Document Detail


Chondrogenic progenitor cells respond to cartilage injury.
MedLine Citation:
PMID:  22777600     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Hypocellularity resulting from chondrocyte death in the aftermath of mechanical injury is thought to contribute to posttraumatic osteoarthritis. However, we observed that nonviable areas in cartilage injured by blunt impact were repopulated within 7-14 days by cells that appeared to migrate from the surrounding matrix. The aim of this study was to assess our hypothesis that the migrating cell population included chondrogenic progenitor cells that were drawn to injured cartilage by alarmins.
METHODS: Osteochondral explants obtained from mature cattle were injured by blunt impact or scratching, resulting in localized chondrocyte death. Injured sites were serially imaged by confocal microscopy, and migrating cells were evaluated for chondrogenic progenitor characteristics. Chemotaxis assays were used to measure the responses to chemokines, injury-conditioned medium, dead cell debris, and high mobility group box chromosomal protein 1 (HMGB-1).
RESULTS: Migrating cells were highly clonogenic and multipotent and expressed markers associated with chondrogenic progenitor cells. Compared with chondrocytes, these cells overexpressed genes involved in proliferation and migration and underexpressed cartilage matrix genes. They were more active than chondrocytes in chemotaxis assays and responded to cell lysates, conditioned medium, and HMGB-1. Glycyrrhizin, a chelator of HMGB-1 and a blocking antibody to receptor for advanced glycation end products (RAGE), inhibited responses to cell debris and conditioned medium and reduced the numbers of migrating cells on injured explants.
CONCLUSION: Injuries that caused chondrocyte death stimulated the emergence and homing of chondrogenic progenitor cells, in part via HMGB-1 release and RAGE-mediated chemotaxis. Their repopulation of the matrix could promote the repair of chondral damage that might otherwise contribute to progressive cartilage loss.
Authors:
Dongrim Seol; Daniel J McCabe; Hyeonghun Choe; Hongjun Zheng; Yin Yu; Keewoong Jang; Morgan W Walter; Abigail D Lehman; Lei Ding; Joseph A Buckwalter; James A Martin
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Arthritis and rheumatism     Volume:  64     ISSN:  1529-0131     ISO Abbreviation:  Arthritis Rheum.     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-31     Completed Date:  2013-01-10     Revised Date:  2014-11-09    
Medline Journal Info:
Nlm Unique ID:  0370605     Medline TA:  Arthritis Rheum     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3626-37     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2012 by the American College of Rheumatology.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology
Cartilage, Articular / injuries*,  pathology
Cattle
Cell Differentiation / physiology
Cell Movement / physiology
Cells, Cultured
Chondrocytes / cytology*,  physiology
Multipotent Stem Cells / cytology*,  physiology
Osteoarthritis, Knee / etiology,  pathology*
Stifle / injuries*,  pathology
Transcriptome
Wounds, Nonpenetrating / pathology
Grant Support
ID/Acronym/Agency:
P50 AR055533/AR/NIAMS NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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