Biointerface topography regulates phenotypic switching and cell apoptosis in vascular smooth muscle cells.


Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
04 06 2020
Historique:
received: 19 02 2020
accepted: 05 03 2020
pubmed: 13 4 2020
medline: 18 12 2020
entrez: 13 4 2020
Statut: ppublish

Résumé

In-stent restenosis (ISR) is a complex disease that occurs after coronary stenting procedures. The development of quality materials and improvement of our understanding on significant factors regulating ISR are essential for enhancing prognosis. Vascular smooth muscle cells (VSMCs) are the main constituent cells of blood vessel walls, and dysfunction of VMSCs can exacerbate ISR. Accordingly, in this study, we explored the influence of wrinkled material topography on the biological functions of VSMCs. Polydimethylsiloxane with a wrinkled topography was synthesized using elastomer base and crosslinking and observed by atomic force microscopy. VSMC proliferation, apoptosis, and morphology were determined by Cell Counting Kit-8 assays, fluorescence-assisted cell sorting, and phalloidin staining. α-Smooth muscle actin (α-SMA), major histocompatibility complex (MHC), and calponin 1 (CNN-1) expression levels were measured by quantitative real-time polymerase chain reaction and western blotting. Moreover, p53 and cleaved caspase-3 expression levels were evaluated by western blotting in VSMCs to assess apoptotic induction. Surface topographies were not associated with a clear orientation or elongation of VSMCs. The number of cells was increased on wrinkled surfaces (0.7 μm in amplitude, and 3 μm in wavelength [W3]) compared with that on other surfaces, contributing to continuously increased cell proliferation. Moreover, interactions of VSMCs with the W3 surface suppressed phenotypic switching, resulting in ISR via regulation of α-SMA, calponin-1, and SM-MHC expression. The surface with an amplitude of 0.05 μm and a wavelength of 0.5 μm (W0.5) promoted apoptosis by inducing caspase 3 and p53 activities. Introduction of aligned topographies on biomaterial scaffolds could provide physical cues to modulate VSMC responses for engineering vascular constructs. Materials with wrinkled topographies could have applications in the development of stents to reduce ISR.

Sections du résumé

BACKGROUND
In-stent restenosis (ISR) is a complex disease that occurs after coronary stenting procedures. The development of quality materials and improvement of our understanding on significant factors regulating ISR are essential for enhancing prognosis. Vascular smooth muscle cells (VSMCs) are the main constituent cells of blood vessel walls, and dysfunction of VMSCs can exacerbate ISR. Accordingly, in this study, we explored the influence of wrinkled material topography on the biological functions of VSMCs.
METHODS
Polydimethylsiloxane with a wrinkled topography was synthesized using elastomer base and crosslinking and observed by atomic force microscopy. VSMC proliferation, apoptosis, and morphology were determined by Cell Counting Kit-8 assays, fluorescence-assisted cell sorting, and phalloidin staining. α-Smooth muscle actin (α-SMA), major histocompatibility complex (MHC), and calponin 1 (CNN-1) expression levels were measured by quantitative real-time polymerase chain reaction and western blotting. Moreover, p53 and cleaved caspase-3 expression levels were evaluated by western blotting in VSMCs to assess apoptotic induction.
RESULTS
Surface topographies were not associated with a clear orientation or elongation of VSMCs. The number of cells was increased on wrinkled surfaces (0.7 μm in amplitude, and 3 μm in wavelength [W3]) compared with that on other surfaces, contributing to continuously increased cell proliferation. Moreover, interactions of VSMCs with the W3 surface suppressed phenotypic switching, resulting in ISR via regulation of α-SMA, calponin-1, and SM-MHC expression. The surface with an amplitude of 0.05 μm and a wavelength of 0.5 μm (W0.5) promoted apoptosis by inducing caspase 3 and p53 activities.
CONCLUSION
Introduction of aligned topographies on biomaterial scaffolds could provide physical cues to modulate VSMC responses for engineering vascular constructs. Materials with wrinkled topographies could have applications in the development of stents to reduce ISR.

Identifiants

pubmed: 32278550
pii: S0006-291X(20)30517-9
doi: 10.1016/j.bbrc.2020.03.038
pii:
doi:

Substances chimiques

ACTA2 protein, human 0
Actins 0
Calcium-Binding Proteins 0
Cross-Linking Reagents 0
Dimethylpolysiloxanes 0
Microfilament Proteins 0
Tumor Suppressor Protein p53 0
baysilon 63148-62-9
CASP3 protein, human EC 3.4.22.-
Caspase 3 EC 3.4.22.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

841-847

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare no conflict of interests.

Auteurs

Lu Han (L)

Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Qingde Yin (Q)

Department of Laboratory Medicine, Linyi Center for Disease Control and Prevention, 276000, China.

Liangliang Yang (L)

University of Groningen, W.J. Kolff Institute for Biomedical Engineering and Materials Science, Department of Biomedical Engineering, University Medical Center Groningen, A. Deusinglaan 1, 9713 AV, Groningen, the Netherlands. Electronic address: l.yang@umcg.nl.

Patrick van Rijn (P)

University of Groningen, W.J. Kolff Institute for Biomedical Engineering and Materials Science, Department of Biomedical Engineering, University Medical Center Groningen, A. Deusinglaan 1, 9713 AV, Groningen, the Netherlands. Electronic address: p.van.rijn@umcg.nl.

Yanyan Yang (Y)

Institute for Translational Medicine, School of Basic Medicine, Qingdao University, Qingdao, 266021, China.

Yan Liu (Y)

Institute for Translational Medicine, School of Basic Medicine, Qingdao University, Qingdao, 266021, China.

Min Li (M)

Institute for Translational Medicine, School of Basic Medicine, Qingdao University, Qingdao, 266021, China.

Mingzhe Yan (M)

Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Qihui Zhou (Q)

Institute for Translational Medicine, School of Basic Medicine, Qingdao University, Qingdao, 266021, China. Electronic address: qihuizhou@qdu.edu.cn.

Tao Yu (T)

Institute for Translational Medicine, School of Basic Medicine, Qingdao University, Qingdao, 266021, China. Electronic address: yutao0112@qdu.edu.cn.

Zhexun Lian (Z)

Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao 266003, China. Electronic address: lianzx566@163.com.

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Classifications MeSH