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AKAP12 mediates barrier functions of fibrotic scars during CNS repair

Authors
 Jong-Ho Cha  ;  Hee-Jun Wee  ;  Ji Hae Seo  ;  Bum Ju Ahn  ;  Ji-Hyeon Park  ;  Jun-Mo Yang  ;  Sae-Won Lee  ;  Eun Hee Kim  ;  Ok-Hee Lee  ;  Ji Hoe Heo  ;  Hyo-Jong Lee  ;  Irwin H. Gelman  ;  Ken Arai  ;  Eng H. Lo  ;  Kyu-Won Kim 
Citation
 PLOS ONE, Vol.9(4) : e94695, 2014 
Journal Title
 PLOS ONE 
Issue Date
2014
MeSH
A Kinase Anchor Proteins/genetics ; A Kinase Anchor Proteins/metabolism* ; Animals ; Blotting, Western ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism* ; Central Nervous System/metabolism* ; Fibrosis/genetics ; Fibrosis/metabolism* ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Rats, Wistar ; Wound Healing/genetics ; Wound Healing/physiology
Abstract
The repair process after CNS injury shows a well-organized cascade of three distinct stages: inflammation, new tissue formation, and remodeling. In the new tissue formation stage, various cells migrate and form the fibrotic scar surrounding the lesion site. The fibrotic scar is known as an obstacle for axonal regeneration in the remodeling stage. However, the role of the fibrotic scar in the new tissue formation stage remains largely unknown. We found that the number of A-kinase anchoring protein 12 (AKAP12)-positive cells in the fibrotic scar was increased over time, and the cells formed a structure which traps various immune cells. Furthermore, the AKAP12-positive cells strongly express junction proteins which enable the structure to function as a physical barrier. In in vivo validation, AKAP12 knock-out (KO) mice showed leakage from a lesion, resulting from an impaired structure with the loss of the junction complex. Consistently, focal brain injury in the AKAP12 KO mice led to extended inflammation and more severe tissue damage compared to the wild type (WT) mice. Accordingly, our results suggest that AKAP12-positive cells in the fibrotic scar may restrict excessive inflammation, demonstrating certain mechanisms that could underlie the beneficial actions of the fibrotic scar in the new tissue formation stage during the CNS repair process.
Files in This Item:
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DOI
10.1371/journal.pone.0094695
Appears in Collections:
5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
Lee, Ok Hee(이옥희)
Heo, Ji Hoe(허지회) ORCID logo https://orcid.org/0000-0001-9898-3321
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/98749
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