Membrane type-1 matrix metalloproteinase is induced following cyclic compression of in vitro grown bovine chondrocytes

Abstract

These data suggest that cyclic compression of chondrocytes in vitro upregulates MT1-MMP via ERK1/2 dependent activation of Egr-1 binding. Delineation of the regulatory pathways activated by mechanical stimulation will further our understating of the mechanisms influencing tissue remodeling.

Integration of Tissue-engineered Cartilage With Host Cartilage: An In Vitro Model

“…Our study showed that bovine chondrocytes are motile although their role in cartilage repair and integration in this model is unknown. Previous studies in our laboratory have highlighted the importance of matrix remodeling, mediated in part by the protease MT1-MMP, in improving tissue formation [9,10]. Given the role of MT1-MMP in cell migration [11,37], it is possible this metalloprotease is involved in chondrocyte motility; however, further study is required to confirm this.…”

Proteomic Analysis Reveals Grb2 as a Key Regulator of Periodic Mechanical Stress Transduction in Chondrocytes

“…Grb2 has been known to play a positive role in receptor tyrosine kinase signaling [24, 25], and the association of Grb2 and Shc/FAK is upstream to the activation of MAPK, which is an important signaling pathway leading to the proliferation and matrix synthesis of chondrocytes when exposed to periodic mechanical stress [26, 27]. We therefore hypothesized that the effect of Grb2 in mechanical signal transduction in chondrocytes may be related to the stimulation of MAPK pathway.…”

EGR-1 decoy ODNs inhibit vascular smooth muscle cell proliferation and neointimal hyperplasia of balloon-injured arteries in rat

“…2000; Ohtani et al 2004), but also regulate the cells' adhesion and migration through participating in the transcription activation of CCN1 (Grote et al 2004) and MT1-MMP (De Croos et al 2007). These results provided the first evidence that TF decoy strategies might be used to prevent and cure diseases (Morishita et al 1998).…”