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pmid:34540913

Knockdown of lnc-KCNC3-3:1 Alleviates the Development of Atherosclerosis via Downregulation of JAK1/STAT3 Signaling Pathway.

Limin Sun · Xin He · Tao Zhang · Guizhou Tao · Xin Wang

Frontiers in cardiovascular medicine · 2021 doi:10.3389/fcvm.2021.701058

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

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title
Knockdown of lnc-KCNC3-3:1 Alleviates the Development of Atherosclerosis via Downregulation of JAK1/STAT3 Signaling Pathway.
doi
10.3389/fcvm.2021.701058
pmid
34540913
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Limin Sun
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Xin He
[2]
Tao Zhang
[3]
Guizhou Tao
[4]
Xin Wang
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Frontiers in cardiovascular medicine
year
2021
abstract
Background: Atherosclerosis is a major cause of coronary artery disease (CAD), and CAD is one of the main causes leading to death in most countries. It has been reported that lncRNAs play important roles in the development of atherosclerosis; thus, we aimed to explore lncRNAs that are closely related to the occurrence and development of atherosclerosis. Methods: The data GSE113079 from the GEO database was used to explore the dysregulated lncRNAs in peripheral blood mononuclear cells (PBMCs) between 93 patients with CAD and 48 healthy controls. Next, RT-qPCR was performed to detect the level of lncRNAs in HUVEC cells and CCK-8 was performed to detect cell viability. Then, flow cytometry assays were used to determine the apoptosis of HUVEC. In addition, ELISA assay was used to measure the concentrations of triglyceride (TG), low density lipoprotein cholesterin (LDL-C), and high density lipoprotein cholesterol (HDL-C). Moreover, western blot assay was used to detect the expression of proteins. Results: lnc-KCNC3-3:1 was significantly upregulated in PBMCs of patients with CAD. In addition, oxidized low density lipoprotein (oxLDL) notably inhibited the proliferation and induced the apoptosis of HUVEC, while this phenomenon was notably reversed by lnc-KCNC3-3:1 knockdown. Moreover, oxLDL significantly promoted the migration of HUVECs, which was significantly restored by knockdown of lnc-KCNC3-3:1. Moreover, lnc-KCNC3-3:1 siRNA1 could reverse oxLDL-induced HUVEC growth inhibition, and lnc-KCNC3-3:1 silencing could inhibit the expressions of p-JAK1 and p-STAT3 in oxLDL-treated HUVECs. Animal study revealed that knockdown of lnc-KCNC3-3:1 alleviated the symptom of atherosclerosis, and it could inhibit the expressions of p-JAK1, p-STAT3 and p-Akt in tissues of atherosclerosis mice. Conclusion: Knockdown of lnc-KCNC3-3:1 alleviates the development of atherosclerosis via downregulation of JAK1/STAT3 signaling pathway. These data indicated that lnc-KCNC3-3:1 might serve as a potential target for the treatment of atherosclerosis.
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Knockdown of lnc-KCNC3-3:1 Alleviates the Development
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omenon was notably reversed by lnc-KCNC3-3:1 knockdown. Moreover, oxLDL significantly promoted the
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ents with CAD and 48 healthy controls. Next, RT-qPCR was performed to detect the level of lncRNAs
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method to obtain their related pathways. (D) RT-qPCR was used to detect the expression levels of
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inhibited the proliferation and induced the apoptosis of HUVEC, while this phenomenon was notably
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evidence array · 1 item
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assay:6
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:34540913", "kind": "science-record", "revision": 7, "content_hash": "sha256:672eaf376f535aec8a480dadd3ba40df2227737a1c81ffbf631bbeff12d1b504", "created_at": "2026-11-01T15:41:53Z", "updated_at": "2026-11-01T22:04:46Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Knockdown of lnc-KCNC3-3:1 Alleviates the Development of Atherosclerosis via Downregulation of JAK1/STAT3 Signaling Pathway.", "doi": "10.3389/fcvm.2021.701058", "pmid": "34540913", "authors": ["Limin Sun", "Xin He", "Tao Zhang", "Guizhou Tao", "Xin Wang"], "journal": "Frontiers in cardiovascular medicine", "year": 2021, "abstract": "Background: Atherosclerosis is a major cause of coronary artery disease (CAD), and CAD is one of the main causes leading to death in most countries. It has been reported that lncRNAs play important roles in the development of atherosclerosis; thus, we aimed to explore lncRNAs that are closely related to the occurrence and development of atherosclerosis. Methods: The data GSE113079 from the GEO database was used to explore the dysregulated lncRNAs in peripheral blood mononuclear cells (PBMCs) between 93 patients with CAD and 48 healthy controls. Next, RT-qPCR was performed to detect the level of lncRNAs in HUVEC cells and CCK-8 was performed to detect cell viability. Then, flow cytometry assays were used to determine the apoptosis of HUVEC. In addition, ELISA assay was used to measure the concentrations of triglyceride (TG), low density lipoprotein cholesterin (LDL-C), and high density lipoprotein cholesterol (HDL-C). Moreover, western blot assay was used to detect the expression of proteins. Results: lnc-KCNC3-3:1 was significantly upregulated in PBMCs of patients with CAD. In addition, oxidized low density lipoprotein (oxLDL) notably inhibited the proliferation and induced the apoptosis of HUVEC, while this phenomenon was notably reversed by lnc-KCNC3-3:1 knockdown. Moreover, oxLDL significantly promoted the migration of HUVECs, which was significantly restored by knockdown of lnc-KCNC3-3:1. Moreover, lnc-KCNC3-3:1 siRNA1 could reverse oxLDL-induced HUVEC growth inhibition, and lnc-KCNC3-3:1 silencing could inhibit the expressions of p-JAK1 and p-STAT3 in oxLDL-treated HUVECs. Animal study revealed that knockdown of lnc-KCNC3-3:1 alleviated the symptom of atherosclerosis, and it could inhibit the expressions of p-JAK1, p-STAT3 and p-Akt in tissues of atherosclerosis mice. Conclusion: Knockdown of lnc-KCNC3-3:1 alleviates the development of atherosclerosis via downregulation of JAK1/STAT3 signaling pathway. These data indicated that lnc-KCNC3-3:1 might serve as a potential target for the treatment of atherosclerosis.", "claims": [{"id": "claim-method", "statement": "R language was used to analyze the differentially expressed genes (DEGs) in PBMCs of 93 patients with CAD and 48 healthy controls.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:34540913", "locator": "sections[3] \"Bioinformatics Analysis\" paragraph 2", "quote": "R language was used to analyze the differentially expressed genes (DEGs) in PBMCs of 93 patients with CAD and 48 healthy controls."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The datasets presented in this study can be found in online repositories. 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