Literature DB >> 29906225

Scleraxis regulates Twist1 and Snai1 expression in the epithelial-to-mesenchymal transition.

Danah S Al-Hattab1, Hamza A Safi1, Raghu S Nagalingam1, Rushita A Bagchi1, Matthew T Stecy1, Michael P Czubryt1.   

Abstract

Numerous physiological and pathological events, from organ development to cancer and fibrosis, are characterized by an epithelial-to-mesenchymal transition (EMT), whereby adherent epithelial cells convert to migratory mesenchymal cells. During cardiac development, proepicardial organ epithelial cells undergo EMT to generate fibroblasts. Subsequent stress or damage induces further phenotype conversion of fibroblasts to myofibroblasts, causing fibrosis via synthesis of an excessive extracellular matrix. We have previously shown that the transcription factor scleraxis is both sufficient and necessary for the conversion of cardiac fibroblasts to myofibroblasts and found that scleraxis knockout reduced cardiac fibroblast numbers by 50%, possibly via EMT attenuation. Scleraxis induced expression of the EMT transcriptional regulators Twist1 and Snai1 via an unknown mechanism. Here, we report that scleraxis binds to E-box consensus sequences within the Twist1 and Snai1 promoters to transactivate these genes directly. Scleraxis upregulates expression of both genes in A549 epithelial cells and in cardiac myofibroblasts. Transforming growth factor-β induces EMT, fibrosis, and scleraxis expression, and we found that transforming growth factor-β-mediated upregulation of Twist1 and Snai1 completely depends on the presence of scleraxis. Snai1 knockdown upregulated the epithelial marker E-cadherin; however, this effect was lost after scleraxis overexpression, suggesting that scleraxis may repress E-cadherin expression. Together, these results indicate that scleraxis can regulate EMT via direct transactivation of the Twist1 and Snai1 genes. Given the role of scleraxis in also driving the myofibroblast phenotype, scleraxis appears to be a critical controller of fibroblast genesis and fate in the myocardium and thus may play key roles in wound healing and fibrosis. NEW & NOTEWORTHY The molecular mechanism by which the transcription factor scleraxis mediates Twist1 and Snai1 gene expression was determined. These results reveal a novel means of transcriptional regulation of epithelial-to-mesenchymal transition and demonstrate that transforming growth factor-β-mediated epithelial-to-mesenchymal transition is dependent on scleraxis, providing a potential target for controlling this process.

Entities:  

Keywords:  epithelial cells; epithelial-to-mesenchymal transition; fibroblasts; gene regulation; transcription

Mesh:

Substances:

Year:  2018        PMID: 29906225     DOI: 10.1152/ajpheart.00092.2018

Source DB:  PubMed          Journal:  Am J Physiol Heart Circ Physiol        ISSN: 0363-6135            Impact factor:   4.733


  15 in total

1.  Getting to the heart of myofibroblast differentiation: implications for scleraxis in ECM remodeling and therapeutic targeting.

Authors:  Ashley L Eadie; Allison J Titus; Keith R Brunt
Journal:  Am J Physiol Heart Circ Physiol       Date:  2018-06-29       Impact factor: 4.733

Review 2.  Extracellular matrix in cardiovascular pathophysiology.

Authors:  Maria Bloksgaard; Merry Lindsey; Luis A Martinez-Lemus
Journal:  Am J Physiol Heart Circ Physiol       Date:  2018-09-21       Impact factor: 4.733

3.  Scleraxis lineage cells contribute to organized bridging tissue during tendon healing and identify a subpopulation of resident tendon cells.

Authors:  Katherine T Best; Alayna E Loiselle
Journal:  FASEB J       Date:  2019-04-05       Impact factor: 5.191

4.  Single-cell dual-omics reveals the transcriptomic and epigenomic diversity of cardiac non-myocytes.

Authors:  Li Wang; Yuchen Yang; Hong Ma; Yifang Xie; Jun Xu; David Near; Haofei Wang; Tiffany Garbutt; Yun Li; Jiandong Liu; Li Qian
Journal:  Cardiovasc Res       Date:  2022-05-06       Impact factor: 13.081

5.  The Transcription Factor SCX is a Potential Serum Biomarker of Fibrotic Diseases.

Authors:  Miguel Ramírez-Aragón; Fernando Hernández-Sánchez; Tatiana S Rodríguez-Reyna; Ivette Buendía-Roldán; Gael Güitrón-Castillo; Carlos A Núñez-Alvarez; Diego F Hernández-Ramírez; Sergio A Benavides-Suárez; Alexia Esquinca-González; Ana Lilia Torres-Machorro; Criselda Mendoza-Milla
Journal:  Int J Mol Sci       Date:  2020-07-16       Impact factor: 5.923

6.  Fangjihuangqi Decoction inhibits MDA-MB-231 cell invasion in vitro and decreases tumor growth and metastasis in triple-negative breast cancer xenografts tumor zebrafish model.

Authors:  Yubo Guo; Yingyi Fan; Xiaohua Pei
Journal:  Cancer Med       Date:  2020-02-09       Impact factor: 4.452

Review 7.  Cardiac Fibroblast to Myofibroblast Phenotype Conversion-An Unexploited Therapeutic Target.

Authors:  Michael P Czubryt
Journal:  J Cardiovasc Dev Dis       Date:  2019-08-16

8.  Scleraxis-lineage cell depletion improves tendon healing and disrupts adult tendon homeostasis.

Authors:  Katherine T Best; Antonion Korcari; Keshia E Mora; Anne Ec Nichols; Samantha N Muscat; Emma Knapp; Mark R Buckley; Alayna E Loiselle
Journal:  Elife       Date:  2021-01-22       Impact factor: 8.140

Review 9.  The NLRP3 Inflammasome: Relevance in Solid Organ Transplantation.

Authors:  Ryan M Burke; Bethany L Dale; Shamik Dholakia
Journal:  Int J Mol Sci       Date:  2021-10-03       Impact factor: 5.923

Review 10.  Homodimeric and Heterodimeric Interactions among Vertebrate Basic Helix-Loop-Helix Transcription Factors.

Authors:  Ana Lilia Torres-Machorro
Journal:  Int J Mol Sci       Date:  2021-11-28       Impact factor: 5.923

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