Corroborating evidence for platelet-induced epithelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation in the development of adenomyosis
| Autor: | Sun-Wei Guo, Qiuming Qi, Minhong Shen, Xishi Liu, Hongqi Zhang |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
CD31 Adult Blood Platelets Pathology medicine.medical_specialty Epithelial-Mesenchymal Transition Platelet Aggregation Angiogenesis Biology 03 medical and health sciences Endometrium 0302 clinical medicine Fibrosis medicine Humans Adenomyosis Epithelial–mesenchymal transition Myofibroblasts Cells Cultured Cell Proliferation 030219 obstetrics & reproductive medicine Neovascularization Pathologic Rehabilitation Obstetrics and Gynecology Fibroblasts Middle Aged medicine.disease 030104 developmental biology Cross-Sectional Studies Reproductive Medicine Cell Transdifferentiation Microvessels Myometrium Immunohistochemistry Hepatocyte growth factor Female Myofibroblast Biomarkers medicine.drug |
| Zdroj: | Human reproduction (Oxford, England). 31(4) |
| ISSN: | 1460-2350 |
| Popis: | STUDY QUESTION Do platelets play any role in the development of adenomyosis? SUMMARY ANSWER As in endometriosis, adenomyotic lesions show significantly increased platelet aggregation, increased expression of transforming growth factor (TGF)-β1, phosphorylated Smad3, markers of epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transdifferentiation (FMT), and smooth muscle metaplasia (SMM), in conjunction with increased fibrosis as compared with normal endometrium. WHAT IS KNOWN ALREADY Both EMT and FMT are known to play vital roles in fibrogenesis in general and in endometriosis in particular. EMT has been implicated in the development of adenomyosis. SMM is universally seen in endometriosis and also in adenomyosis, and is correlated positively with the extent of fibrosis. However, there has been no published study on the role of platelets in fibrogenesis in adenomyosis, even though adenomyotic lesions undergo repeated cycles of tissue injury and repair, which suggests the involvement of platelets and their possible roles in fibrogenesis. STUDY DESIGN, SIZE, DURATION Cross-sectional studies of ectopic endometrial and control endometrial tissue samples from three sets of women with and without adenomyosis (n= 34 and 20, 12 and 10, and 8 and 8, respectively) were carried out from 2014 to 2015. PARTICIPANTS/MATERIALS, SETTING, METHODS Immunohistochemistry analysis of ectopic endometrial tissues from women with (n= 34) and without (n= 20) adenomyosis with respect to biomarkers of EMT, FMT and highly differentiated smooth muscle cells as well as TGF-β1, phosphorylated Smad3, markers of proliferation, angiogenesis and extracellular matrix (ECM) deposits. Masson trichrome staining, Van Gieson staining and Pico-Sirius staining were performed to evaluate and quantify the extent of fibrosis in lesions. Progesterone receptor isoform B (PR-B) staining also was performed. In addition, CD42b-positive platelets in ectopic (n= 12) and control (n= 10) endometrium were counted by confocal microscopy and compared. The protein expression levels of TGF-β1 and phosphorylated Smad3 in both ectopic (n= 8) and control (n= 8) endometrium were measured by western blot analysis. Immunofluorescent staining of both platelets and hepatocyte growth factor (HGF) was also performed for adenomyotic tissue samples (n= 10). MAIN RESULTS AND THE ROLE OF CHANCE Adenomyotic lesions had a significantly higher extent of platelet aggregation and increased staining for TGF-β1 and phosphorylated Smad3 (both P-values |
| Databáze: | OpenAIRE |
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