Local activation of TGF-beta1 at endometriosis sites.
article
OA: closed
CC0
⤵ 30 in-corpus citations
AI-generated summary
Endometriotic cysts exhibit increased TGF-beta1 activity due to elevated uPA production by glandular epithelium, which converts plasminogen to plasmin, subsequently activating TGF-beta1.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
OBJECTIVE: To investigate the factors related to activation of transforming growth factor-beta 1 (TGF-beta1) at sites of endometriosis. STUDY DESIGN: TGF-beta1 is activated by plasmin, which is formed when plasminogen is activated by urokinase-type plasminogen activator (uPA). We studied these factors by immunohistochemistry or immunoassay. RESULTS: TGF-beta1 protein was localized mainly in the cytoplasm of glandular epithelial cells in both endometriotic cysts and normal endometrium, but strongly positive immunostaining was significantly more common in cysts. The levels of TGF-beta1, uPA and plasmin/alpha2-plasmin inhibitor complex were all higher in cyst fluid than in peritoneal fluid. There was little uPA protein expression in the glandular epithelium of normal endometrium, but it was prominent in the cytoplasm of glandular epithelial cells from endometriotic cysts, and strongly positive immunostaining was significantly more common in cysts. CONCLUSION: These results suggest that TGF-beta1 activity is increased at sites of endometriosis due to enhanced production of both uPA and TGF-beta1 by glandular epithelium and because plasmin activates TGF-beta1 after being converted from plasminogen by uPA.
My notes (saved in your browser only)
Condition tags
MeSH descriptors
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.
Cited by (30)
- The long road of drug development for endometriosis – Pains, gains, and hopes 2024
- Lysine acetyltransferase 14 mediates TGF-β-induced fibrosis in ovarian endometrioma via co-operation with serum response factor 2024
- The Expression of TGF-β1, SMAD3, ILK and miRNA-21 in the Ectopic and Eutopic Endometrium of Women with Endometriosis 2023
- Circulating oncomiR-21 as a potential biomarker of mild and severe forms of endometriosis for early diagnosis and management 2022
- Papel de MICA na endometriose 2022
- Focal Adhesion Kinase-Mediated Sequences, Including Cell Adhesion, Inflammatory Response, and Fibrosis, as a Therapeutic Target in Endometriosis 2020
- Anti-inflammatory cytokines in endometriosis 2019
- A high level of TGF-B1 promotes endometriosis development via cell migration, adhesiveness, colonization, and invasiveness† 2018
- Seminal plasma (SP) induces a rapid transforming growth factor beta 1 (TGFβ1)—independent up-regulation of epithelial–mesenchymal transdifferentiation (EMT) and myofibroblastic metaplasia-markers in endometriotic (EM) and endometrial cells 2018
- Arrangement of myofibroblastic and smooth muscle-like cells in superficial peritoneal endometriosis and a possible role of transforming growth factor beta 1 (TGFβ1) in myofibroblastic metaplasia 2018
- Platelets impair natural killer cell reactivity and function in endometriosis through multiple mechanisms 2017
- Myofibroblasts Are Evidence of Chronic Tissue Microtrauma at the Endometrial-Myometrial Junctional Zone in Uteri With Adenomyosis 2017
- Transforming growth factor beta1 from endometriomas promotes fibrosis in surrounding ovarian tissues via Smad2/3 signaling† 2017
- <i>mir-126</i> rs4636297 and <i>TGF</i> <b>β</b> <i>RI</i> rs334348 functional gene variants are associated with susceptibility to endometriosis and its severity 2017
- The role of TGF-β in the pathophysiology of peritoneal endometriosis 2017
- Platelets drive smooth muscle metaplasia and fibrogenesis in endometriosis through epithelial–mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation 2016
- Platelet-derived TGF-β1 mediates the down-modulation of NKG2D expression and may be responsible for impaired natural killer (NK) cytotoxicity in women with endometriosis 2016
- Cytokins as the markers for non-invasive diagnosis of pelvic endometriosis 2015
- The Peritoneum Is Both a Source and Target of TGF-β in Women with Endometriosis 2014
- The effect of macrophages on fibroblast activity and lesion development in mouse models of endometriosis. 2014
- Endometriosis and Angiogenic Factors 2012
- Raf-1, a Potential Therapeutic Target, Mediates Early Steps in Endometriosis Lesion Development by Endometrial Epithelial and Stromal Cells 2012
- MiRNA-130a, a potential endometriosis-inducing factor 2012
- TGF- 1 induces proteinase-activated receptor 2 (PAR2) expression in endometriotic stromal cells and stimulates PAR2 activation-induced secretion of IL-6 2011
- Endometriosis‐associated nerve fibers and pain 2009
- Induction of endometrial epithelial cell invasion and c-fms expression by transforming growth factor beta 2009
- The role of iron in the pathogenesis of endometriosis 2009
- Role of TGF- s in normal human endometrium and endometriosis 2009
- The role of microRNAs in endometriosis and associated reproductive conditions 2009
- Endometrial-Peritoneal Interactions during Endometriotic Lesion Establishment 2008
Source provenance
- europepmc
- last seen: 2026-06-04T01:30:01.192114+00:00
- openalex
- last seen: 2026-06-04T00:00:01.174412+00:00
- pubmed
- last seen: 2026-05-13T22:15:00.519696+00:00
License: CC0
· commercial use OK