Substrate-induced phenotypic switches of human smooth muscle cells: an<i>in vitro</i>study of in-stent restenosis activation pathways

Guildford, Anna; Stewart, Helen; Morris, Christopher G.; Santin, Matteo

doi:10.1098/rsif.2010.0532

Cited by 10 publications

(6 citation statements)

References 38 publications

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“…His findings highlighted the induction of a phenotypic pattern in VSMC using a stainless steel substrate, where the formation of an HA-rich neointimal tissue was enhanced. 37 Similar results were obtained in this study. The BMS have induced the VSMC phenotype to change from contractile to synthetic, and the amount of ECM, especially the collagen, increased.…”

Section: Discussionsupporting

confidence: 90%

Endothelialization and in‐stent restenosis on the surface of glycoprotein IIIa monoclonal antibody eluting stent

Yin

Wang

Zhang

et al. 2012

J Biomedical Materials Res

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Since the percutaneous transtuminal coronary angioplasty was introduced into China in 1984, this procedure has become widely accepted as an important step in coronary revascularization. This study shows the effect of the monoclonal antibody (mAb) on the platelet glycoprotein IIIa receptor during endothelialization and in-stent restenosis by implanting the mAb-eluting stents into iliac arteries of rabbits. The hard tissue cross sections of the stent-implanted arterial segments were made by polymethylmethacrylate embedding. Arterial intima proliferation was observed and analyzed. The endothelialization of the stent surface was observed using scanning electron microscope, whereas the ultrastructure of the neointima was observed using transmission electron microscope. After one month of stent implantation, the surfaces of both groups were covered by intact endothelial layers, but the neointimal areas and the ratio of stenosis were significantly lesser in the mAb-eluting stent group (p < 0.01). After 3 months, the ratio of stenosis in the mAb-eluting stent group was 14.67 ± 0.79, whereas that of the bare stent group was 21.58 ± 1.76 (p < 0.01). Therefore, the mAb eluting from the stent surface has the potential to accelerate endothelialization, prevent thrombosis formation due to the interaction of stent with blood, and decrease the stenosis ratio by inhibiting neointima proliferation.

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Section: Discussionsupporting

confidence: 90%

Endothelialization and in‐stent restenosis on the surface of glycoprotein IIIa monoclonal antibody eluting stent

Yin

Wang

Zhang

et al. 2012

J Biomedical Materials Res

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“…A similar research was conducted by Guildford in VSMCs. His findings highlighted the induction of a phenotypic pattern in VSMC using a stainless steel substrate, where the formation of an HA‐rich neointimal tissue was enhanced 37. Similar results were obtained in this study.…”

Section: Discussionsupporting

confidence: 89%

Amphiphilic diblock copolymers containing poly(N‐hexylisocyanate): Monolayer behavior at the air–water interface

Gargallo

Becerra

Sandoval

et al. 2011

J of Applied Polymer Sci

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The behavior of amphiphilic diblock copolymers containing 80-89% of poly(N-hexylisocyanate) (PHIC) with different hydrophobic segments spread at the air-water interface has been studied. Surface pressure-area isotherms (p-A) at the air-water interface were determined. It was found that these diblock copolymers form stable monolayers and the isotherms present a pseudoplateau region at low surface pressure, irrespective of the nature of the partner block: poly(styrene) (PS) or poly(isoprene). Surface pressure variation at the semidilute region of the monolayer was expressed in terms of the scaling laws as power function of the surface concentration. The critical exponents of the excluded volume m obtained for copolymers with PHIC and PS blocks are 0.58 for the copolymer with 85% of PHIC and 15% of PS, and 0.63 for the copolymer with 89% of PHIC and 11% of PS. The hydrophobicity degree of the diblock copolymers was estimated from the determination of the surface energy values by wettability measurements. The morphology of the monolayers was determined by means of Brewster angle microscopy. Molecular dynamic simulation was performed to explain the experimental behavior of diblock copolymers at the air-water interface.

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“…Bare metal stent increased PDGF-BB receptor expression in VSMCs; moreover, under this stimulus, VSMCs secreted growth factors, including PDGF-BB. Cells in direct contact with the stent may activate distant cells and themselves in a paracrine and autocrine manner, respectively [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNAs Might Regulate Phenotypic Switch of Vascular Smooth Muscle Cells Acting as ceRNA: Implications for In-Stent Restenosis

Arencibia

Lanas

Salazar

2022

IJMS

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Coronary in-stent restenosis is a late complication of angioplasty. It is a multifactorial process that involves vascular smooth muscle cells (VSMCs), endothelial cells, and inflammatory and genetic factors. In this study, the transcriptomic landscape of VSMCs’ phenotypic switch process was assessed under stimuli resembling stent injury. Co-cultured contractile VSMCs and endothelial cells were exposed to a bare metal stent and platelet-derived growth factor (PDGF-BB) 20 ng/mL. Migratory capacity (wound healing assay), proliferative capacity, and cell cycle analysis of the VSMCs were performed. RNAseq analysis of contractile vs. proliferative VSMCs was performed. Gene differential expression (DE), identification of new long non-coding RNA candidates (lncRNAs), gene ontology (GO), and pathway enrichment (KEGG) were analyzed. A competing endogenous RNA network was constructed, and significant lncRNA–miRNA–mRNA axes were selected. VSMCs exposed to “stent injury” conditions showed morphologic changes, with proliferative and migratory capacities progressing from G0-G1 cell cycle phase to S and G2-M. RNAseq analysis showed DE of 1099, 509 and 64 differentially expressed mRNAs, lncRNAs, and miRNAs, respectively. GO analysis of DE genes showed significant enrichment in collagen and extracellular matrix organization, regulation of smooth muscle cell proliferation, and collagen biosynthetic process. The main upregulated nodes in the lncRNA-mediated ceRNA network were PVT1 and HIF1-AS2, with downregulation of ACTA2-AS1 and MIR663AHG. The PVT1 ceRNA axis appears to be an attractive target for in-stent restenosis diagnosis and treatment.

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Substrate-induced phenotypic switches of human smooth muscle cells: anin vitrostudy of in-stent restenosis activation pathways

Cited by 10 publications

References 38 publications

Endothelialization and in‐stent restenosis on the surface of glycoprotein IIIa monoclonal antibody eluting stent

Endothelialization and in‐stent restenosis on the surface of glycoprotein IIIa monoclonal antibody eluting stent

Amphiphilic diblock copolymers containing poly(N‐hexylisocyanate): Monolayer behavior at the air–water interface

Long Non-Coding RNAs Might Regulate Phenotypic Switch of Vascular Smooth Muscle Cells Acting as ceRNA: Implications for In-Stent Restenosis

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