title: Exercise Training Inhibits the Nogo-A/NgR1/Rho-A Signals in the Cortical Peri-infarct Area in Hypertensive Stroke Rats.
abstract: OBJECTIVE
  The aim of this study was to test the hypothesis that exercise training promotes motor recovery after stroke by facilitating axonal remodeling via inhibition of the Nogo-A/NgR1 and Rho-A pathway.
  
  
  METHODS
  A distal middle cerebral artery occlusion model was generated in stroke-prone renovascular hypertensive rats. Stroke-prone renovascular hypertensive rats were randomly divided into a control group, an exercise training group, and a sham group. Motor function was measured using the grip strength test. Axon and myelin remodeling markers, growth-associated protein 43, myelin basic protein, Tau, and amyloid precursor protein were detected by immunofluorescence. The expression of Nogo-A, NgR1, and Rho-A was demonstrated by immunofluorescence and Western blotting in the peri-infarction area at 7, 14, 28, and 52 days after distal middle cerebral artery occlusion.
  
  
  RESULTS
  Grip strength was higher in the exercise training group (P < 0.05). Exercise training increased the expression of growth-associated protein 43, myelin basic protein (at 7, 14, and 28 days), and Tau (at 7 and 14 days), and decreased the expression of axonal damage amyloid precursor protein (at 7 and 14 days), compared with the control group. The protein levels of Nogo-A (at 7 and 14 days), NgR1 (at 7, 14, and 28 days), and Rho-A (at 14 and 28 days) were reduced after exercise training.
  
  
  CONCLUSIONS
  Exercise training promotes axonal recovery, which is associated with functional improvement after cerebral infarction. Down-regulation of the Nogo-A/NgR1/Rho-A may mediate the axonal remodeling induced by exercise training.
authors.affiliation: From the Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, China (CL, HMW, CJZ, LJ, ZLD); Stroke Biological Recovery Laboratory, Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Charlestown, Massachusetts (QMW); Department of Rehabilitation Medicine, The Fourth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China (XL); and Department of Neurology and Stroke Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, China (JSZ).
authors.forename: Chao
authors.initials: C
authors.lastname: Li
authors.forename: HongMei
authors.initials: H
authors.lastname: Wen
authors.forename: QingMei
authors.initials: Q
authors.lastname: Wang
authors.forename: ChanJuan
authors.initials: C
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Jiang
authors.forename: ZuLin
authors.initials: Z
authors.lastname: Dou
authors.forename: Xun
authors.initials: X
authors.lastname: Luo
authors.forename: JinSheng
authors.initials: J
authors.lastname: Zeng
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism / Q000534:rehabilitation; D004195:Disease Models, Animal; D005081:Exercise Therapy; D058851:GPI-Linked Proteins / Q000378:metabolism; D008297:Male; D009185:Myelin Proteins / Q000378:metabolism*; D000070798:Nogo Proteins; D000070816:Nogo Receptor 1; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000378:metabolism*; D020127:Recovery of Function; D020521:Stroke / Q000209:etiology / Q000378:metabolism*; D000071939:Stroke Rehabilitation; D020742:rhoA GTP-Binding Protein / Q000378:metabolism*
chemical_list: D058851:GPI-Linked Proteins; D009185:Myelin Proteins; D000070798:Nogo Proteins; D000070816:Nogo Receptor 1; D011956:Receptors, Cell Surface; C000603197:Rtn4 protein, rat; C486581:Rtn4r protein, rat; D020742:rhoA GTP-Binding Protein