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Abstract <p>Endothelial-to-mesenchymal transition (EndoMT) is an essentialprocess in cardiac development and maintenance of postnatal tissues.It also contributes to the development of various cardiovascular disorders.The Notch signaling pathway plays a crucial role in endothelialbiology and is essential for EndoMT, although the exact mechanismsinvolved are still not fully understood. This study aims to: 1. Comparethe mechanisms and roles of the Notch signaling pathway in severalprimary human endothelial cell lines, including human aortic endothelialcells, human valvular endothelial cells, and human umbilical veinendothelial cells. 2. Explore the consequences of activating orsuppressing Notch on EndoMT. 3. Identify which components of theNotch pathway trigger or inhibit EndoMT in endothelial cells. Forthis, Notch signaling was activated via lentiviral transductionof either NOTCH1 intracellular domain (NICD) or full ligand JAG1(JAGGED1). JAG1 alone did not induce EndoMT, causing only slightexpression of Notch components. Unlike JAG1, NICD dose-dependentlyincreased activity of the CSL luciferase reporter while inhibitionvia downregulation of CSL inhibited Notch as well as EndoMT. Wehave found similarity of all three endothelial cell types studiedin terms of Notch-dependent induction of EndoMT as well as a possibilityto activate and inactivate the EndoMT program in the endothelialcells by activation and inactivation of Notch pathway components.This knowledge may be significant in the development of treatmentstrategies for managing endothelial cells in cardiovascular disease.</p>

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Notch Signaling as a Way to Control the Endothelial-To-Mesenchymal Transition

  • 期刊论文

  • 发表日期：

    2025年1月1日

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  • D. Evensen,
  • D. Smirnova,
  • A. Belyaeva,
  • N. Boyarskaya,
  • V. Uspensky,
  • F. Vieceli Dalla Sega,
  • P. Rizzo,
  • A. Malashicheva

摘要

Abstract

Endothelial-to-mesenchymal transition (EndoMT) is an essentialprocess in cardiac development and maintenance of postnatal tissues.It also contributes to the development of various cardiovascular disorders.The Notch signaling pathway plays a crucial role in endothelialbiology and is essential for EndoMT, although the exact mechanismsinvolved are still not fully understood. This study aims to: 1. Comparethe mechanisms and roles of the Notch signaling pathway in severalprimary human endothelial cell lines, including human aortic endothelialcells, human valvular endothelial cells, and human umbilical veinendothelial cells. 2. Explore the consequences of activating orsuppressing Notch on EndoMT. 3. Identify which components of theNotch pathway trigger or inhibit EndoMT in endothelial cells. Forthis, Notch signaling was activated via lentiviral transductionof either NOTCH1 intracellular domain (NICD) or full ligand JAG1(JAGGED1). JAG1 alone did not induce EndoMT, causing only slightexpression of Notch components. Unlike JAG1, NICD dose-dependentlyincreased activity of the CSL luciferase reporter while inhibitionvia downregulation of CSL inhibited Notch as well as EndoMT. Wehave found similarity of all three endothelial cell types studiedin terms of Notch-dependent induction of EndoMT as well as a possibilityto activate and inactivate the EndoMT program in the endothelialcells by activation and inactivation of Notch pathway components.This knowledge may be significant in the development of treatmentstrategies for managing endothelial cells in cardiovascular disease.