Chondrogenic progenitor cells respond to cartilage injury

Abstract

Styrene oligomers (Mn, 2500–3000 g/mol) with low polydispersity index and containing peroxidic groups within their structure were synthesized using a novel trifunctional cyclic radical initiator, diethylketone triperoxide (DEKTP), through nitroxide‐mediated radical polymerization (NMRP), using OH‐TEMPO. During the synthesis of the polystyrene (PS) oligomers, camphorsulfonic acid (CSA) was used to inhibit the thermal autoinitiation of styrene at the evaluated temperatures (T = 120–130°C). The polymerization rate, which can be related to the slope of the plot of monomer conversion with reaction time, was monitored as a function of OH‐TEMPO, DEKTP, and CSA concentrations. The experimental results showed that all the synthesized polymers presented narrow molecular weight distributions, and the monomer conversion and the molecular weight of the polymers increased as a function of reaction time. Under the experimental conditions, T = 130°C, [DEKTP] = 10 mM, and [DEKTP]/[OH‐TEMPO] = 6.5, PS oligomers containing unreacted OO sites in their inner structure were obtained. © 2011 Wiley Periodicals, Inc. J Appl Polym Sci, 2012

Genomic Analysis and Differential Expression of HMG and S100A Family in Human Arthritis: Upregulated Expression of Chemokines, IL-8 and Nitric Oxide by HMGB1

“…It should be noted that the lack of HMGB1 expression in mice had detrimental effects on homeostasis of bone and cartilage (Taniguchi et al, 2007). Seol et al (2012) showed that injury to bovine cartilage and chondrocyte death stimulated the emergence of chondrogenic progenitor cells via HMGB1 release and RAGEmediated chemotaxis. This process could be inhibited by Glycrrhizin, a chelator of HMGB1 and anti-HMGB1 antibodies.…”

Effect of Short-Term Enzymatic Treatment on Cell Migration and Cartilage Regeneration:In VitroOrgan Culture of Bovine Articular Cartilage

“…In our previous study, we identified the characteristics of these chondrogenic progenitor cells (CPCs) isolated from injured articular cartilage. 21 These cells showed notable chemotatic activity, clonogenicity, and side populations like MSCs. On the other hand, they underexpressed cartilage-specific genes, such as type II, IX, and X collagens and aggrecan, compared with normal chondrocytes.…”

“…21 The control cartilage in our explant model begins to deteriorate after *3 weeks, due possibly to the lack of mechanical stimulation in culture. This may not have been long enough to fully evaluate the potential for matrix regeneration in defects.…”

Induced superficial chondrocyte death reduces catabolic cartilage damage in murine posttraumatic osteoarthritis

“…Although cell death and cartilage failure are correlated, the relationship between chondrocyte loss and cartilage degeneration is unknown. Some studies indicate chondrocyte loss precedes cartilage damage after injury and that chondrocyte repopulation in damaged areas can promote cartilage repair (13,14). Other studies indicate that injured chondrocytes produce factors, such as matrix metallopeptidase 13 (MMP13), ADAM metallopeptidase with thrombospondin type 1 motif 4 (ADAMTS4), and ADAMTS5, that cause cartilage degeneration (15)(16)(17)(18).…”