The uterine secretome initiates growth of gynecologic tissues in ectopic locations

Jan Sunde, Morgan Wasickanin, Tiffany A Katz, Laurel Gillette, Sanam Bidadi, Derek O'Neil, Derek O’Neil, Ramya P. Masand, Ramya Masand, Richard O Burney, Kathleen A. Pennington
PloS one · 2024 · vol. 19(5) , pp. e0292978 · doi:10.1371/journal.pone.0292978 · PMID:38728307 · W4396790048
article OA: gold CC0
🔓 Open OA copy View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Endometrial-derived factors like LIF are necessary for initiating ectopic gynecologic tissue growth, as demonstrated in a new mouse model of endosalpingiosis and endometriosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

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

The study investigated whether “uterine secretome” factors from post-ovulatory uterine tissue drive the implantation and growth of ectopic gynecologic epithelium by developing a fluorescent mouse model using tdTomato donor tissues injected intraperitoneally into synchronized wild-type recipients to visualize lesions over time as endometriosis (endometrial tissue) or endosalpingiosis (oviductal tissue). Lesion implantation was higher when tdT oviductal tissue was co-implanted with wild-type endometrium, and implantation was markedly reduced when progesterone knockout (PKO) tdT endometrium was used; additionally, exogenous leukemia inhibitory factor (LIF) promoted lesion implantation, with LIF serving as an implantation factor mimic. A key limitation is that the work relies on experimentally manipulated donor/recipient hormone states and tissue implantation (minced tissue/implantation into the peritoneum), which may not fully recapitulate natural lesion development. This paper is centrally about endometriosis—specifically testing that endometrial implantation factors within the uterine secretome (including LIF) are necessary to initiate ectopic growth in vivo.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endosalpingiosis (ES) and endometriosis (EM) refer to the growth of tubal and endometrial epithelium respectively, outside of their site of origin. We hypothesize that uterine secretome factors drive ectopic growth. To test this, we developed a mouse model of ES and EM using tdTomato (tdT) transgenic fluorescent mice as donors. To block implantation factors, progesterone knockout (PKO) tdT mice were created. Fluorescent lesions were present after oviduct implantation with and without WT endometrium. Implantation was increased (p<0.05) when tdt oviductal tissue was implanted with endometrium compared to oviductal tissue alone. Implantation was reduced (p<0.0005) in animals implanted with minced tdT oviductal tissue with PKO tdT endometrium compared to WT endometrium. Finally, oviductal tissues was incubated with and without a known implantation factor, leukemia inhibitory factor (LIF) prior to and during implantation. LIF promoted lesion implantation. In conclusion, endometrial derived implantation factors, such as LIF, are necessary to initiate ectopic tissue growth. We have developed an animal model of ectopic growth of gynecologic tissues in a WT mouse which will potentially allow for development of new prevention and treatment modalities.

My notes (saved in your browser only)

Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Endometrium Uterus Uterus Uterus Uterus Uterus Animals Animals Animals

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (72)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-29T00:32:39.447666+00:00
License: CC0 · commercial use OK