Proinflammatory cytokine-induced matrix metalloproteinase-9 expression in temporomandibular joint osteoarthritis is regulated by multiple intracellular mitogen-activated protein kinase pathways.

Objectives: Temporomandibular joint (TMJ) osteoarthritis (OA) is an inflammatory disease that involves periarthritis of the TMJ and destruction of cartilage tissue in the mandibular condyle. However, the role of proinflammatory cytokines in the expression levels of matrix metalloproteinase (MMP) remains inconclusive. Thus, in this study, we aimed to investigate the effect of proinflammatory cytokines on the expression of MMPs.

Connective tissue growth factor enhances TGF-β1-induced osteogenic differentiation via activation of p38 MAPK in mesenchymal stem cells.

Objectives: Cellular differentiation is based on the effects of various growth factors. Transforming growth factor (TGF)-β1 plays a pivotal role in inducing osteogenic differentiation of mesenchymal stem cells (MSCs). In this study, we investigated the influence of connective tissue growth factor (CTGF), known to function synergistically with TGF-β1, on osteogenic differentiation in MSCs.

Disruption of CADM1-dependent cell-cell adhesion in human oral squamous cell carcinoma cells results in tumor progression, possibly through an increase of MMP-2 and MMP-9 expression.

Objectives: This study aimed to clarify the molecular mechanism underlying the higher invasion and metastasis abilities of LMF4 cells than those of HSC-3 cells by comparing the expression levels of the tumor suppressor factor, cell adhesion molecule 1 (CADM1).

Methods: We explored 1) whether CADM1 expression level was downregulated in LMF4 cells compared with HSC-3 cells, 2) whether CADM1 expression knockdown increased the expression levels of matrix metalloproteinases (MMPs), 3) the exact cellular signaling pathways responsible for increased MMP expression after knockdown of CADM1 expression, and 4) whether disruption of CADM1-dependent HSC-3 cell adhesion increased the migratory and invasive activities of HSC-3 cells.

Results: CADM1 expression was lower in the LMF4 than in the HSC-3 cells.

Hydrogen peroxide-induced oxidative stress promotes expression of CXCL15/Lungkine mRNA in a MEK/ERK-dependent manner in fibroblast-like synoviocytes derived from mouse temporomandibular joint.

Objectives: Temporomandibular joint osteoarthritis (TMJ-OA) is a multifactorial disease caused by inflammation and oxidative stress. It has been hypothesized that mechanical stress-induced injury of TMJ tissues induces the generation of reactive oxygen species (ROS), such as hydroxyl radical (OH∙), in the synovial fluid (SF). In general, the overproduction of ROS contributes to synovial inflammation and dysfunction of the subchondral bone in OA.

Extracellular adenosine 5'-diphosphate promotes MCP-1/CCL2 expression via the P2Y purinergic receptor/ERK signaling axis in temporomandibular joint-derived mouse fibroblast-like synoviocytes.

Background: Temporomandibular joint osteoarthritis (TMJ-OA) causes cartilage degeneration, bone cavitation, and fibrosis of the TMJ. However, the mechanisms underlying the fibroblast-like synoviocyte (FLS)-mediated inflammatory activity in TMJ-OA remain unclear.

Methods And Results: Reverse transcription-quantitative polymerase chain reaction analysis revealed that the P2Y, P2Y, and P2Y purinergic receptor agonist adenosine 5'-diphosphate (ADP) significantly induces monocyte chemotactic protein 1 (MCP-1)/ C-C motif chemokine ligand 2 (CCL2) expression in the FLS1 synovial cell line.