Entity

Time filter

Source Type

Murviel-lès-Montpellier, France

Landes T.,Toulouse 1 University Capitole | Leroy I.,Toulouse 1 University Capitole | Bertholet A.,Toulouse 1 University Capitole | Diot A.,Toulouse 1 University Capitole | And 11 more authors.
Seminars in Cell and Developmental Biology | Year: 2010

Mitochondrial morphology varies according to cell type and cellular context from an interconnected filamentous network to isolated dots. This morphological plasticity depends on mitochondrial dynamics, a balance between antagonistic forces of fission and fusion. DRP1 and FIS1 control mitochondrial outer membrane fission and Mitofusins its fusion. This review focuses on OPA1, one of the few known actors of inner membrane dynamics, whose mutations provoke an optic neuropathy. Since its first identification in 2000 the characterization of the functions of OPA1 has made rapid progress thus providing numerous clues to unravel the pathogenetic mechanisms of ADOA-1. © 2009 Elsevier Ltd. Source


M'Kadmi C.,Max Mousseron Institute of Biomolecules | Leyris J.-P.,Institute Des Neurosciences Of Montpellier | Onfroy L.,French Institute of Health and Medical Research | Gales C.,French Institute of Health and Medical Research | And 11 more authors.
Journal of Biological Chemistry | Year: 2015

Background: GHS-R1a activates multiple signaling pathways mediating feeding and addictive behaviors. Results: Some GHS-R1a ligands activate Gq but not Gi/o and fail to recruit β-arrestin2; others act as selective inverse agonists at Gq compared with G13. Conclusion: Synthetic ligands can selectively activate or reverse Gq-dependent signaling at GHS-R1a. Significance: Ligand-biased signaling can be exploited for the development of selective drugs to treat GHS-R1a-mediated Disorders. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Source


Gannouni N.,Laboratoire Of Physiologie Integree | Gannouni N.,Laboratoire Of Toxicologie | Mhamdi A.,Laboratoire Of Toxicologie | Lenoir M.,Institute Des Neurosciences Of Montpellier | And 6 more authors.
Tunisie Medicale | Year: 2015

Background: The noise is considered as a factor of environmental stress, causing a wide range of health effects such as acoustic, cardiovascular, nervous and endocrine systems. Purpose: The present study was conducted to examine the affects of repeated exposure to noise on the peripheral auditory system, adrenal gland and heart tissue. Method: The White strain rats “Wistar” were exposed to chronic and repetitive exposure noise at two different intensity levels of 70 and 85dB (A). The noise level was generated by the Audacity® software to an octave-band noise (8616 kHz). The sound exposure duration was 6 hr/day, 5 days per week for 3 months. Quantitative and qualitative investigations were performed by using electron microscopy. The ganglion neuron counting was examined via light microscopy. Results : The results show that exposure to sound intensities 70 and 85 dB (A) for long periods, lead to changes in the morphological structure of the cochlea (inner ear), adrenal cortex and cardiac tissue which involve cell disruption which over time can lead to pathological effects. Conclusion : This study provides morphological evidence that repetitive exposure noise at moderate sound levels to 70 and 85 dB (A) induces changes in the peripheral auditory system, the adrenal cortex and heart tissue. © 2015, Maison du Medicine. All rights reserved. Source


Guichet P.-O.,Institute Des Neurosciences Of Montpellier | Guelfi S.,Institute Des Neurosciences Of Montpellier | Teigell M.,Institute Des Neurosciences Of Montpellier | Hoppe L.,Institute Des Neurosciences Of Montpellier | And 10 more authors.
Stem Cells | Year: 2015

Glioblastoma multiforms (GBMs) are highly vascularized brain tumors containing a subpopulation of multipotent cancer stem cells. These cells closely interact with endothelial cells in neurovascular niches. In this study, we have uncovered a close link between the Notch1 pathway and the tumoral vascularization process of GBM stem cells. We observed that although the Notch1 receptor was activated, the typical target proteins (HES5, HEY1, and HEY2) were not or barely expressed in two explored GBM stem cell cultures. Notch1 signaling activation by expression of the intracellular form (NICD) in these cells was found to reduce their growth rate and migration, which was accompanied by the sharp reduction in neural stem cell transcription factor expression (ASCL1, OLIG2, and SOX2), while HEY1/2, KLF9, and SNAI2 transcription factors were upregulated. Expression of OLIG2 and growth were restored after termination of Notch1 stimulation. Remarkably, NICD expression induced the expression of pericyte cell markers (NG2, PDGFRβ, and α-smooth muscle actin [αSMA]) in GBM stem cells. This was paralleled with the induction of several angiogenesis-related factors most notably cytokines (heparin binding epidermal growth factor [HB-EGF], IL8, and PLGF), matrix metalloproteinases (MMP9), and adhesion proteins (vascular cell adhesion molecule 1 [VCAM1], intercellular adhesion molecule 1 [ICAM1], and integrin alpha 9 [ITGA9]). In xenotransplantation experiments, contrasting with the infiltrative and poorly vascularized tumors obtained with control GBM stem cells, Notch1 stimulation resulted in poorly disseminating but highly vascularized grafts containing large vessels with lumen. Notch1-stimulated GBM cells expressed pericyte cell markers and closely associated with endothelial cells. These results reveal an important role for the Notch1 pathway in regulating GBM stem cell plasticity and angiogenic properties. Stem Cells 2015;33:21-34 © 2014 AlphaMed Press. Source


Schindler M.,Institute Des Neurosciences Of Montpellier | Schindler M.,National Graduate School of Chemistry, Montpellier | Fabre C.,Institute Des Neurosciences Of Montpellier | Fabre C.,National Graduate School of Chemistry, Montpellier | And 5 more authors.
Molecular Endocrinology | Year: 2012

As one of the nine hereditary neurodegenerative polyQ disorders, spinal and bulbar muscular atrophy (SBMA) results from a polyQ tract expansion in androgen receptor (AR). Although protein aggregates are the pathological hallmark of many neurodegenerative diseases, their direct role in the neurodegeneration is more and more questioned. To determine the early molecular mechanisms causing motor neuron degeneration in SBMA, we established an in vitro system based on the tetracycline-inducible expression of normal (AR20Q), the mutated, 51 glutamine-extended (AR51Q), or polyQ-deleted (AR0Q) AR in NSC34, a motor neuron-like cell line lacking endogenous AR. Although no intracellular aggregates were formed, the expression of the AR51Q leads to a loss of function characterized by reduced neurite outgrowth and to a toxic gain of function resulting in decreased cell viability. In this study, we show that both AR20Q and AR51Q are recruited to lipid rafts in response to testosterone stimulation. However, whereas testosterone induces the activation of the c-jun N-terminal kinase/c-jun pathway via membrane-associated AR20Q, it does not so in NSC34 expressing AR51Q. Phosphorylation of c-jun N-terminal kinase plays a crucial role in AR20Q-depen-dent survival and differentiation of NSC34. Moreover, c-jun protein levels decrease more slowly in AR20Q-than in AR51Q-expressing NSC34 cells. This is due to a rapid and transient inhibition of glycogen synthase kinase 3a occurring in a phosphatidylinositol 3-kinase-independent manner. Our results demonstrate that the deregulation of nongenomic AR signaling may be involved in SBMA establishment, opening new therapeutic perspectives. © 2012 by The Endocrine Society. Source

Discover hidden collaborations