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Publication : Inhibition of fibrous adhesion formation in the temporomandibular joint of tenascin-C knockout mice.

First Author  Shinohara Y Year  2014
Journal  Eur J Histochem Volume  58
Issue  4 Pages  2337
PubMed ID  25578971 Mgi Jnum  J:318298
Mgi Id  MGI:6859111 Doi  10.4081/ejh.2014.2337
Citation  Shinohara Y, et al. (2014) Inhibition of fibrous adhesion formation in the temporomandibular joint of tenascin-C knockout mice. Eur J Histochem 58(4):2337
abstractText  Tenascin-C (TNC) is a large hexameric extracellular matrix glycoprotein that is expressed in developing organs and tumors. It has been reported that TNC is expressed in inflamed synovial membranes and deformed discs of temporomandibular joint (TMJ) disorder. However, the role of TNC in TMJ is not fully known. In this study, the role of TNC in fibrous adhesion formation of TMJ was examined using TNC knockout (TNCKO) mice. Hypermobility was produced by excessive mouth opening method on the TMJ of both wild-type (WT) and TNCKO mice. TMJ wound healing was compared histologically, and the expression of TNC, fibronectin (FN) and alpha-smooth muscle actin (alpha-SMA) in the wounded TMJ was examined by immunohistochemical and immunoblot analyses. Based on histologic analysis, fibrous adhesions were observed in the TMJ of both TNCKO and wild-type (WT) mice after excessive mouth opening. However, fibrous adhesion formation in TNCKO mice occurred later than in WT mice. TNC was expressed in the wounded TMJ disc and mandibular fossa. Although FN and alpha-SMA expression in the TMJ of TNCKO and WT mice was up-regulated after excessive mouth opening, FN and alpha-SMA protein levels were higher in WT mice at the same time points. In the wounded TMJ, TNC appears to enhance the expression of FN and alpha-SMA, and a lack of TNC may reduce fibrous adhesion formation in the TMJ. TNC plays an important role in TMJ wound healing, especially for wounds generated by mechanical stress.
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