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pmid:41294029

LncRNA LINC01605 Regulates Smooth Muscle Cell Functions and Participates in the Development of Aortic Dissection Through Regulating SGK1.

Mingliang Li · Ruonan Li · Zihe Zheng · Changbo Xiao · Quanlin Yang · Bo Chen · Xiaofu Dai

Journal of cellular and molecular medicine · 2025 doi:10.1111/jcmm.70963

Paper

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Experiment

complete

Data

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Analysis

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Execution

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title
LncRNA LINC01605 Regulates Smooth Muscle Cell Functions and Participates in the Development of Aortic Dissection Through Regulating SGK1.
doi
10.1111/jcmm.70963
pmid
41294029
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Mingliang Li
[1]
Ruonan Li
[2]
Zihe Zheng
[3]
Changbo Xiao
[4]
Quanlin Yang
[5]
Bo Chen
[6]
Xiaofu Dai
journal
Journal of cellular and molecular medicine
year
2025
abstract
Long noncoding RNAs (lncRNAs) are emerging as key regulators in cardiovascular diseases. This study investigated the role of lncRNA LINC01605 in aortic dissection (AD) pathogenesis through its effects on vascular smooth muscle cells (VSMCs). Bioinformatics analysis of GEO datasets (GSE107844, GSE147026) identified LINC01605 as differentially expressed in AD. Its expression was validated in human aortic tissues and VSMCs using RT-qPCR and FISH. Functional assays (CCK-8, Transwell, Western blot) assessed VSMC proliferation, migration, phenotypic switching and autophagy. SGK1 was predicted as a target via bioinformatics and confirmed by RIP assays. Ang II-induced AD mice with LINC01605 knockdown were used for in vivo validation. LINC01605 was significantly upregulated in AD aortic tissues and VSMCs. Functional studies demonstrated that LINC01605 promoted VSMC proliferation, migration, invasion, phenotypic switching and autophagy, particularly under Ang II stimulation. Mechanistically, LINC01605 targeted SGK1 to regulate VSMC function. Knockdown of LINC01605 alleviated AD pathology in mice, modulating synthetic phenotype and autophagy markers. LINC01605 plays an important role in AD. It regulates the function of VSMCs by targeting SGK1 and promotes the pathological process of AD. LINC01605 may be a potential target for AD treatment, providing new directions for the mechanism research and treatment strategies of AD.
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For comparisons involving more than two groups, a one‐way analysis of variance (ANOVA) was conducted.
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It regulates the function of VSMCs by targeting SGK1 and promotes the pathological process of AD.
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This study investigated the role of lncRNA LINC01605 in aortic dissection (AD) pathogenesis through its effects on vascular smooth muscle cells (VSMCs). Bioinformatics analysis of GEO datasets (GSE107844, GSE147026) identified LINC01605 as differentially expressed in AD. Its expression was validated in human aortic tissues and VSMCs using RT-qPCR and FISH. Functional assays (CCK-8, Transwell, Western blot) assessed VSMC proliferation, migration, phenotypic switching and autophagy. SGK1 was predicted as a target via bioinformatics and confirmed by RIP assays. Ang II-induced AD mice with LINC01605 knockdown were used for in vivo validation. LINC01605 was significantly upregulated in AD aortic tissues and VSMCs. Functional studies demonstrated that LINC01605 promoted VSMC proliferation, migration, invasion, phenotypic switching and autophagy, particularly under Ang II stimulation. Mechanistically, LINC01605 targeted SGK1 to regulate VSMC function. Knockdown of LINC01605 alleviated AD pathology in mice, modulating synthetic phenotype and autophagy markers. LINC01605 plays an important role in AD. It regulates the function of VSMCs by targeting SGK1 and promotes the pathological process of AD. LINC01605 may be a potential target for AD treatment, providing new directions for the mechanism research and treatment strategies of AD.", "claims": [{"id": "claim-method", "statement": "Raw count data from these datasets were preprocessed and analysed using the DESeq2 package in R. To evaluate the differences in means between two distinct groups, an independent samples t‐test was employed. 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Functional assays (CCK-8, Transwell, Western blot) assessed VSMC proliferation, migration, phe", "r Ang II‐induced and basal conditions. (A–P) Western blot analysis of matrix metalloproteinases (MMP‐2"], "order_basis": "paper_text_order:578", "id": "assay:3"}, {"role": "data_generation", "definition_id": "transfection", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["ssays. Ang II-induced AD mice with LINC01605 knockdown were used for in vivo validation. LINC01605", "605 targeted SGK1 to regulate VSMC function. Knockdown of LINC01605 alleviated AD pathology in mice", "e staining [13]. Cell Culture and Lentiviral Transfection Human aortic vascular smooth muscle cells (V", "in six‐well plates (5 × 104 cells/well) and transfected 24 h later with lentivirus at a multiplicity"], "order_basis": "paper_text_order:785", "id": "assay:4"}, {"role": "data_generation", "definition_id": "animal_model", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["mice with LINC01605 knockdown were used for in vivo validation. LINC01605 was significantly upre", "ockdown of LINC01605 alleviated AD pathology in mice, modulating synthetic phenotype and autophag", "infusion continued for 28 days. At endpoint, mice were euthanised with pentobarbital sodium (100 mg/kg), and a", "ntation to ensure preemptive gene knockdown. Mice were anaesthetised with 2% isoflurane (Vet One),"], "order_basis": "paper_text_order:810", "id": "assay:5"}, {"role": "data_generation", "definition_id": "ihc", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.93, "evidence": ["ollagenase digestion and identified by α‐SMA immunofluorescence staining [13]. Cell Culture and Lentiviral T"], "order_basis": "paper_text_order:1943", "id": "assay:6"}, {"role": "data_generation", "definition_id": "cell_culture", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.77, "evidence": ["ology Co. Ltd., Wuhan, China. The cells were cultured in Ham's F‐12 K medium (PM150910) supplemented"], "order_basis": "paper_text_order:2170", "id": "assay:7"}, {"role": "data_generation", "definition_id": "cell_imaging", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["d using GAPDH as an internal control. (D, E) Confocal microscopy was employed to visualise the cell nuclei (s", "autophagosome formation was achieved through confocal microscopy by observing the cell nuclei (DAPI, blue), L", "APDH as an internal control. 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