SNHG16 suppression enhances M2 macrophage polarization and inhibits VSMC migration in atherosclerosis

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica Pub Date : 2025-05-06 DOI:10.1016/j.acthis.2025.152248

Bing Gao , Maogong Xi , Ying Cui , Kai Wang , Hui Zhang , Yiyong Wang

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引用次数: 0

Abstract

Atherosclerosis (AS) significantly impacts both cardiovascular and cerebrovascular health, making it an important area of research for potential therapeutic interventions. This study investigates the role of lncRNA SNHG16 in macrophage polarization and its effects on the progression of AS. We assessed the expression of SNHG16 in macrophages and vascular smooth muscle cells (VSMCs) treated with oxidized low-density lipoprotein (ox-LDL) using qPCR. Cell proliferation was evaluated via EdU assay and western blotting, while flow cytometry and immunofluorescence were employed to analyze the polarization of macrophages. Foam cell formation was examined using Oil Red O staining. In a co-culture system, VSMCs treated with ox-LDL were cultured alongside macrophages pretreated with sh-SNHG16, and VSMC viability, migration, and motility were assessed using CCK-8, migration, and scratch assays. The levels of inflammatory cytokines, including IL-6, IL-10, TGFβ, and TNFα, were quantified by ELISA. Our results show that SNHG16 expression is upregulated in ox-LDL-treated cells, which correlates with enhanced macrophage proliferation. Inhibition of SNHG16 promoted M1-to-M2 macrophage polarization, reducing foam cell formation and inflammation. Furthermore, SNHG16 knockdown limited VSMC viability and motility, while attenuating ox-LDL-induced inflammatory responses. In conclusion, suppression of SNHG16 favors M2 macrophage polarization and presents a potential therapeutic target for AS management.

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抑制SNHG16可增强动脉粥样硬化中M2巨噬细胞极化，抑制VSMC迁移

动脉粥样硬化（AS）显著影响心脑血管健康，使其成为潜在治疗干预的重要研究领域。本研究探讨lncRNA SNHG16在巨噬细胞极化中的作用及其对AS进展的影响。我们使用qPCR方法评估了氧化低密度脂蛋白（ox-LDL）处理巨噬细胞和血管平滑肌细胞（VSMCs）中SNHG16的表达。EdU法、western blotting法检测细胞增殖，流式细胞术、免疫荧光法检测巨噬细胞极化情况。油红O染色检测泡沫细胞形成。在共培养系统中，用ox-LDL处理的VSMC与用sh-SNHG16预处理的巨噬细胞一起培养，使用CCK-8、迁移和划痕试验评估VSMC的活力、迁移和运动性。ELISA法测定各组炎症因子IL-6、IL-10、tgf - β、tnf - α水平。我们的研究结果表明，SNHG16在ox- ldl处理的细胞中表达上调，这与巨噬细胞增殖增强有关。抑制SNHG16促进巨噬细胞M1-to-M2极化，减少泡沫细胞形成和炎症。此外，SNHG16敲低限制了VSMC的活力和运动，同时减轻了ox- ldl诱导的炎症反应。综上所述，抑制SNHG16有利于M2巨噬细胞极化，是治疗AS的潜在靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Acta histochemica 生物-细胞生物学

CiteScore

4.60

自引率

4.00%

发文量

107

审稿时长

23 days

期刊介绍： Acta histochemica, a journal of structural biochemistry of cells and tissues, publishes original research articles, short communications, reviews, letters to the editor, meeting reports and abstracts of meetings. The aim of the journal is to provide a forum for the cytochemical and histochemical research community in the life sciences, including cell biology, biotechnology, neurobiology, immunobiology, pathology, pharmacology, botany, zoology and environmental and toxicological research. The journal focuses on new developments in cytochemistry and histochemistry and their applications. Manuscripts reporting on studies of living cells and tissues are particularly welcome. Understanding the complexity of cells and tissues, i.e. their biocomplexity and biodiversity, is a major goal of the journal and reports on this topic are especially encouraged. Original research articles, short communications and reviews that report on new developments in cytochemistry and histochemistry are welcomed, especially when molecular biology is combined with the use of advanced microscopical techniques including image analysis and cytometry. Letters to the editor should comment or interpret previously published articles in the journal to trigger scientific discussions. Meeting reports are considered to be very important publications in the journal because they are excellent opportunities to present state-of-the-art overviews of fields in research where the developments are fast and hard to follow. Authors of meeting reports should consult the editors before writing a report. The editorial policy of the editors and the editorial board is rapid publication. Once a manuscript is received by one of the editors, an editorial decision about acceptance, revision or rejection will be taken within a month. It is the aim of the publishers to have a manuscript published within three months after the manuscript has been accepted