Covalently Immobilized Mitomycin C on Polypropylene Sutures Creates a Non-Releasing Bioactive Interface That Modulates Vascular Smooth Muscle Cell Fate and Prevents Intimal Hyperplasia.

Tzu-Yen Huang, Wei-Chieh Chiu, Ko-Shao Chen, Ya-Jyun Liang, Pin-Yuan Chen, Yao-Chang Wang, Feng-Huei Lin

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Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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7 authors.

Tzu-Yen HuangInstitute of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd, Taipei City 10617, Taiwan.ORCID 0000-0003-1907-1514

Wei-Chieh ChiuInstitute of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd, Taipei City 10617, Taiwan.

Ko-Shao ChenDepartment of Materials Engineering, Tatung University, No. 40, Sec. 3, Zhongshan N. Rd., Taipei City 10452, Taiwan.

Ya-Jyun LiangInstitute of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd, Taipei City 10617, Taiwan.ORCID 0000-0002-3353-1524

Pin-Yuan ChenDepartment of Neurosurgery, Chang Gung Memorial Hospital at Keelung, 222 Mai-Chin Road, Keelung 204201, Taiwan.

Yao-Chang WangDepartment of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital at Keelung, 222 Mai-Chin Road, Keelung 204201, Taiwan.

Feng-Huei LinInstitute of Biomedical Engineering, College of Medicine and College of Engineering, National Taiwan University, No. 1, Sec. 4, Roosevelt Rd, Taipei City 10617, Taiwan.ORCID 0000-0002-2994-6671

Funding

Keelung Chang Gung Memorial Hospital CMRPG2N0421

6 · The paper itself

Abstract

Intimal hyperplasia (IH) at vascular anastomosis sites arises from endothelial injury, thrombin activation, and the subsequent proliferation and phenotypic modulation of vascular smooth muscle cells (VSMCs). Existing clinically used systemic pharmacologic regimens (e.g., antiplatelet/anticoagulant therapy) and reported local material-based strategies in the literature (e.g., drug-eluting sutures, hydrogels, or coatings) largely rely on drug release, which can result in burst kinetics, finite duration, and off-target/systemic exposure. We developed a covalently immobilized, non-releasing biointerface in which mitomycin C (MMC) is stably anchored onto polypropylene sutures via low-pressure, non-thermal acetic-acid plasma (AAP) activation. AAP functionalization introduced reactive oxygen-containing groups on polypropylene, enabling amide-bond immobilization of MMC while preserving suture mechanics. Anchored MMC exhibited potent contact-mediated regulation of VSMC fate, reducing metabolic activity to 81% of control, suppressing G

Indexed as

HyperplasiaMitomycinMuscle, Smooth, VascularMyocytes, Smooth MusclePolypropylenesSuturesTunica IntimaAnimalsCell ProliferationMaleRatsRats, WistarMitomycinPolypropylenescontact-dependent bioactivitycovalent surface graftingintimal hyperplasiaMitomycin Cnon-releasing biointerfacevascular anastomosis

Identifiers

PMID41683753

DOI10.3390/ijms27031328

PMCPMC12897631

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LicenceCC BY

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.