Expression And Significance Of Neural Cell Adhesion Molecule-1 In Adenomyosis

BackgroundAdenomyosis is a common but complex gynecologic disease which involves the glands and stroma from the endometrium invading into the myometrium, accompanied with hypertrophy and hyperplasia in the surrounding tissue. Progressive dysmenorrhea and abnormal uterine bleeding are the two most common complaints of patients with adenomyosis. Although recently the incidence of adenomyosis is higher and the age becomes younger, the pathogenesis is still not very clear.Neural cell adhesion molecule-1 (NCAM1), also known as CD56, was first discovered in the chicken retina and brain in 1976. NCAM1 was found expressed on immunocytes and neural cells, which not only is the surface marker of NK cells, but also expressed in neural tissues, neuroendocrine tissues and tumors and play an important role in the growth and aggregation of nerve fibers and neuroendocrine tumor metastases. NCAM1 has been detected in the interstitial tissue of both human and rat endometriotic foci, but it has not been reported in adenomyosis.Though both of adenomyosis and endometriosis belongs to the ectopic invading of endometrium, the clinical features and pathogenesis of them are quite different. Thus, we design this study to investigate NCAM1 expression in the ectopic and eutopic endometrium of adenomyosis and its possible role in the pathogenesis of this disease.ObjectiveTo investigate the expression of NCAM1 in the eutopic endometrium and ectopic lesions from patients in adenomyosis and its possible role in the pethogenesis of adenomyosis. Besides, we also investigate the correlation between NCAM1 expression in the patients with adenomyosis and the severity of dysmenorrhea.MethodsThe expression of NCAM1 was assayed by immunohistochemical staining and the result was compared with the control group by H-score method. The severity of dymenorrhea was valued by NRS (Numerical rating scale) and then compared with the NCAM1 staining.ResultNCAM1 was observed in the endometrial glandular epithelium of all the ectopic and ectopic samples and 19 normal samples. Positive results can be hardly observed in the stroma and myometrium.The staining intensity of NCAM1 in ectopic lesion was significantly higher than it was in the eutopic endometrium and normal endometrium (P<0.01), whereas no statistical difference was observed in the expression between the eutopic endometrium and normal endometrium of patients with adenomyosis. For eutopic endometrium of adenomyosis, expression was higher in the secretory phase than in the proliferative phase (P<0.05). The expression of NCAM1 in ectopic lesion of adenomyosis is positively correlated with the severity of dysmenorrhea (spearman rho=0.84, P<0.01)ConclusionsNCAM1 may participate in the occurrence and development of adenomyosis and may contributes to the severity of dymenorrhea, but the exact moleculor mechanisms still remain to be discovered.