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  Vasorin plays a critical role in vascular smooth muscle cells and arterial functions

Louvet, L., Lenglet, G., Krautzberger, A. M., Mentaverri, R., Hague, F., Kowalewski, C., et al. (2022). Vasorin plays a critical role in vascular smooth muscle cells and arterial functions. Journal of Cellular Physiology. doi:10.1002/jcp.30838.

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JCellPhysiol_Louvet et al_2022.pdf (Publisher version), 3MB
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Louvet, Loïc , Author
Lenglet, Gaëlle , Author
Krautzberger, A. Michaela 1, Author
Mentaverri, Romuald , Author
Hague, Frédéric , Author
Kowalewski, Clara , Author
Mahtal, Nassim , Author
Lesieur, Julie , Author
Bonnet, Anne-Laure , Author
Andrique, Caroline , Author
Gaucher, Céline , Author
Gomila, Cathy , Author
Schrewe, Heinrich1, Author           
Tharaux, Pierre-Louis , Author
Kamel, Said , Author
Chaussain, Catherine , Author
Six, Isabelle , Author
Affiliations:
1Dept. of Developmental Genetics (Head: Bernhard G. Herrmann), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433548              

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Free keywords: angiotensin II, artery, nitric oxide, smooth muscle cells, vascular function, vasorin
 Abstract: Within the cardiovascular system, the protein vasorin (Vasn) is predominantly expressed by vascular smooth muscle cells (VSMCs) in the coronary arteries and the aorta. Vasn knockout (Vasn−/−) mice die within 3 weeks of birth. In the present study, we investigated the role of vascular Vasn expression on vascular function. We used inducible Vasn knockout mice (VasnCRE-ERT KO and VasnSMMHC-CRE-ERT2 KO, in which respectively all cells or SMCs only are targeted) to analyze the consequences of total or selective Vasn loss on vascular function. Furthermore, in vivo effects were investigated in vitro using human VSMCs. The death of VasnCRE-ERT KO mice 21 days after tamoxifen injection was concomitant with decreases in blood pressure, angiotensin II levels, and vessel contractibility to phenylephrine. The VasnSMMHC-CRE-ERT2 KO mice displayed concomitant changes in vessel contractibility in response to phenylephrine and angiotensin II levels. In vitro, VASN deficiency was associated with a shift toward the SMC contractile phenotype, an increase in basal intracellular Ca2+ levels, and a decrease in the SMCs' ability to generate a calcium signal in response to carbachol or phenylephrine. Additionally, impaired endothelium-dependent relaxation (due to changes in nitric oxide signaling) was observed in all Vasn knockout mice models. Our present findings highlight the role played by Vasn SMC expression in the maintenance of vascular functions. The mechanistic experiments suggested that these effects are mediated by SMC phenotype switching and changes in intracellular calcium homeostasis, angiotensin II levels, and NO signaling.

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Language(s): eng - English
 Dates: 2022-07-122022-07-26
 Publication Status: Published online
 Pages: -
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 Table of Contents: -
 Rev. Type: -
 Identifiers: DOI: 10.1002/jcp.30838
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Title: Journal of Cellular Physiology
  Other : J. Cell. Physiol.
Source Genre: Journal
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Publ. Info: Hoboken, NJ : Wiley Subscription Services, Inc.
Pages: - Volume / Issue: - Sequence Number: - Start / End Page: - Identifier: ISSN: 0021-9541
CoNE: https://pure.mpg.de/cone/journals/resource/110992357271180