Abnormal expression of connective tissue growth factor and its correlation with fibrogenesis in adenomyosis.

RESEARCH QUESTION: Does connective tissue growth factor (CTGF) expression relate to adenomyotic fibrosis and determine the correlation between fibrosis with adenomyosis-associated dysmenorrhoea? DESIGN: Protein and mRNA expression of CTGF was detected by Western blots and real-time quantitative polymerase chain reaction in the endometrium of the control group and the eutopic and ectopic endometrium of the adenomyosis group. Collagen fibres and type I collagen in the myometrium were detected by immunohistochemistry and Masson's trichrome staining, and the correlations of CTGF protein and mRNA levels with the degree of fibrosis were analysed. Furthermore, the relationship between the severity of dysmenorrhoea and the degree of fibrosis was determined, and the correlation between uterus size and the degree of fibrosis was also analysed. RESULTS: Levels of CTGF mRNA and protein were significantly higher in patients with adenomyosis than in controls, and CTGF mRNA and protein expression in adenomyosis was positively correlated with fibrosis severity (r = 0.57, P < 0.001 and r = 0.39, P = 0.012), which correlated positively with dysmenorrhoea and uterus size (r = 0.42 and r = 0.6, P < 0.002). CONCLUSIONS: Increased CTGF may contribute to the occurrence and fibrogenic progression of adenomyosis and may play an important role in dysmenorrhoea. The present study may provide ideas for treating adenomyosis-associated dysmenorrhoea.

FAK regulates epithelial­mesenchymal transition in adenomyosis.

Epithelial­mesenchymal transition (EMT) has been associated with the pathogenesis of adenomyosis; focal adhesion kinase (FAK) serves an important role in the EMT process. The aim of the present study was to determine whether FAK regulates EMT in adenomyosis and to investigate the potential pathway in this process. The expression of FAK and EMT­associated molecules in adenomyosis and control cells were determined by immunohistochemical staining and immunofluorescence at the protein level, and at the mRNA level by reverse transcription­quantitative polymerase chain reaction (RT­qPCR). Small interfering RNAs were designed to knock down FAK expression. Subsequently, molecular expression was detected by immunofluorescence, RT­qPCR and western blotting; cell migration was investigated via Transwell assays. In addition, the expression levels of members of the phosphoinositide 3­kinase (PI3K)/protein kinase B (AKT) signaling pathway was also analyzed by RT­qPCR and western blotting to determine the association between these members and EMT in adenomyosis. The results of the present study revealed that FAK was upregulated and the expression levels of EMT­associated molecules were altered in adenomyosis. Silencing FAK expression inhibited adenomyosis cell migration in vitro and the expression of EMT­promoting molecules, suggesting that the FAK/PI3K/AKT signaling pathway may participate in the EMT of endometrial cells in adenomyosis. In conclusion, FAK may regulate EMT in adenomyosis, and this process may be associated with the PI3K/AKT signaling pathway.