Proteomic analysis of masticatory muscle tendon–aponeurosis hyperplasia: A preliminary study using a 2D-DIGE system

Masticatory muscle tendon–aponeurosis hyperplasia (MATAPHY) exhibits hyperplasia on tendon and aponeurosis of the masticatory muscles histopathologically. This disease is characterized by a palpable dense band of the anterior border of the masseter muscle on maximum mouth opening, strike root appearance on MR imaging and square mandible configuration. However, the common useful diagnostic markers of this disease are still unknown. Here we performed a preliminary study to identify potential therapeutic targets and diagnostic markers that may indicate disease progression of MATAPHY using a proteomic analysis method, two-dimensional fluorescence difference gel electrophoresis and liquid chromatography coupled with tandem mass spectrometry. We have found that myosin regulatory light chain 2 and myosin regulatory light chain 3 were down-regulated in MATAPHY. This result is consistent with the observation that muscle tissues showed atrophic changes. We have also demonstrated that aortic smooth muscle actin was down-regulated in MATAPHY, suggesting that this down-regulation is due to decreasing in muscle tissues that blood vessels are abundant and increasing in tendon tissues that blood vessels are exiguous. Furthermore, collagen alpha-1(VI) chain (COL6A1) was up-regulated in MATAPHY. COL6A1, which is essential for tendon fibrillogenesis, expressed in the masticatory muscle, indicating that tendon-aponeurosis hyperplasia is due to the overexpression of COL6A1. Facial deformity, which we choose as a control in this study, is sometimes congenital and may be complicated with deficiency of the skeletal proteins. Although this report has some limitations, this is the first report to describe the relationship between the variation of specific molecules and histopathological observation in MATAPHY.