AKAP12 mediates barrier functions of fibrotic scars during CNS repair.

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...

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Main 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
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0094695&type=printable
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author 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
author_facet 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
author_sort Jong-Ho Cha
collection DOAJ
description 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.
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publishDate 2014-01-01
publisher Public Library of Science (PLoS)
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spelling doaj-art-3d669d77a7bf4175a36a6ae26c8739f92025-08-20T03:00:30ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0194e9469510.1371/journal.pone.0094695AKAP12 mediates barrier functions of fibrotic scars during CNS repair.Jong-Ho ChaHee-Jun WeeJi Hae SeoBum Ju AhnJi-Hyeon ParkJun-Mo YangSae-Won LeeEun Hee KimOk-Hee LeeJi Hoe HeoHyo-Jong LeeIrwin H GelmanKen AraiEng H LoKyu-Won KimThe 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.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0094695&type=printable
spellingShingle 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
AKAP12 mediates barrier functions of fibrotic scars during CNS repair.
PLoS ONE
title AKAP12 mediates barrier functions of fibrotic scars during CNS repair.
title_full AKAP12 mediates barrier functions of fibrotic scars during CNS repair.
title_fullStr AKAP12 mediates barrier functions of fibrotic scars during CNS repair.
title_full_unstemmed AKAP12 mediates barrier functions of fibrotic scars during CNS repair.
title_short AKAP12 mediates barrier functions of fibrotic scars during CNS repair.
title_sort akap12 mediates barrier functions of fibrotic scars during cns repair
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0094695&type=printable
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