| Summary: | 碩士 === 國防醫學院 === 牙醫科學研究所 === 99 === Epithelial to mesenchymal transition (EMT) occurs normally in development. In pathology, EMT drives fibrosis and cancer. EMT is an underlying mechanism of tissue fibrosis, generating myofibroblasts, which serve as the primary source of extracellular matrix production from tissue epithelial cells.
Cyclosporin A (CsA) is one of the most widely used immunosuppressive drugs in the organ transplantation and in the therapy of autoimmune disorders, but CsA induces side effects, including gingival overgrowth. Based on the findings of decreased E-cadherin and enhanced FSP-1 in the overgrown gingival tissue (mainly for the phynetoin-induced gingival overgrowth) in a recent study, the authors first suggested that EMT might participate in the pathogenesis of drug-induced gingival overgrowth.
In this study, the CsA-induced EMT in gingiva was observed in vivo & in vitro because the direct evidences are still limited. The expressions of EMT markers (E-cadherin,α-SMA and TGF-β1) were analyzed by RT-PCR and ICC/IHC in cultured primary human gingival epithelial cells after CsA treatment and in CsA-treated SD rats. In CsA-treated cultured epithelial cells and rat gingival tissue were decreased expressions of E-cadherin, but increased expressions of α-SMA, and loss of epithelial morphology. In summary, CsA treatment resulted in the EMT genes changed in the gingival epithelial cells; as well as the EMT markers altered in the gingival overgrowth tissues of rats. These findings support the hypothesis that EMT occurs in CsA-induced gingival overgrowth. And TGF-β1 might play an important role for the development of EMT.
|
|---|
