Inflammation, but not infection, induces EMT in human amnion epithelial cells
Autor: | Ramkumar Menon, Mariana de Castro Silva, Rheanna Urrabaz-Garza, Lauren Richardson, Talar Kechichian, Márcia Guimarães da Silva |
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Přispěvatelé: | University of Texas Medical Branch at Galveston, Universidade Estadual Paulista (Unesp) |
Rok vydání: | 2020 |
Předmět: |
Lipopolysaccharides
0301 basic medicine Embryology Epithelial-Mesenchymal Transition Vimentin Inflammation Infections Proinflammatory cytokine Transforming Growth Factor beta1 03 medical and health sciences Fetus 0302 clinical medicine Endocrinology Western blot Antigens CD Pregnancy Fetal membrane medicine Humans Amnion Epithelial–mesenchymal transition 030219 obstetrics & reproductive medicine medicine.diagnostic_test biology Chemistry Mesenchymal stem cell Obstetrics and Gynecology Epithelial Cells Cell Biology Transforming growth factor beta Cadherins 030104 developmental biology Reproductive Medicine embryonic structures biology.protein Cancer research Premature Birth Female medicine.symptom |
Zdroj: | Scopus Repositório Institucional da UNESP Universidade Estadual Paulista (UNESP) instacron:UNESP |
ISSN: | 1741-7899 1470-1626 |
Popis: | Made available in DSpace on 2020-12-12T02:20:36Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-10-01 A non-reversible state of epithelial to mesenchymal transition (EMT) at term accumulates proinflammatory mesenchymal cells and predisposes fetal membrane to weakening prior to delivery at term. We investigated the induction of EMT in amnion epithelial cells (AEC) in response to inflammation and infection associated with spontaneous preterm birth (SPTB). For this, membranes from SPTB were screened for EMT markers. Primary AEC in culture were treated with TNF-α (10 and 50 ng/mL) and LPS (50 and 100 ng/mL) for 72 h. Cell shape index (SI) was determined based on morphological shift (microscopy followed by ImageJ software analysis). Immunocytochemistry and Western blot assessed changes in epithelial markers (cytokeratin-18 and E-cadherin) and mesenchymal markers (vimentin and N-cadherin). Involvement of transforming growth factor beta (TGF-β) in EMT induction and EMT associated inflammation was tested using specific markers (Western blot) and by measuring MMP9 (ELISA), respectively. We report that PTB is associated with fetal membrane EMT. TNF-α produced dose- and time-dependent induction of EMT; within 24 h by 50 ng/mL and after 72 h by 10 ng/mL. AEC showed mesenchymal morphology, lower E-cadherin, higher vimentin and N-cadherin and higher MMP9 compared to control. TNF-α-induced EMT was not associated with canonical TGF-β pathway. LPS, regardless of dose or time, did not induce EMT in AEC. We conclude that PTB with intact membranes is associated with EMT. Our data suggest that inflammation, but not infection, is associated with non-canonical activation of EMT and inflammation that can predispose membrane to undergo weakening. Division of Maternal-Fetal Medicine and Perinatal Research Department of Obstetrics & Gynecology University of Texas Medical Branch at Galveston Department of Pathology Botucatu Medical School Universidade Estadual Paulista UNESP Department of Pathology Botucatu Medical School Universidade Estadual Paulista UNESP |
Databáze: | OpenAIRE |
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