Senior Lecturer – CN 24 du CNRS
Email : email@example.com
1986 - 1990 B.S., Biology (Biochemistry), University of Paris VI, FRANCE
1991 - 1995 Ph.D., Microbiology, Institut Curie – Orsay - France (E. De Maeyer - advisor)
1997 - 1999 Postdoctoral Fellow, The University of Edinburgh, Edinburgh, UK (David J. Price -
2009- Senior Lecturer CNRS – UMR_968-Institut de la Vision-75012 Paris
2004 - 2008 Senior Lecturer CNRS – UMR676- Hôpital Robert Debré- 75019 Paris.
2000 - 2004 Lecturer Centre National de la Recherche Scientifique (CNRS)- U106/616 INSERM – Hôpital de la Pitié Salpétrière, 75013 Paris.
Production and Supervision
- 25 original papers; Reviewer J Comp Neurol, Eur J Neurosci, Neurosci, Brain Res.
2004-2007 : Fondation EDF contre l’autisme
2005-2007 : Fondation Lejeune
2007-2008 : French-Indian research grant
SELECTION OF FIVE ORIGINAL PUBLICATIONS
Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, Muller U, Aguet M, Babinet C, Shih JC, De Maeyer E. 1995. Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. Science 268: 1763-1766.
Cases O, Vitalis T, Seif I, De Maeyer E, Sotelo C, Gaspar P. 1996. Lack of barrels in the somatosensory cortex of monoamine oxidase A-deficient mice: role of a serotonin excess during the critical period. Neuron 16: 297-307.
Gaspar P, Cases O, Maroteaux L. 2003. The developmental role of serotonin: news from mouse molecular genetics. Nat Rev Neurosci 4: 1002-1012.
Chen K, Cases O, Rebrin I, Wu W, Gallaher TK, Seif I, Shih JC. 2007. Forebrain specific expression of MAO A reduces neurotransmitter levels, restores the brain structure and rescues aggressive behavior in MAO A deficient mice. J Biol Chem 282, 115-123.
Stankovski L, Alvarez C, Ouimet T, Vitalis T, El-Hachimi KH, Price DJ, Deneris E, Gasapr P, Cases O. 2007. Developmental cell death is enhanced in the cerebral cortex of mice lacking the brain vesicular monoamine transporter. J Neurosci. 27, 1315-24.
The anterior-posterior (axial) length of the eye depends on the coordinated cross-talk between genetic, developmental and environmental factors. Early post-natal growth appears to be a crucial determinant of axial length whereas later, visual experience fine-tunes the size of the eyeball by constant adaptive remodeling. Altered composition of the vitreous and/or aqueous humour, abnormal intra-ocular pressure or remodeling of the sclera, aberrant growth factor production are thus some of the factors that may contribute to axial length elongation independently of visual experience.
In the present proposal we focus on the function of the ciliary epithelium (CE), necessary for the synthesis of the aqueous (AH) and vitreous humour (VH), under normal and pathological (excessive axial elongation) conditions. The CE is composed of an outer layer of pigmented cells attached to the stroma of the ciliary body and an inner layer of nonpigmented (NPE) cells facing the AH of the posterior chamber. The two cell layers are arranged apex to apex and are connected by gap junctions whose composition and function is well characterized. Much less is known about the proteins expressed at the apical pole of the NPE cells and their contribution to the formation of the AH and VH.
We previously reported (Assemat E. 2005) that the multiligand receptors Lrp2/Megalin and Cubilin (Cubn) are expressed in the NPE during development and in the adult. We recently generated several mutant mice. In these mice the eyeballs are excessively large, and the protein concentration in the VH is increased. Our current data indicate that the onset of the defects is between the post-natal day 5 (P5) and P10.
We plan to a) isolate NPE cells and b) characterize the transcriptional profile of control and mutant NPE cells; c) characterize the protein composition of the mutant AH and VH; d) characterize the function of mutated proteins expressed in the NPE cells in vitro.