Hepatocyte Growth Factor/Met System Promotes Endometrial and Endometriotic Stromal Cell Invasion via Autocrine and Paracrine Pathways

Souichi Yoshida, Tasuku Harada, Masahiro Mitsunari, Tomio Iwabe, Yasuko Sakamoto, Satoru Tsukihara, Yumiko Iba, Sayako Horie, Naoki Terakawa
The Journal of clinical endocrinology and metabolism · 2004 · vol. 89(2) , pp. 823–832 · doi:10.1210/jc.2003-030874 · PMID:14764801 · W2033389118
article OA: bronze CC0 ⤵ 34 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that elevated HGF/Met system signaling in peritoneal fluid promotes endometrial and endometriotic stromal cell proliferation and invasion via autocrine and paracrine pathways, contributing to endometriosis pathogenesis.

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Abstract

Endometrial stromal cells reportedly have a role in the initial invasion of endometrial tissue into the peritoneum. Hepatocyte growth factor (HGF), which is a ligand for the c-met protooncogene product (Met), stimulates proliferation and invasion of a large number of cells. In this study we investigated the role of the HGF/Met system in the pathogenesis of endometriosis. HGF concentrations in the peritoneal fluid of patients with endometriosis were significantly higher than in those without endometriosis and correlated positively with revised American Society of Reproductive Medicine scores. We showed that the peritoneum and endometriotic stromal cells may be major sources of HGF in peritoneal fluid. Endometrial and endometriotic stromal cells expressed the Met receptor, which was activated by endogenous and exogenous HGF. HGF enhanced stromal cell proliferation and invasion. We also demonstrated that the HGF-stimulated stromal cell invasion was due in part to the induction of urokinase-type plasminogen activator, a member of the extracellular proteolysis system. In conclusion, the HGF/Met system is involved in the pathogenesis of endometriosis by promoting stromal cell proliferation and invasion of shed endometria and endometrial lesions via autocrine and paracrine pathways.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Autocrine Communication Endometriosis Endometriosis Endometrium Hepatocyte Growth Factor Paracrine Communication Proto-Oncogene Proteins c-met Stromal Cells Stromal Cells Adult Ascitic Fluid Ascitic Fluid Cell Division Cell Division Cells, Cultured Endometriosis Endometriosis Endometrium Endometrium Endometrium

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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 (47)

Cited by (34)

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