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pmid:40233150

Long noncoding RNA MIAT regulates VSMC migration by sponging miR-326.

Yuxin Bao · Yinzhou Luo · Hanjie Zhai · Jie Lu · Man Zhang · Ningning Wang

Science progress · 2025 doi:10.1177/00368504251335854

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

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absent

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title
Long noncoding RNA MIAT regulates VSMC migration by sponging miR-326.
doi
10.1177/00368504251335854
pmid
40233150
authors array · 6 items
[0]
Yuxin Bao
[1]
Yinzhou Luo
[2]
Hanjie Zhai
[3]
Jie Lu
[4]
Man Zhang
[5]
Ningning Wang
journal
Science progress
year
2025
abstract
ObjectiveThe current study aimed to investigate the role of the myocardial infarction-associated transcript (MIAT)/microRNA-326 (miR-326) axis in regulating the migration of vascular smooth muscle cells (VSMCs) during the progression of atherosclerosis (AS).MethodsBioinformatic analysis of MIAT and miR-326 in two AS-related GEO datasets was performed via the online web tool GEO2R. MIAT and miR-326 expression in 46 paired plasma samples and in oxidized low-density lipoprotein (ox-LDL)-treated VSMCs was analysed via RT-qPCR. Western blot analysis was used to determine the expression of monocyte chemotactic protein 1 (MCP-1) after diverse ox-LDL treatments. The correlation between MIAT and miR-326 was analysed by Spearman correlation analysis. Transwell assays were performed to determine the changes in migration after different MIAT or miR-326 interventions. RNA-fluorescence in situ hybridization (FISH) assays were performed to determine the subcellular localization of MIAT and miR-326. The targeted binding effect between MIAT and miR-326 was confirmed via a luciferase assay.ResultsMIAT was upregulated and miR-326 was downregulated in 46 plasma samples from patients with AS compared with those from patients without AS (non-AS). A negative correlation was found between MIAT and miR-326 (r = - 0.6591, P < 0.0001). The expression of MIAT in plaque samples from advanced AS patients was markedly greater than that in plaque samples from early AS patients according to the GEO dataset GSE28829 (P < 0.0001). The expression of miR-326 in platelet samples from patients with first acute myocardial infarction (FAMI) was significantly lower than that in healthy controls (P = 0.0034). MCP-1 was upregulated in ox-LDL-treated VSMCs. MIAT knockdown by specific MIAT small interfering RNAs (siRNAs) suppressed VSMC migration. Upregulation of miR-326 by transfection of miR-326 mimics also inhibited VSMC migration. Dual luciferase assays indicated that miR-326 targets MIAT. The upregulation of MIAT increased the migration of VSMCs. However, this effect was attenuated by a miR-326 mimic.ConclusionsMIAT was upregulated and miR-326 was downregulated in AS plasma and in ox-LDL-treated VSMCs. MIAT binds to miR-326 via theoretical miRNA response elements. MIAT promoted migration by sponging miR-326 in ox-LDL-induced VMSCs. The MIAT/miR-326 axis may represent a novel therapeutic target for the treatment of AS, offering potential insights into AS progression and its clinical management.
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The correlation between MIAT and miR-326 was analysed by Spearman correlation analysis.
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A negative correlation was found between MIAT and miR-326 (r = − 0.6591, P < 0.0001).
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tein (ox-LDL)-treated VSMCs was analysed via RT-qPCR. Western blot analysis was used to determine
[1]
n (ox-LDL)-treated VSMCs was analysed via RT-qPCR. Western blot analysis was used to determine
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rom patients without AS was determined by RT–qPCR. As shown in Figure 1(d) and (e), the expres
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LDL)-treated VSMCs was analysed via RT-qPCR. Western blot analysis was used to determine the expressio
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lammatory marker of VSMCs, was measured by a western blot analysis. 26 The treated VSMCs were used for
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AS in the above cell models, was detected by western blot analysis. As shown in the representative ima
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d VSMC migration. Upregulation of miR-326 by transfection of miR-326 mimics also inhibited VSMC migrat
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as upregulated in ox-LDL-treated VSMCs. MIAT knockdown by specific MIAT small interfering RNAs (siR
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ml amphoteracin B (Solarbio). The VSMCs were cultured in a humidified atmosphere containing 5% CO2 at
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:40233150", "kind": "science-record", "revision": 3, "content_hash": "sha256:5dafb5600b5a0efea092e0aa78c5760dfbaccb4968c76de18a9599dbbad29b96", "created_at": "2026-11-01T20:30:23Z", "updated_at": "2026-11-01T22:13:53Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Long noncoding RNA MIAT regulates VSMC migration by sponging miR-326.", "doi": "10.1177/00368504251335854", "pmid": "40233150", "authors": ["Yuxin Bao", "Yinzhou Luo", "Hanjie Zhai", "Jie Lu", "Man Zhang", "Ningning Wang"], "journal": "Science progress", "year": 2025, "abstract": "ObjectiveThe current study aimed to investigate the role of the myocardial infarction-associated transcript (MIAT)/microRNA-326 (miR-326) axis in regulating the migration of vascular smooth muscle cells (VSMCs) during the progression of atherosclerosis (AS).MethodsBioinformatic analysis of MIAT and miR-326 in two AS-related GEO datasets was performed via the online web tool GEO2R. MIAT and miR-326 expression in 46 paired plasma samples and in oxidized low-density lipoprotein (ox-LDL)-treated VSMCs was analysed via RT-qPCR. Western blot analysis was used to determine the expression of monocyte chemotactic protein 1 (MCP-1) after diverse ox-LDL treatments. The correlation between MIAT and miR-326 was analysed by Spearman correlation analysis. Transwell assays were performed to determine the changes in migration after different MIAT or miR-326 interventions. RNA-fluorescence in situ hybridization (FISH) assays were performed to determine the subcellular localization of MIAT and miR-326. The targeted binding effect between MIAT and miR-326 was confirmed via a luciferase assay.ResultsMIAT was upregulated and miR-326 was downregulated in 46 plasma samples from patients with AS compared with those from patients without AS (non-AS). A negative correlation was found between MIAT and miR-326 (r = - 0.6591, P < 0.0001). The expression of MIAT in plaque samples from advanced AS patients was markedly greater than that in plaque samples from early AS patients according to the GEO dataset GSE28829 (P < 0.0001). The expression of miR-326 in platelet samples from patients with first acute myocardial infarction (FAMI) was significantly lower than that in healthy controls (P = 0.0034). MCP-1 was upregulated in ox-LDL-treated VSMCs. MIAT knockdown by specific MIAT small interfering RNAs (siRNAs) suppressed VSMC migration. Upregulation of miR-326 by transfection of miR-326 mimics also inhibited VSMC migration. Dual luciferase assays indicated that miR-326 targets MIAT. The upregulation of MIAT increased the migration of VSMCs. However, this effect was attenuated by a miR-326 mimic.ConclusionsMIAT was upregulated and miR-326 was downregulated in AS plasma and in ox-LDL-treated VSMCs. MIAT binds to miR-326 via theoretical miRNA response elements. MIAT promoted migration by sponging miR-326 in ox-LDL-induced VMSCs. The MIAT/miR-326 axis may represent a novel therapeutic target for the treatment of AS, offering potential insights into AS progression and its clinical management.", "claims": [{"id": "claim-method", "statement": "The correlation between MIAT and miR-326 was analysed by Spearman correlation analysis.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:40233150", "locator": "sections[0] \"Abstract\" paragraph 2", "quote": "The correlation between MIAT and miR-326 was analysed by Spearman correlation analysis."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The authors declare that the data supporting this study's findings are available within the paper. 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