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Transforming growth factor beta1 induces epithelial-to-mesenchymal transition of A549 cells.
J Korean Med Sci. 2007 Oct; 22(5):898-904.JK

Abstract

Idiopathic pulmonary fibrosis (IPF) comprises an aggregate of mesenchymal cells. However, the cellular origin of these mesenchymal phenotypes remains unclear. Transforming growth factor beta1 (TGF-beta1) has been known as the main cytokine involved in the pathogenesis of IPF. We examined whether the potent fibrogenic cytokine TGF-beta1 could induce the epithelial-to-mesenchymal transition (EMT) in the human alveolar epithelial cell line, A549, and determined whether snail expression is associated with the phenotypic changes observed in the A549 cells. EMT was investigated with cells morphology changes under phase-contrast microscopy, western blotting, and indirect immunofluorescence stains. E-cadherin and transcription factor, snail, were also evaluated by measuring mRNA levels using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. The data showed that TGF-beta1 induced A549 cells with epithelial cell characteristics to undergo EMT in a concentration-dependent manner. Following TGF-beta1 treatment, A549 cells induced EMT characterized by cells morphological changes, loss of epithelial markers Ecaherin and cytokeratin, increased stress fiber reorganization by F-actin, and cytokeratin replacement by vimentin. Although IL-1beta failed to induce A549 cells to undergo EMT, the combination of TGF-beta1 and IL-1beta showed synergy effects in cells morphology changes and the expression of mesenchymal markers. The snail expression study using RT-PCR analysis provided that loss of E-cadherin expression was associated with snail expression. Stimulation of A54 cells with TGF-beta1 plus IL-1beta revealed a higher level of snail expression. Our data showed that EMT of A549 cells might be closely associated with snail expression.

Authors+Show Affiliations

Department of Internal Medicine, Hallym University Sacred Heart Hospital, College of Medicine, Hallym University, Anyang, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17982242

Citation

Kim, Ju Hee, et al. "Transforming Growth Factor Beta1 Induces Epithelial-to-mesenchymal Transition of A549 Cells." Journal of Korean Medical Science, vol. 22, no. 5, 2007, pp. 898-904.
Kim JH, Jang YS, Eom KS, et al. Transforming growth factor beta1 induces epithelial-to-mesenchymal transition of A549 cells. J Korean Med Sci. 2007;22(5):898-904.
Kim, J. H., Jang, Y. S., Eom, K. S., Hwang, Y. I., Kang, H. R., Jang, S. H., Kim, C. H., Park, Y. B., Lee, M. G., Hyun, I. G., Jung, K. S., & Kim, D. G. (2007). Transforming growth factor beta1 induces epithelial-to-mesenchymal transition of A549 cells. Journal of Korean Medical Science, 22(5), 898-904.
Kim JH, et al. Transforming Growth Factor Beta1 Induces Epithelial-to-mesenchymal Transition of A549 Cells. J Korean Med Sci. 2007;22(5):898-904. PubMed PMID: 17982242.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transforming growth factor beta1 induces epithelial-to-mesenchymal transition of A549 cells. AU - Kim,Ju Hee, AU - Jang,Young Sook, AU - Eom,Kwang-Seok, AU - Hwang,Young Il, AU - Kang,Hae Raen, AU - Jang,Seung Hun, AU - Kim,Cheol Hong, AU - Park,Young Bum, AU - Lee,Myung Goo, AU - Hyun,In Gyu, AU - Jung,Ki-Suck, AU - Kim,Dong-Gyu, PY - 2007/11/6/pubmed PY - 2008/1/11/medline PY - 2007/11/6/entrez SP - 898 EP - 904 JF - Journal of Korean medical science JO - J Korean Med Sci VL - 22 IS - 5 N2 - Idiopathic pulmonary fibrosis (IPF) comprises an aggregate of mesenchymal cells. However, the cellular origin of these mesenchymal phenotypes remains unclear. Transforming growth factor beta1 (TGF-beta1) has been known as the main cytokine involved in the pathogenesis of IPF. We examined whether the potent fibrogenic cytokine TGF-beta1 could induce the epithelial-to-mesenchymal transition (EMT) in the human alveolar epithelial cell line, A549, and determined whether snail expression is associated with the phenotypic changes observed in the A549 cells. EMT was investigated with cells morphology changes under phase-contrast microscopy, western blotting, and indirect immunofluorescence stains. E-cadherin and transcription factor, snail, were also evaluated by measuring mRNA levels using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. The data showed that TGF-beta1 induced A549 cells with epithelial cell characteristics to undergo EMT in a concentration-dependent manner. Following TGF-beta1 treatment, A549 cells induced EMT characterized by cells morphological changes, loss of epithelial markers Ecaherin and cytokeratin, increased stress fiber reorganization by F-actin, and cytokeratin replacement by vimentin. Although IL-1beta failed to induce A549 cells to undergo EMT, the combination of TGF-beta1 and IL-1beta showed synergy effects in cells morphology changes and the expression of mesenchymal markers. The snail expression study using RT-PCR analysis provided that loss of E-cadherin expression was associated with snail expression. Stimulation of A54 cells with TGF-beta1 plus IL-1beta revealed a higher level of snail expression. Our data showed that EMT of A549 cells might be closely associated with snail expression. SN - 1011-8934 UR - https://www.unboundmedicine.com/medline/citation/17982242/Transforming_growth_factor_beta1_induces_epithelial_to_mesenchymal_transition_of_A549_cells_ L2 - https://jkms.org/DOIx.php?id=10.3346/jkms.2007.22.5.898 DB - PRIME DP - Unbound Medicine ER -