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Gas6 Prevents Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells via Production of PGE(2), PGD(2) and Their Receptors

Title
Gas6 Prevents Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells via Production of PGE(2), PGD(2) and Their Receptors
Authors
Jung, JihyeLee, Ye-JiChoi, Youn-HeePark, Eun-MiKim, Hee-SunKang, Jihee L.
Ewha Authors
이지희김희선박은미최윤희
SCOPUS Author ID
이지희scopus; 김희선scopus; 박은미scopus; 최윤희scopus
Issue Date
2019
Journal Title
CELLS
ISSN
2073-4409JCR Link
Citation
CELLS vol. 8, no. 7
Keywords
Gas6prostaglandinsepithelial-mesenchymal transitionalveolar epithelial cells
Publisher
MDPI
Indexed
SCIE; SCOPUS WOS
Document Type
Article
Abstract
The epithelial-mesenchymal transition (EMT) is important in organ fibrosis. We hypothesized that growth arrest -specific protein 6 (Gas6) and its underlying mechanisms play roles in the prevention of EMT in alveolar epithelial cells (ECs). In this study, to determine whether Gas6 prevents TGF-beta 1-induced EMT in LA-4 and primary alveolar type II ECs, real-time PCR and immunoblotting in cell lysates and ELISA in culture supernatants were performed. Migration and invasion assays were performed using Transwell chambers. Pretreatment of ECs with Gas6 inhibited TGF-beta 1-induced EMT based on cell morphology, changes in EMT marker expression, and induction of EMT-activating transcription factors. Gas6 enhanced the levels of cyclooxygenase-2 (COX-2)-derived prostaglandin E-2 (PGE(2)) and PGD(2) as well as of their receptors. COX -2 inhibitors and antagonists of PGE(2) and PGD2 receptors reversed the inhibition of TGF-beta 1-induced EMT, migration, and invasion by Gas6. Moreover, knockdown of Axl or Mer reversed the enhancement of PGE(2) and PGD(2) and suppression of EMT, migration and invasion by Gas6. Our data suggest Gas6-Axl or -Mer signalling events may reprogram ECs to resist EMT via the production of PGE(2), PGD(2), and their receptors.
DOI
10.3390/cells8070643
Appears in Collections:
의과대학 > 의학과 > Journal papers
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