Endometriosis is an estrogen-dependent disease. A theory of deficient HSD17B2 activity in endometriotic lesions leading to high local levels of estradiol has been described as a potential molecular mechanism for the disease progression. However, HSD17B2 mRNA is normally expressed in endometriotic tissue, leading us to question whether an excess of microRNAS (miRNAs) could be involved in post-transcriptional silencing of HSD17B2.

This was a prospective, cross-sectional, pilot study. The study included seven samples of superficial peritoneal endometriosis and 22 samples of eutopic endometrium from 22 reproductive-aged patients submitted to laparoscopy for symptomatic endometriosis. We searched in an experimentally validated microRNA-target interaction online database (miRTarBase) for miRNAs that target the HSD17B2 gene and performed RT-PCR to evaluate their expression in endometriotic lesions and eutopic endometrium.

We found two miRNAs on the miRTarBase search that interact with HSD17B2: miR-124-3p and miR-26b-5p. RT-PCR analysis showed that both miRNAs were expressed in ectopic tissues as well as in eutopic endometrium. Quantitatively, no significant difference existed between the two tissue groups in either miR-26b-5p (p = 0.08) or miR-124-3p (p = 0.09) expression levels, although the observed trend was towards lower levels of both miRNAs in the endometriotic lesions.

The expression of miRNAs miR-26b-5p and miR-124-3p is not increased in peritoneal endometriosis compared to eutopic endometrium. The regulation of HSD17B2 expression may be more complex than assumed, and it must be further investigated in different clinical scenarios.