4.5 Article

MRTFA overexpression promotes conversion of human coronary artery smooth muscle cells into lipid-laden foam cells

期刊

VASCULAR PHARMACOLOGY
卷 138, 期 -, 页码 -

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.vph.2021.106837

关键词

Atherosclerosis; Transdifferentiation; Myocardin; Pinocytosis; LDL receptor

资金

  1. Novo Nordisk Foundation
  2. Swedish Research Council [2017-00860]
  3. Swedish Heart and Lung Foundation
  4. Crafoord foundation
  5. Magnus Bergvall foundation
  6. Lars Hierta Memorial Foundation
  7. Royal Physiographic Society
  8. Swedish Research Council [2017-00860] Funding Source: Swedish Research Council

向作者/读者索取更多资源

This study reveals that the transcriptional co-activator MRTFA promotes lipid accumulation in smooth muscle cells through various mechanisms, and plays an important role in vascular remodeling in humans. Thus, MRTFA could potentially be a new therapeutic target for inhibiting vascular lipid accumulation.
Objective: Smooth muscle cells contribute significantly to lipid-laden foam cells in atherosclerotic plaques. However, the underlying mechanisms transforming smooth muscle cells into foam cells are poorly understood. The purpose of this study was to gain insight into the molecular mechanisms regulating smooth muscle foam cell formation. Approach and results: Using human coronary artery smooth muscle cells we found that the transcriptional co activator MRTFA promotes lipid accumulation via several mechanisms, including direct transcriptional control of LDL receptor, enhanced fluid-phase pinocytosis and reduced lipid efflux. Inhibition of MRTF activity with CCG1423 and CCG203971 significantly reduced lipid accumulation. Furthermore, we demonstrate enhanced MRTFA expression in vascular remodeling of human vessels. Conclusions: This study demonstrates a novel role for MRTFA as an important regulator of lipid homeostasis in vascular smooth muscle cells. Thus, MRTFA could potentially be a new therapeutic target for inhibition of vascular lipid accumulation.

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