BACKGROUND AND PURPOSE: NB-3 is a member of the F3/contactin family of neural recognition molecules, which are crucial for cell morphogenesis and motility. NB-3 is expressed in neurons and plays an important role in axonal extension and neuronal survival. However, the role of NB-3 in cerebral ischemic injury remains unknown. METHODS: Adult male wild-type and NB-3 knockout mice were subjected to ischemic injury by unilateral middle cerebral carotid artery occlusion for 3 hours, 6 hours, and 12 hours. Ischemic infarction volumes were then determined by 2, 3, 5-triphenyltetrazolium chloride staining. Neurological dysfunction analysis was also performed. Primary culture of neuronal cells from wild-type and knockout animals was also used for analysis of neuronal survival and neurite outgrowth. RESULTS: NB-3 expression in the ischemic hemisphere was decreased after transient middle cerebral artery occlusion (MCAO). NB-3-knockout mice developed a 2.6-fold larger infarct volume and exhibited increased neurological deficit scores after transient middle cerebral artery occlusion compared with control mice. Substrate with NB-3 promoted neuronal survival and neurite outgrowth in vitro, whereas neurite outgrowth and neuronal survival were significantly reduced in NB-3-deficient neurons. In addition, NB-3 deficiency renders neurons more susceptible to oxygen-glucose deprivation-induced damage and NB-3 as substrate could partially through homophilic mechanisms. CONCLUSIONS: These data demonstrate that NB-3 deficiency may aggravate brain damage after middle cerebral artery occlusion by impairing neuronal survival and neurite growth.
BACKGROUND AND PURPOSE:NB-3 is a member of the F3/contactin family of neural recognition molecules, which are crucial for cell morphogenesis and motility. NB-3 is expressed in neurons and plays an important role in axonal extension and neuronal survival. However, the role of NB-3 in cerebral ischemic injury remains unknown. METHODS: Adult male wild-type and NB-3 knockout mice were subjected to ischemic injury by unilateral middle cerebral carotid artery occlusion for 3 hours, 6 hours, and 12 hours. Ischemic infarction volumes were then determined by 2, 3, 5-triphenyltetrazolium chloride staining. Neurological dysfunction analysis was also performed. Primary culture of neuronal cells from wild-type and knockout animals was also used for analysis of neuronal survival and neurite outgrowth. RESULTS:NB-3 expression in the ischemic hemisphere was decreased after transient middle cerebral artery occlusion (MCAO). NB-3-knockout mice developed a 2.6-fold larger infarct volume and exhibited increased neurological deficit scores after transient middle cerebral artery occlusion compared with control mice. Substrate with NB-3 promoted neuronal survival and neurite outgrowth in vitro, whereas neurite outgrowth and neuronal survival were significantly reduced in NB-3-deficient neurons. In addition, NB-3 deficiency renders neurons more susceptible to oxygen-glucose deprivation-induced damage and NB-3 as substrate could partially through homophilic mechanisms. CONCLUSIONS: These data demonstrate that NB-3 deficiency may aggravate brain damage after middle cerebral artery occlusion by impairing neuronal survival and neurite growth.
Authors: Amila Zuko; Asami Oguro-Ando; Roland van Dijk; Sara Gregorio-Jordan; Bert van der Zwaag; J Peter H Burbach Journal: Cell Adh Migr Date: 2016-03-03 Impact factor: 3.405
Authors: Amila Zuko; Asami Oguro-Ando; Harm Post; Renske L R E Taggenbrock; Roland E van Dijk; A F Maarten Altelaar; Albert J R Heck; Alexander G Petrenko; Bert van der Zwaag; Yasushi Shimoda; R J Pasterkamp; J P H Burbach Journal: Front Mol Neurosci Date: 2016-12-15 Impact factor: 5.639
Authors: O Mercati; G Huguet; A Danckaert; G André-Leroux; A Maruani; M Bellinzoni; T Rolland; L Gouder; A Mathieu; J Buratti; F Amsellem; M Benabou; J Van-Gils; A Beggiato; M Konyukh; J-P Bourgeois; M J Gazzellone; R K C Yuen; S Walker; M Delépine; A Boland; B Régnault; M Francois; T Van Den Abbeele; A L Mosca-Boidron; L Faivre; Y Shimoda; K Watanabe; D Bonneau; M Rastam; M Leboyer; S W Scherer; C Gillberg; R Delorme; I Cloëz-Tayarani; T Bourgeron Journal: Mol Psychiatry Date: 2016-05-10 Impact factor: 15.992