title: Class A plexin expression in axotomized rubrospinal and facial motoneurons.
abstract: The semaphorin family of guidance molecules plays a role in many aspects of neural development, and more recently semaphorins have been implicated to contribute to the failure of injured CNS neurons to regenerate. While semaphorin expression patterns after neural injury are partially understood, little is known about the expression of their signal transducing transmembrane receptors, the plexins. Therefore, in this study, we compared the expression patterns of all class A plexins (Plxn-A1, A2, A3, A4) in mouse CNS (rubrospinal) and peripheral nervous system (PNS)-projecting (facial) motoneurons for up to two weeks following axonal injury. Using in situ hybridization, immunohistochemistry, and Western blot analysis, in rubrospinal neurons, Plxn-A1 mRNA and protein and Plxn-A4 expression did not change as a result of injury while Plxn-A2 mRNA increased and Plxn-A3 mRNA was undetectable. In facial motoneurons, Plxn-A1, -A3 and -A4 mRNA expression increased, Plxn-A2 mRNA decreased while Plxn-A1 protein expression did not change following injury. We demonstrate that with the exception of the absence of Plxn-A3 mRNA in rubrospinal neurons, both injured rubrospinal (CNS) and facial (PNS) neurons maintain expression of all plexin A family members tested. Hence, there are distinct expression patterns of the individual plexin-A family members suggesting that regenerating rubrospinal and facial motoneurons have a differential ability to transduce semaphorin signals.
authors.affiliation: International Collaboration on Repair Discoveries, 6270 University Boulevard, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z4.
authors.forename: E D
authors.initials: ED
authors.lastname: Spinelli
authors.forename: L T
authors.initials: LT
authors.lastname: McPhail
authors.forename: L W
authors.initials: LW
authors.lastname: Oschipok
authors.forename: J
authors.initials: J
authors.lastname: Teh
authors.forename: W
authors.initials: W
authors.lastname: Tetzlaff
mesh_terms: D000818:Animals; D019771:Axotomy; D002490:Central Nervous System / Q000378:metabolism / Q000503:physiopathology; D005154:Facial Nerve / Q000378:metabolism* / Q000503:physiopathology; D005786:Gene Expression Regulation / Q000502:physiology; D008297:Male; D051379:Mice; D009046:Motor Neurons / Q000378:metabolism*; D009416:Nerve Regeneration / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D009434:Neural Pathways / Q000378:metabolism* / Q000503:physiopathology; D017933:Peripheral Nervous System / Q000378:metabolism / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D012012:Red Nucleus / Q000378:metabolism* / Q000503:physiopathology; D039961:Semaphorins / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D015854:Up-Regulation / Q000502:physiology
chemical_list: D009419:Nerve Tissue Proteins; C492114:Plxna1 protein, mouse; C492113:Plxna2 protein, mouse; C492112:Plxna3 protein, mouse; C492110:Plxna4 protein, mouse; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D039961:Semaphorins