title: Temporal changes in the expression of TGF-beta 1 and EGF in the ventral horn of the spinal cord and associated precentral gyrus in adult Rhesus monkeys subjected to cord hemisection.
abstract: It is well known that some growth factors can not only rescue neurons from death, but also improve motor functions following spinal cord injury. However, their cellular distribution in situ and temporal expressions following spinal cord injury have not been determined, especially in primates. This study investigated the temporal changes in the expression of two growth factors--epidermal growth factor (EGF) and transforming growth factor-beta 1 (TGF-beta1) in the injured motoneurons of the spinal cord and the associated precentral gyrus in adult Rhesus monkeys subjected to spinal cord hemisection. Animals were allowed to survive 7, 14, 30 and 90 days post operation (dpo). Functional recovery of the hindlimbs was assessed using Tarlov scale. The immunohistological expressions of EGF and TGF-beta1 in the ventral horn motoneurons decreased sharply at 7 dpo in the cord segments caudal to the lesion site, which was followed by an increase and a peak between 14 and 30 dpo for EGF and at 90 dpo for TGF-beta1. Changes in the expression of EGF in the precentral gyrus were similar to that in the spinal cord. No TGF-beta1 immunoreactive neurons were detected in the precentral gyrus. In the spinal segments rostral to the lesion, the expressions of EGF and TGF-beta1 peaked at 30 dpo. The mRNA of EGF was detected in both spinal motoneurons and the precentral gyrus, while that of TGF-beta1, only in the spinal motoneuons, suggesting that the spinal motoneurons themselves could synthesize both the growth factors. Partial locomotor recovery in hindlimbs was seen, especially after 14 dpo. It was concluded that a possible association existed between the modulation of EGF and TGF-beta1 and the recovery of locomotor function, and their roles differed somewhat in the neuroplasticity observed after spinal cord injury in primates.
authors.affiliation: Institute of Neurological Disease, West China Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Xiao-Li
authors.initials: XL
authors.lastname: Li
authors.forename: Jia
authors.initials: J
authors.lastname: Liu
authors.forename: Xu-Yang
authors.initials: XY
authors.lastname: Wang
authors.forename: Li-Yan
authors.initials: LY
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Ni
authors.forename: Rong-Yuan
authors.initials: RY
authors.lastname: Zheng
authors.forename: Hui-Juan
authors.initials: HJ
authors.lastname: Yang
authors.forename: Yong-Chao
authors.initials: YC
authors.lastname: Lu
authors.forename: Jian-Guo
authors.initials: JG
authors.lastname: Qi
authors.forename: Ting-Hua
authors.initials: TH
authors.lastname: Wang
mesh_terms: D000818:Animals; D000870:Anterior Horn Cells / Q000378:metabolism*; D004195:Disease Models, Animal; D004815:Epidermal Growth Factor / Q000235:genetics / Q000378:metabolism*; D007839:Functional Laterality; D005786:Gene Expression Regulation / Q000502:physiology*; D008253:Macaca mulatta; D008297:Male; D009043:Motor Activity / Q000502:physiology; D020127:Recovery of Function / Q000502:physiology; D013116:Spinal Cord / Q000473:pathology*; D013119:Spinal Cord Injuries / Q000401:mortality / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D053773:Transforming Growth Factor beta1; D004815:Epidermal Growth Factor