In-depth evaluation of commercially available human vascular smooth muscle cells phenotype: Implications for vascular tissue engineering

Timraz, Sara B. H.; Farhat, Ilyas A. H.; Alhussein, Ghada; Christoforou, Nicolas; Teo, Jeremy C. M.

doi:10.1016/j.yexcr.2016.04.004

Cited by 19 publications

(11 citation statements)

References 25 publications

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“…Immunostaining of the VSMCs cultured on tissue culture polystyrene revealed the expression of α-SMA but minimal SM-MHC in most VSMCs used in this study (Figure S5). This observation indicated that the conventional 2D culture induced a spontaneous shift of VSMCs from a contractile phenotype to a more synthetic state by losing SM-MHC expression, which is in agreement with previous findings [26].…”

Section: Resultssupporting

confidence: 93%

Biomimetic soft fibrous hydrogels for contractile and pharmacologically responsive smooth muscle

Ding

Sharma

et al. 2018

Acta Biomaterialia

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Engineering functional smooth muscle in vitro holds the great potential for diseased tissue replacement and drug testing. A central challenge is recapitulating the smooth muscle contractility and pharmacological responses given its significant phenotypic plasticity in response to changes in environment. We present a biomimetic fibrous hydrogel with tunable structure, stiffness, and composition that enables the creation of functional smooth muscle tissues in the native-like vascular tissue microenvironment. Such fibrous hydrogel is further combined with the combinatory protein array technology to construct a cellular array for evaluation of smooth muscle phenotype, contraction, and cell mechanics. The integrated platform produced here could be promising for developing a broad range of normal or diseased in vitro tissue models.

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Section: Resultssupporting

confidence: 93%

Biomimetic soft fibrous hydrogels for contractile and pharmacologically responsive smooth muscle

Ding

Sharma

et al. 2018

Acta Biomaterialia

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“…Our study has limitations. To achieve sufficient cell numbers for our experimental studies we used VSMCs of early passages (≤ P4) that while an accepted approach is not as close to the in vivo state as freshly dispersed VSMCs [53][54][55][56] . Another limitation was the mortality in SMC-overexpressing IL11 transgenic mice driven, in part, by inflammatory bowel disease 30 .…”

Section: Discussionmentioning

confidence: 99%

Interleukin-11 is important for vascular smooth muscle phenotypic switching and aortic inflammation, fibrosis and remodeling in mouse models

Lim

Corden

et al. 2020

Sci Rep

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Transforming growth factor beta-1 (TGFβ1) is a major driver of vascular smooth muscle cell (VSMC) phenotypic switching, an important pathobiology in arterial disease. We performed RNA-sequencing of TGFβ1-stimulated human aortic or arterial VSMCs which revealed large and consistent upregulation of Interleukin 11 (IL11). IL11 has an unknown function in VSMCs, which highly express the IL11 receptor alpha, suggestive of an autocrine loop. In vitro, IL11 activated ERK signaling, but inhibited STAT3 activity, and caused VSMC phenotypic switching to a similar extent as TGFβ1 or angiotensin II (ANGII) stimulation. Genetic or therapeutic inhibition of IL11 signaling reduced TGFβ1- or ANGII-induced VSMC phenotypic switching, placing IL11 activity downstream of these factors. Aortas of mice with Myh11-driven IL11 expression were remodeled and had reduced contractile but increased matrix and inflammatory genes expression. In two models of arterial pressure loading, IL11 was upregulated in the aorta and neutralizing IL11 antibodies reduced remodeling along with matrix and pro-inflammatory gene expression. These data show that IL11 plays an important role in VSMC phenotype switching, vascular inflammation and aortic pathobiology.

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“…Primary human aortic smooth muscle cells (VSMC) from healthy donors were purchased from Cell Applications Inc. (354K-05a), California, USA. In order to preserve cell identity all experiments were carried out at passages 1–5 62 . Primary VSMC from wild-type and Hdac9 −/− mice were isolated from the proximal ascending section of aortas by standard explant protocol.…”

Section: Methodsmentioning

confidence: 99%

An HDAC9-MALAT1-BRG1 complex mediates smooth muscle dysfunction in thoracic aortic aneurysm

et al. 2018

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Thoracic aortic aneurysm (TAA) has been associated with mutations affecting members of the TGF-β signaling pathway, or components and regulators of the vascular smooth muscle cell (VSMC) actomyosin cytoskeleton. Although both clinical groups present similar phenotypes, the existence of potential common mechanisms of pathogenesis remain obscure. Here we show that mutations affecting TGF-β signaling and VSMC cytoskeleton both lead to the formation of a ternary complex comprising the histone deacetylase HDAC9, the chromatin-remodeling enzyme BRG1, and the long noncoding RNA MALAT1. The HDAC9–MALAT1–BRG1 complex binds chromatin and represses contractile protein gene expression in association with gain of histone H3-lysine 27 trimethylation modifications. Disruption of Malat1 or Hdac9 restores contractile protein expression, improves aortic mural architecture, and inhibits experimental aneurysm growth. Thus, we highlight a shared epigenetic pathway responsible for VSMC dysfunction in both forms of TAA, with potential therapeutic implication for other known HDAC9-associated vascular diseases.

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In-depth evaluation of commercially available human vascular smooth muscle cells phenotype: Implications for vascular tissue engineering

Cited by 19 publications

References 25 publications

Biomimetic soft fibrous hydrogels for contractile and pharmacologically responsive smooth muscle

Biomimetic soft fibrous hydrogels for contractile and pharmacologically responsive smooth muscle

Interleukin-11 is important for vascular smooth muscle phenotypic switching and aortic inflammation, fibrosis and remodeling in mouse models

An HDAC9-MALAT1-BRG1 complex mediates smooth muscle dysfunction in thoracic aortic aneurysm

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