lncRNA ZFAS1 promotes the ox‑LDL induced proliferation, invasion and migration of vascular smooth muscle cells

Wang, Hao; Hu, Huajie; Ma, Junjie; Jiang, Yafeng; Cheng, Ruifei

doi:10.3892/etm.2021.10267

Cited by 5 publications

(3 citation statements)

References 34 publications

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“…When the blood vessels are stimulated by pathological factors, multiple signaling pathways on VSMCs are activated and the number of “synthetic” phenotypes of VSMCs gradually increases. While synthetic VSMCs have the functions of secretion, migration, and proliferation, the excessive proliferation and migration of VSMCs are the pathophysiological basis of atherosclerosis and vascular stenosis diseases [ 18 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

Role of miR-181b/Notch1 Axis in circ_TNPO1 Promotion of Proliferation and Migration of Atherosclerotic Vascular Smooth Muscle Cells

Chen

Jiang

et al. 2022

Journal of Healthcare Engineering

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Background. The role and expression level change in circ_TNPO1 (hsa_circ_0072951) in atherosclerosis (AS) and VSMC dysfunction remain unknown. In this study, we try to explore the effects of circ_TNPO1 on oxidized low-density lipoprotein (ox-LDL)-induced human vascular smooth muscle cell (VSMC) excessive proliferation and migration, and the potential molecular mechanism. Methods. Quantitative real-time polymerase chain reaction (RT-qPCR) and western blot experiment were used to detect the serum samples from AS patients and healthy controls. CCK-8, Transwell, and the dual-luciferase reporter gene assay were used to detect the cell biology. Results. In human AS serum and ox-LDL-induced VSMCs, circ_TNPO1 was increased, whereas miR-181b was decreased. Silencing circ_TNPO1 inhibited proliferation and migration activity and reduced protein expression of PCNA, Ki-67, MMP2, and E-cadherin and promoted N-cadherin protein expression in ox-LDL induced VSMCs. Remarkably, miR-181b knockdown or Notch1 overexpression could efficiently offset the proliferation and migration inhibiting effect of circ_TNPO1 knockdown in ox-LDL-induced VSMCs. Furthermore, a molecular mechanism study pointed out that circ_TNPO1 and Notch1 are direct-acting targets of miR-181b. Conclusions. In conclusion, our study indicated that circ_TNPO1 promotes the proliferation and migration progression of VSMCs in atherosclerosis through the miR-181b/Notch1 axis.

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Section: Discussionmentioning

confidence: 99%

Role of miR-181b/Notch1 Axis in circ_TNPO1 Promotion of Proliferation and Migration of Atherosclerotic Vascular Smooth Muscle Cells

Chen

Jiang

et al. 2022

Journal of Healthcare Engineering

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“…In our EBs several of the genes more strongly altered by hypoxia (Neat1, Zfas1, supplementary Fig. S5) have been described as regulatory elements of SMC phenotypes or associated processes [62][63][64]. Here, we can see a significant reduction in some contractile genes (Actb, Tpm2, Tpm3, Cald1 ), especially in the HX10d sample.…”

Section: Discussionmentioning

confidence: 56%

An exploration of vascular cell development in mouse embryoid bodies under hypoxia through single cell RNA-seq

Acosta-Iborra,

Puente-Santamaría,

Berrouayel

et al. 2024

Preprint

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Background: Differentiation of mouse stem cells (mESC) to embryonic bodies (EBs) is a widely used approach to model early stages of development. In this study, we employed single-cell transcriptomics to examine the effect of hypoxia on the differentiation of different cell populations in EBs. Results: We differentiated EBs for 8 or 10 days, with two time frames of hypoxic or normoxic exposure: a short window of 16h for the 8-day samples, and a 48h window for the 10-day samples, totaling four experimental conditions. The EBs were composed mainly of broad mesodermal progenitors, a limited number of endodermal precursors, and smaller groups of cells that were more advanced in their differentiation pathways. These developed groups included hemoendothelial progenitors, endothelium, cardiomyocytes, and monocyte and erythrocyte precursors. Both O2 and time of differentiation significantly influenced the distribution of cell types across conditions. Our findings revealed that hypoxia induces a pervasive cell cycle arrest signature across all identified cell populations within the EB. Despite the cell cycle arrest, vascular smooth muscle (vSMCs), endothelial, and cardiac cell populations exhibit expansion under hypoxic conditions, while normoxia favours an increase in the monocyte population. Differential proliferation of hemoendothelial progenitors does not appear to be the primary driver of endothelial cells expansion in hypoxia, as their distribution remained similar across treatments and depleted over time. We observed delays in the terminal differentiation pathway of vSMCs precursors in hypoxic conditions, which may contribute to their expansion and migration by switching to a synthetic phenotype. Additionally, oxygen concentration influenced the developmental path of hemangioblasts towards either an endothelial, or myeloid lineage. In the EBs, this was coupled with a shift in presomitic mesoderm differentiation towards endotome or musculoskeletal precursors, which may provide an additional source of progenitors with endothelial potential during oxygen deprivation. Conclusion: Our study provides novel insights into the cellular responses to hypoxia in the context of early embryonic development, thus unveiling potential mechanisms underlying blood vessel growth.

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“…ZFAS1 overexpression enhanced vascular smooth muscle cells (VSMCs) proliferation, migration, and invasion in response to oxidized low-density lipoprotein (ox LDL), as well as raised the expression of proteins involved in cell proliferation, migration, and invasion (Ki67, PCNA, MMP2, and MMP9). ZFAS1 knockdown partially reversed the effect of ox LDL treatment on VSMC proliferation, migration, and invasion, as well as the protein expression involved in cell proliferation, migration, and invasion [ 54 ].…”

Section: Zfas1 In Apoptosis Cell Proliferation and Cell Cyclementioning

confidence: 99%

An update on the molecular mechanisms of ZFAS1 as a prognostic, diagnostic, or therapeutic biomarker in cancers

Mehrab Mohseni,

Zamani,

Momeni

et al. 2024

Discov Onc

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Zinc finger antisense 1 (ZFAS1), a newly discovered long noncoding RNA, is expressed in various tissues and organs and has been introduced an oncogenic gene in human malignancies. In various cancers, ZFAS1 regulates apoptosis, cell proliferation, the cell cycle, migration, translation, rRNA processing, and spliceosomal snRNP assembly; targets signaling cascades; and interacts with transcription factors via binding to key proteins and miRNAs, with conflicting findings on its effect on these processes. ZFAS1 is elevated in different types of cancer, like colorectal, colon, osteosarcoma, and gastric cancer. Considering the ZFAS1 expression pattern, it also has the potential to be a diagnostic or prognostic marker in various cancers. The current review discusses the mode of action of ZFAS1 in various human cancers and its regulation function related to chemoresistance comprehensively, as well as the potential role of ZFAS1 as an effective and noninvasive cancer-specific biomarker in tumor diagnosis, prognosis, and treatment. We expected that the current review could fill the current scientific gaps in the ZFAS1-related cancer causative mechanisms and improve available biomarkers.

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lncRNA ZFAS1 promotes the ox‑LDL induced proliferation, invasion and migration of vascular smooth muscle cells

Cited by 5 publications

References 34 publications

Role of miR-181b/Notch1 Axis in circ_TNPO1 Promotion of Proliferation and Migration of Atherosclerotic Vascular Smooth Muscle Cells

Role of miR-181b/Notch1 Axis in circ_TNPO1 Promotion of Proliferation and Migration of Atherosclerotic Vascular Smooth Muscle Cells

An exploration of vascular cell development in mouse embryoid bodies under hypoxia through single cell RNA-seq

An update on the molecular mechanisms of ZFAS1 as a prognostic, diagnostic, or therapeutic biomarker in cancers

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