Abstract
Human endometrium is a highly regenerative and dynamic tissue that undergoes cyclic changes during menstrual cycle. It has been reported that endometrial epithelium contains a population of progenitor/stem cells. Increasing amount of evidence indicates that progenitor/stem cells are involved in the pathogenesis of endometriosis. Proteins belonging to the aldehyde dehydrogenase 1 (ALDH1A) family have been reported to be markers of normal tissue stem cells and cancer stem cells. In this study, by using immunohistochemistry, we examined the expression of ALDH1A isozymes in human endometrial tissue, including that affected by endometriosis, and in ovarian endometrioma. Positive staining for ALDH1A isozymes was observed in the stroma of the endometrium and in endometriotic ovarian tissue. In the glands, expression patterns were distinct for different ALDH1A isozymes. ALDH1A1 and ALDH1A3 were highly expressed in the epithelium of stratum basalis of the endometrium and in the epithelium of ovarian endometrioma irrespective of the menstrual cycle, whereas ALDH1A2 was highly expressed only in the epithelium of endometrioma. Furthermore, ALDH1A1 co-localized with N-cadherin, which is a marker of endometrial epithelial progenitor cells, in the glands of stratum basalis. These findings support and reinforce the notion about the presence of progenitor/stem cells in endometrial glands in stratum basalis and in endometriotic glands, suggesting that these cells are involved in the physiology of the endometrium and in the pathology of endometriosis.
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We would like to thank Editage (www.editage.jp) for English language review.
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This work was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology and the Japan Agency for Medical Research and Development.
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Ma, S., Hirata, T., Arakawa, T. et al. Expression of ALDH1A Isozymes in Human Endometrium with and without Endometriosis and in Ovarian Endometrioma. Reprod. Sci. 27, 443–452 (2020). https://doi.org/10.1007/s43032-019-00041-4
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DOI: https://doi.org/10.1007/s43032-019-00041-4