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血浆微小细胞外囊泡携带的 miRNA-501-5p 促进血管平滑肌细胞表型调节介导的支架内再狭窄。

Plasma Small Extracellular Vesicle-Carried miRNA-501-5p Promotes Vascular Smooth Muscle Cell Phenotypic Modulation-Mediated In-Stent Restenosis.

机构信息

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

Department of Cardiology, Nanjing Heart Centre, Nanjing, China.

出版信息

Oxid Med Cell Longev. 2021 Apr 21;2021:6644970. doi: 10.1155/2021/6644970. eCollection 2021.

DOI:10.1155/2021/6644970
PMID:33968296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8084657/
Abstract

Vascular smooth muscle cell (VSMC) phenotypic modulation plays an important role in the occurrence and development of in-stent restenosis (ISR), the underlying mechanism of which remains a key issue needing to be urgently addressed. This study is designed to investigate the role of plasma small extracellular vesicles (sEV) in VSMC phenotypic modulation. sEV were isolated from the plasma of patients with ISR (ISR-sEV) or not (Ctl-sEV) 1 year after coronary stent implantation using differential ultracentrifugation. Plasma sEV in ISR patients are elevated markedly and decrease the expression of VSMC contractile markers -SMA and calponin and increase VSMC proliferation. miRNA sequencing and qRT-PCR validation identified that miRNA-501-5p was the highest expressed miRNA in the plasma ISR-sEV compared with Ctl-sEV. Then, we found that sEV-carried miRNA-501-5p level was significantly higher in ISR patients, and the level of plasma sEV-carried miRNA-501-5p linearly correlated with the degree of restenosis ( = 0.62). Moreover, miRNA-501-5p inhibition significantly increased the expression of VSMC contractile markers -SMA and calponin and suppressed VSMC proliferation and migration; in vivo inhibition of miRNA-501-5p could also blunt carotid artery balloon injury induced VSMC phenotypic modulation in rats. Mechanically, miRNA-501-5p promoted plasma sEV-induced VSMC proliferation by targeting Smad3. Notably, endothelial cells might be the major origins of miRNA-501-5p. Collectively, these findings showed that plasma sEV-carried miRNA-501-5p promotes VSMC phenotypic modulation-mediated ISR through targeting Smad3.

摘要

血管平滑肌细胞 (VSMC) 表型调节在支架内再狭窄 (ISR) 的发生和发展中起着重要作用，其潜在机制仍然是一个亟待解决的关键问题。本研究旨在探讨血浆小细胞外囊泡 (sEV) 在 VSMC 表型调节中的作用。使用差速超速离心法从支架植入 1 年后患有 ISR（ISR-sEV）或未患有 ISR（Ctl-sEV）的患者血浆中分离 sEV。与 Ctl-sEV 相比，ISR 患者血浆中的 sEV 明显升高，并降低 VSMC 收缩标志物 -SMA 和钙调蛋白的表达，增加 VSMC 的增殖。miRNA 测序和 qRT-PCR 验证表明，与 Ctl-sEV 相比，ISR-sEV 中表达最高的 miRNA 是 miRNA-501-5p。然后，我们发现 ISR 患者的 sEV 携带 miRNA-501-5p 水平显著升高，并且血浆 sEV 携带 miRNA-501-5p 的水平与再狭窄程度呈线性相关（ = 0.62）。此外，miRNA-501-5p 抑制显著增加 VSMC 收缩标志物 -SMA 和钙调蛋白的表达，并抑制 VSMC 的增殖和迁移；体内抑制 miRNA-501-5p 也可以抑制大鼠颈动脉球囊损伤诱导的 VSMC 表型调节。在机制上，miRNA-501-5p 通过靶向 Smad3 促进 sEV 诱导的 VSMC 增殖。值得注意的是，内皮细胞可能是 miRNA-501-5p 的主要来源。总之，这些发现表明，血浆 sEV 携带的 miRNA-501-5p 通过靶向 Smad3 促进 VSMC 表型调节介导的 ISR。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/63caee1dc027/OMCL2021-6644970.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/996504bfcf68/OMCL2021-6644970.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/fa7cdc3d17ce/OMCL2021-6644970.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/fcfabac9bfb1/OMCL2021-6644970.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/63caee1dc027/OMCL2021-6644970.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/996504bfcf68/OMCL2021-6644970.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/47d245ddc7c2/OMCL2021-6644970.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/5c77dc379663/OMCL2021-6644970.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/fa7cdc3d17ce/OMCL2021-6644970.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/fcfabac9bfb1/OMCL2021-6644970.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f61c/8084657/63caee1dc027/OMCL2021-6644970.007.jpg

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