Human endometriotic lesion expression of the miR-144-3p/miR-451a cluster, its correlation with markers of cell survival and origin of lesion content

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AI-generated summary by claude@2026-06, 2026-06-07

The miR-144-3p/miR-451a cluster is upregulated in endometriotic lesions, with miR-451a potentially originating exogenously, and lesion expression correlates with cell survival.

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AI-generated deep summary by claude@2026-06, 2026-06-07

This study examined whether the miR-144-3p/miR-451a microRNA cluster is expressed in human endometriotic lesions and how lesion levels relate to cell survival markers and lesion cellular origin. In matched patient samples, both pri- and mature miR-144-3p and pri- and mature miR-451a were elevated in endometriotic lesions versus eutopic endometrium, with heterogeneous lesion-to-lesion expression and correlations between pri- and mature forms that differed by miRNA. In DROSHA knockdown experiments using an endometriotic epithelial cell line (12Z), pri-miR-144-3p increased but pri-miR-451a did not, and in an ectopic-lesion mouse model lacking both miRNAs, miR-451a—but not miR-144-3p—rose over time while miR-451a target Mif was reduced, supporting exogenous derivation of miR-451a such as from circulation/erythrocytes; a key caveat is that exogenous contributions were inferred from expression changes rather than directly tracing the source. This paper is centrally about endometriosis — it characterizes lesion expression and putative exogenous origin of the miR-144-3p/miR-451a cluster in human and mouse endometriotic lesions.

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Abstract

Endometriosis is an inflammatory condition in which endometrial tissue grows in ectopic locations. Survival and growth of these ectopic lesions is associated with pain and infertility. MicroRNAs (miRNAs) have been postulated to play a role in the pathophysiology of the disease and we have previously demonstrated expression of miR-451 in human endometriotic lesion tissue. Here we report elevated expression of the miR-144-3p/miR-451a cluster in human endometriotic lesion tissue. Use of an endometriotic epithelial cell line (12Z) in which the miRNA processing enzyme, DROSHA, was knocked down resulted in an enrichment in the primary (pri) form of miR-144-3p but not that of pri-miR-451a. Using an experimental mouse model of endometriosis in which ectopic endometriotic lesions were deficient for both of these miRNAs revealed that miR-451a, but not miR-144-3p may be derived from exogenous sources such as the circulation/erythrocytes. Together, these data suggest that the miR-144-3p/miR-451a cluster is expressed in human endometriotic lesion tissue, the level of expression correlates with survival status of the lesion tissue and that miR-451a, but not miR-144-3p may be derived from exogenous sources such as erythrocytes.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometrium Endometrium Gene Expression Regulation MicroRNAs Adult Cell Survival Cell Survival Endometrium Female Humans MicroRNAs MicroRNAs Middle Aged Ribonuclease III Ribonuclease III RNA, Messenger RNA, Messenger RNA, Messenger Young Adult

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europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
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pubmed
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