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The following is a summary of “Endometriotic lesions express microRNAs that potentially regulate the transcription of hydroxysteroid 17-beta dehydrogenase 2 (HSD17B2): a pilot study,” published in the December 2024 issue of Obstetrics and Gynecology by Coutinho et al. 

Endometriosis, an estrogen-dependent disease, was thought to involve deficient HSD17B2 activity in endometriotic lesions, leading to elevated estradiol levels, despite normal HSD17B2 mRNA expression, suggesting a potential role for microRNAs (miRNAs) in post-transcriptional silencing.  

Researchers conducted a retrospective study to analyze the potential role of miRNAs in post-transcriptional silencing of HSD17B2 in endometriotic tissue.  

They included 7 samples of superficial peritoneal endometriosis and 22 samples of eutopic endometrium from 22 reproductive-aged individuals who underwent laparoscopy for symptomatic endometriosis. Using the miRTarBase (an experimentally validated microRNA-target interaction online database) and identified microRNAs that target the HSD17B2 gene. RT-PCR was performed to assess the expression of microRNAs in both endometriotic lesions and eutopic endometrium.  

The results showed that miR-124-3p and miR-26b-5p were identified as interacting with HSD17B2 in the miRTarBase search. RT-PCR analysis revealed the expression of both miRNAs in both ectopic and eutopic endometrium. There was no significant difference in expression levels between the 2 tissue types for either miRNA (miR-26b-5p: P = 0.08; miR-124-3p: P = 0.09), though a trend toward lower levels of both miRNAs was observed in endometriotic lesions.  

Investigators concluded the expression levels of miRNAs miR-26b-5p and miR-124-3p were not elevated in peritoneal endometriosis as compared to eutopic endometrium, suggesting that the regulation of HSD17B2 expression in the disease might involve more intricate mechanisms than initially hypothesized. 

Source: sciencedirect.com/science/article/pii/S2949838424000355