Paracrine action of vascular endothelial growth factor in the human endometrium: production and target sites, and hormonal regulation

Pedro Bausero, F. Cavaillé, Geri Méduri, Sayonara Freitas, Martine Perrot‐Applanat
In: Angiogenesis · 1998 · vol. 2(2) , pp. 167–182 · doi:10.1023/a:1009292506879 · PMID:14517472 · W1537729141
article OA: closed CC0 ⤵ 10 in-corpus citations
Limited metadata. Only one source feed has indexed this record so far — no abstract, full text, or open-access copy is available through Endo Lab. The publisher's page (linked below) is the canonical location for the actual content. If you have institutional access, use "Find at my library".
View at publisher → View on OpenAlex View on PubMed
⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

VEGF is localized in the human endometrium, is upregulated by estradiol and progesterone in stromal cells, and controls angiogenesis and hyperpermeability necessary for implantation.

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 ⓘ

This study examined VEGF protein localization across the menstrual cycle in human endometrium and assessed hormonal regulation of VEGF mRNA in isolated human endometrial stromal cells using immunohistochemistry and steroid treatments. VEGF was localized not only in glandular epithelium and stroma but also on capillaries and spiral arterioles, with the strongest endothelial immunoreactivity in late proliferative and secretory phases; staining of endothelial-bound VEGF decreased after heparinase, and receptor expression (flt-1 and flk/KDR) aligned with vascular target sites, including mid-secretory capillary strands before lumen formation. In stromal cells, estradiol and estradiol plus progesterone increased VEGF mRNA dose-dependently, with an estrogen response detectable by 3 hours and persisting with continuous estradiol, producing VEGF splice variants VEGF121, VEGF165, and VEGF189; cycloheximide did not block estradiol effects, while the pure anti-estrogen ICI 182,780 did, supporting estrogen receptor–mediated transcription without new protein synthesis. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via keyword match in the upstream search index.

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

My notes (saved in your browser only)

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 (43)

Cited by (10)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK