhizomelic chondrodysplasia punctata is a human autosomal recessive disorder characterized by skeletal, eye and brain abnormalities. The disorder is caused by mutations in the PEX7 gene, which encodes the receptor for a class of peroxisomal matrix enzymes. We describe the generation and characterization of a Pex7 mouse knockout (Pex7(-/-)). Pex7(-/-) mice are born severely hypotonic and have a growth impairment. Mortality in Pex7(-/-) mice is highest in the perinatal period although some Pex7(-/-) mice survived beyond 18 months. Biochemically Pex7(-/-) mice display the abnormalities related to a Pex7 deficiency, i.e. a severe depletion of plasmalogens, impaired alpha-oxidation of phytanic acid and impaired beta-oxidation of very-long-chain fatty acids. In the intermediate zone of the developing cerebral cortex Pex7(-/-) mice have an increase in neuronal density. In vivo neuronal birthdating revealed that Pex7(-/-) mice have a delay in neuronal migration. Analysis of bone ossification in newborn Pex7(-/-) mice revealed a defect in ossification of distal bone elements of the limbs as well as parts of the skull and vertebrae. These findings demonstrate that Pex7 knockout mice provide an important model to study the role of peroxisomal functioning in the pathogenesis of the human disorder.
    Human Molecular Genetics 10/2003; 12(18):2255-67. · 7.69 Impact Factor

Publication Stats

4k Citations
551.85 Total Impact Points

Institutions

  • 1999–2007
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
    • Centre Hospitalier Universitaire Mont-Godinne
      Yvoir, Walloon Region, Belgium
  • 1996–2004
    • Hôpital Universitaire Robert Debré
      • Service de Néphrologie Pédiatrique
      Lutetia Parisorum, Île-de-France, France
  • 2003
    • Université de Vincennes - Paris 8
      Saint-Denis, Île-de-France, France
  • 2001
    • Paris Diderot University
      • Faculté de Médecine Xavier Bichat
      Paris, Ile-de-France, France
  • 1998
    • Holiste Laboratoire et Développement
      Lyons, Rhône-Alpes, France
  • 1985–1998
    • Cliniques Universitaires Saint-Luc
      • • Division of Pediatric Neurology
      • • Department of Medical Imaging
      Bruxelles, Brussels Capital Region, Belgium
  • 1978–1998
    • Catholic University of Louvain
      • Department of Radiology and Medical Imaging - RAIM
      Louvain-la-Neuve, WAL, Belgium
  • 1997
    • Centre Hospitalier Universitaire Rouen
      Rouen, Upper Normandy, France
  • 1992–1996
    • University of California, San Francisco
      San Francisco, California, United States
  • 1994
    • Massachusetts General Hospital
      Boston, Massachusetts, United States