MeCP2, known as a transcriptional regulator, has been suggested to play an essential role in myofibroblast differentiation in the lung. The purpose of this study was to investigate the role of MeCP2 in TGF-β1-induced myofibroblast differentiation and ECM production in NPDFs.

Researchers conducted this study to identify the expression of MeCP2 in nasal polyp tissues, immunohistochemistry staining, and Western blot were performed. TGF-β1-induced NPDFs were treated with 5-azacytidine, a DNA methylation inhibitor. The expression levels of α-SMA and fibronectin were determined by a semiquantitative reverse transcription-polymerase chain reaction, immunofluorescent staining, and Western blotting. The Sircol collagen assay analyzed the total soluble collagen. MeCP2 silenced by MeCP2-specific small interference (si) RNA was verified by Western blot.

The expression levels of MeCP2 increased in nasal polyp tissues compared to normal inferior turbinate tissues. 5-Azacytidine significantly inhibited the expression of α-SMA and fibronectin mRNA in a dose-dependent manner. Besides, 5-azacytidine suppressed collagen production and the manifestation of MeCP2 in the same way. The expression levels of a-SMA and collagen production were significantly blocked by MeCP2 silencing in TGF-β1-induced NPDFs.

The study concluded that MeCP2 plays an essential role in TGF-β1-induced myofibroblast differentiation and ECM production in NPDFs.