Different macrophages equally induce EMT in endometria of adenomyosis and normal

Min An, Min Sung An, An M, Li D, Li Dong, Dong Li, Ming Yuan, Li Q, Qiuju Li, Zhang L, Lu Zhang, Guoyun Wang, Wang G, Guo Yun Wang
Reproduction (Cambridge, England) · 2017 · vol. 154(1) , pp. 79–92 · doi:10.1530/rep-17-0174 · PMID:28495851 · W2612638783
Lab / animal OA: bronze CC0 ⤵ 20 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-08 ⓘ

Macrophages induce epithelial-mesenchymal transition in both normal and adenomyotic endometria, with M2 polarization observed in both groups, though less pronounced in the adenomyosis group.

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

Abstract

Endometrial cells and microenvironment are two important factors in the pathogenesis of adenomyosis. Our previous study demonstrated that macrophages can induce eutopic epithelial cells of adenomyosis to suffer from epithelial-mesenchymal transition (EMT). The aim of this study is to detect whether macrophages interacting with epithelial cells equally induce the EMT process in normal and eutopic endometria of healthy and adenomyotic patients; and whether macrophages parallelly polarize to M2. We investigated the expression levels of epithelial cadherin (E-cadherin), neural cadherin (N-cadherin), cytokeratin7 (CK7), vimentin, transforming growth factor-β1 (TGFB1), SMAD3 and pSMAD3 using immunohistochemistry and western blot, and then estimated the genetic levels of CD163, IL10 and MMP12 using real-time quantitative polymerase chain reaction (RT-PCR) in macrophages. Eutopic and normal endometrial tissues were obtained from 20 patients with adenomyosis and 11 control patients without adenomyosis, respectively. The immunohistochemical analysis shows distinct EMT in eutopic endometria in secretory phase; the expression levels of TGFB1, SMAD3 and pSMAD3 that indicate signal pathway of EMT were also higher in secretory phase. Macrophages can induce EMT process in primary endometrial epithelial cells derived from normal and eutopic endometria. After co-culturing, THP-1-derived macrophages polarized to M2. Compared with the eutopic endometrium group, further polarization to M2 was observed in the normal endometrium group. These results indicate that adenomyosis may be promoted by the pathologic EMT of epithelial cells, which is induced by macrophages that incapably polarize to M2.

My notes (saved in your browser only)

Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Endometrium Epithelial-Mesenchymal Transition Macrophages Adenomyosis Adenomyosis Adenomyosis Adult Adult Cells, Cultured Cells, Cultured Coculture Techniques Coculture Techniques Endometrium Endometrium Epithelial Cells Epithelial Cells Epithelial Cells Epithelial Cells Epithelial-Mesenchymal Transition

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (42)

Cited by (20)

Source provenance

europepmc
last seen: 2026-10-15T06:08:49.021275+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:19:54.474666+00:00
License: CC0 · commercial use OK