The Double Face of Smooth Muscle Cells in Vascular Biology—Friends or Foes, Damage or Regeneration?

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 771

Special Issue Editor


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Guest Editor
Department of Biomaterials and Tissue Engineering, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, 142 20 Prague 4, Czech Republic
Interests: vascular smooth muscle cells; phenotypic modulation; vascular disease; stem cell differentiation; vascular tissue engineering; regenerative medicine

Special Issue Information

Dear Colleagues,

Smooth muscle cells (SMCs) are the most numerous cellular component of the arterial wall, where they form the middle layer called tunica media. They ensure the basic physiological functions of blood vessels, namely contraction, relaxation, and thus regulation of blood flow and pressure. Therefore, in advanced tissue engineering, the layer of SMCs in vascular replacements should always be reconstructed. Nevertheless, tissue engineers have often avoided the presence of SMCs in vascular substitutes. The reason was a high readiness of SMCs for migration and proliferation, which often exceeded the scope of normal regeneration, and led to restenosis of the vascular replacement. A similar mechanism also leads to the formation of atherosclerotic lesions and thickening of the vascular wall in hypertension and other vascular disorders. SMCs undergo a so-called phenotypic modulation, i.e., a transition from a resting, non-proliferative, differentiated contractile phenotype to a less mature, synthetic phenotype, in some ways reminiscent of stem cells. Therefore, during the reconstruction of the vessel wall (whether directly from SMCs or from stem cells), it is necessary to differentiate the cells towards a contractile phenotype via suitable biochemical and mechanical stimuli. These factors include suitable properties of the scaffolds, a suitable composition of the culture medium, suitable mechanical stress in dynamic bioreactors, as well as the presence of a mature semipermeable endothelial cell layer.

In this Special Issue of Cells, I invite you to contribute with original research articles, reviews, or communication articles on all aspects related to the theme of “The double face of smooth muscle cells in vascular biology – from blood vessel damage to regeneration”. Expert articles describing mechanistic, functional, biochemical, cellular, molecular, or genetic aspects of the role of SMCs in blood vessel wall damage or regeneration are highly welcome. Relevant topics include but are not limited to:

  • Role of SMCs in vascular diseases;
  • Phenotypic switching;
  • Contractile phenotype and its achieving/maintaining;
  • Synthetic phenotype and its potential reversal;
  • Role of extracellular matrix and scaffolds;
  • Role of cytokines, chemokines, growth factors, and hormones;
  • Role of oxidative damage and inflammation;
  • Vascular replacements and vascular tissue engineering;
  • Differentiation of SMCs from stem cells;
  • Genetic and RNA modifications of stem cells and SMCs;
  • In vitro SMC-based models of the vascular wall or vascular diseases;
  • Differences in SMC behavior related to gender, age, species, and localization in the vascular bed, etc.

Dr. Lucie Bacakova
Guest Editor

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Keywords

  • vascular smooth muscle cells
  • phenotypic modulation
  • vascular disease
  • stem cell differentiation
  • vascular tissue engineering
  • regenerative medicine

Published Papers (1 paper)

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22 pages, 6368 KiB  
Article
Divergent and Compensatory Effects of BMP2 and BMP4 on the VSMC Phenotype and BMP4’s Role in Thoracic Aortic Aneurysm Development
by Daniel Klessinger, Argen Mamazhakypov, Sophie Glaeser, Ramona Emig, Remi Peyronnet, Lena Meier, Kora Proelss, Katia Marenne, Christian Smolka, Sebastian Grundmann, Franziska Pankratz, Philipp R. Esser, Martin Moser, Qian Zhou and Jennifer S. Esser
Cells 2024, 13(9), 735; https://doi.org/10.3390/cells13090735 - 24 Apr 2024
Viewed by 439
Abstract
Vascular smooth muscle cells (VSMCs) play a key role in aortic aneurysm formation. Bone morphogenetic proteins (BMPs) have been implicated as important regulators of VSMC phenotype, and dysregulation of the BMP pathway has been shown to be associated with vascular diseases. The aim [...] Read more.
Vascular smooth muscle cells (VSMCs) play a key role in aortic aneurysm formation. Bone morphogenetic proteins (BMPs) have been implicated as important regulators of VSMC phenotype, and dysregulation of the BMP pathway has been shown to be associated with vascular diseases. The aim of this study was to investigate for the first time the effects of BMP-4 on the VSMC phenotype and to understand its role in the development of thoracic aortic aneurysms (TAAs). Using the angiotensin II (AngII) osmotic pump model in mice, aortas from mice with VSMC-specific BMP-4 deficiency showed changes similar to AngII-infused aortas, characterised by a loss of contractile markers, increased fibrosis, and activation of matrix metalloproteinase 9. When BMP-4 deficiency was combined with AngII infusion, there was a significantly higher rate of apoptosis and aortic dilatation. In vitro, VSMCs with mRNA silencing of BMP-4 displayed a dedifferentiated phenotype with activated canonical BMP signalling. In contrast, BMP-2-deficient VSMCs exhibited the opposite phenotype. The compensatory regulation between BMP-2 and BMP-4, with BMP-4 promoting the contractile phenotype, appeared to be independent of the canonical signalling pathway. Taken together, these results demonstrate the impact of VSMC-specific BMP-4 deficiency on TAA development. Full article
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