Preliminary study on the mechanism of long noncoding RNA SENCR regulating the proliferation and migration of vascular smooth muscle cells

Ye, Famin; Zhang, Jing; Zhang, Qiaoling; Zhang, Jingjing; Chen, Cheng

doi:10.1002/jcp.29775

Cited by 18 publications

(14 citation statements)

References 28 publications

(29 reference statements)

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“…Some functions of lncRNAs include structural scaffolding, RNA processing, apoptosis and cell invasion regulation, and chromatin rearrangement [30]. The lncRNA SENCR is highly expressed in endothelial cells, vascular smooth muscle cells, and aortic tissues in the heart [31,32]. Silencing SENCR down-regulates the expression of some vascular smooth muscle contractile proteins [33].…”

Section: Discussionmentioning

confidence: 99%

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Long-chain noncoding RNA-GAS5/hsa-miR-138-5p attenuates high glucose-induced cardiomyocyte damage by targeting CYP11B2

et al. 2021

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Objective: Diabetic cardiomyopathy (DCM) is one of the complications experienced by patients with diabetes. In recent years, long noncoding RNAs (lncRNAs) have been investigated because of their role in the progression of various diseases, including DCM. The purpose of this study was to explore the role of lncRNA GAS5 in high-glucose (HG)-induced cardiomyocyte injury and apoptosis. Materials and methods: We constructed HG-induced AC16 cardiomyocytes and a streptozotocin-induced rat diabetes model. GAS5 was overexpressed and knocked out at the cellular level, and GAS5 was knocked down by lentiviruses at the animal level to observe its effect on myocardial injury. Real-time quantitative polymerase chain reaction was used to detect the expression of GAS5. Cell proliferation and apoptosis after GAS5 knockout were detected by CCK-8, TUNEL, and flow cytometry assays. ELISA was used to detect the changes in myocardial enzyme content in cells and animal myocardial tissues during the action of GAS5 on myocardial injury. Results: GAS5 expression was up-regulated in HG-treated AC16 cardiomyocytes and the rat diabetic myocardial injury model. The down-regulation of GAS5 inhibited HG-induced myocardial damage. This work proved that GAS5 konckdown reversed cardiomyocyte injury and apoptosis by targeting miR-138 to down-regulate CYP11B2. Conclusion: We confirmed for the first time that the down-regulation of GAS5 could reverse CYP11B2 via the miR-138 axis to reverse HG-induced cardiomyocyte injury. This research might provide a new direction for explaining the developmental mechanism of DCM and potential targets for the treatment of myocardial injury.

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Section: Discussionmentioning

confidence: 99%

“…The lncRNA SENCR is highly expressed in endothelial cells, vascular smooth muscle cells, and aortic tissues in the heart [31,32]. Silencing SENCR down-regulates the expression of some vascular smooth muscle contractile proteins [33]. The lncRNA Mhrt is rich in ncRNA and is unique to human heart tissue.…”

Section: Discussionmentioning

confidence: 99%

Long-chain noncoding RNA-GAS5/hsa-miR-138-5p attenuates high glucose-induced cardiomyocyte damage by targeting CYP11B2

et al. 2021

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“…However, SENCR was proved to be downregulated in the plasma of patients with coronary heart disease. Upregulation of SENCR could effectively inhibit the stimulatory effect of platelet-derived growth factor (PDGF)-BB on human aortic VSMC proliferation and migration [ 31 ]. SENCR may be involved in the development of AAA.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SENCR suppresses abdominal aortic aneurysm formation by inhibiting smooth muscle cells apoptosis and extracellular matrix degradation

Cai

Huang

Yang

et al. 2020

Bosn J of Basic Med Sci

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Abdominal aortic aneurysm (AAA) is a progressive chronic dilatation of the abdominal aorta without effective medical treatment. This study aims to clarify the potential of long non-coding RNA SENCR as a treatment target in AAA. Angiotensin II (Ang-II) was used to establish AAA mouse model as well as a cell model based on the mouse aortic vascular smooth muscle cells (VSMCs). Reverse transcription quantitative PCR and western blot were performed to measure the expression of SENCR and proteins, respectively. Apoptotic rate in VSMCs was determined using Annexin V-FITC/PI double staining, and cell apoptosis in aortic tissues was determined by TUNEL staining. Hematoxylin and eosin and Elastica van Gieson staining were used for histological analysis of aortic tissues. SENCR was downregulated in AAA tissues and Ang-II-stimulated VSMCs. Overexpression of SENCR inhibited Ang-II-induced VSMC apoptosis, while inhibition of SENCR facilitated VSMC apoptosis. Moreover, overexpression of SENCR suppressed matrix metalloproteinase (MMP)-2 and MMP-9 expression and promoted tissue inhibitor of metalloproteinases 1 (TIMP-1) expression in Ang-II-induced VSMCs, while inhibition of SENCR expression led to the opposite results. In vivo, overexpressed SENCR improved the pathological change in aortic tissues and the damage in arterial wall elastic fibres induced by Ang-II, as well as it suppressed Ang-II-induced cell apoptosis and extracellular matrix degradation in aortic tissues. Overall, overexpression of SENCR inhibited AAA formation via suppressing VSMC apoptosis and extracellular matrix degradation. We provided a reliable evidence for SENCR acting as a potential target for AAA treatment.

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“…Then, 10 µl CCK-8 reagent (Dojindo Molecular Technologies, Inc.) was added to each well and further incubated for 2 h at 37°C. The absorbance of each well was measured at a wavelength of 450 nm using a spectrophotometer (Bio-Rad Laboratories, Inc.) ( 17 ).…”

Section: Methodsmentioning

confidence: 99%

Cinnamaldehyde inhibits psoriasis‑like inflammation by suppressing proliferation and inflammatory response of keratinocytes via inhibition of NF‑κB and JNK signaling pathways

et al. 2021

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Psoriasis is a systemic immune-mediated inflammatory disease characterized by uncontrolled keratinocyte proliferation and poor differentiation. Cinnamaldehyde (CIN) has been shown to inhibit the proliferation and inflammatory response of primary and immortalized immune cells. However, to the best of our knowledge, the role of CIN in the progression of psoriasis remains unclear. Therefore, the present study aimed to investigate the biological role of CIN in psoriasis. To mimic abnormal proliferation and differentiation in keratinocytes in vitro, normal human epidermal keratinocytes (NHEKs) were stimulated with M5 (IL-1α, IL-17A, IL-22, oncostatin M and TNF-α). The viability and proliferation of NHEKs were analyzed using Cell Counting Kit-8 and 5-Ethynyl-2'-deoxyuridine assays, respectively. Western blotting was used to analyze the expression levels of keratin 1, filaggrin and loricrin in NHEKs. The results of the present study revealed that CIN significantly inhibited the proliferation and cell cycle progression, and promoted the differentiation of M5-stimulated NHEKs. CIN also markedly attenuated the extent of oxidative stress-induced damage in M5-stimulated NHEKs. Moreover, CIN ameliorated M5-induced inflammatory injury in NHEKs, as evidenced by the decreased levels of multiple inflammatory factors. Furthermore, CIN notably downregulated the expression levels of phosphorylated (p)-inhibitor of NF-κB, p-p65 and p-JNK in M5-stimulated NHEKs. In conclusion, the present data suggested that CIN may protect NHEKs against M5-induced hyperproliferation and inflammatory injury via inhibition of NF-κB and JNK signaling pathways. These results provide a novel insight on the role of CIN in psoriasis.

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Preliminary study on the mechanism of long noncoding RNA SENCR regulating the proliferation and migration of vascular smooth muscle cells

Cited by 18 publications

References 28 publications

Long-chain noncoding RNA-GAS5/hsa-miR-138-5p attenuates high glucose-induced cardiomyocyte damage by targeting CYP11B2

Long-chain noncoding RNA-GAS5/hsa-miR-138-5p attenuates high glucose-induced cardiomyocyte damage by targeting CYP11B2

LncRNA SENCR suppresses abdominal aortic aneurysm formation by inhibiting smooth muscle cells apoptosis and extracellular matrix degradation

Cinnamaldehyde inhibits psoriasis‑like inflammation by suppressing proliferation and inflammatory response of keratinocytes via inhibition of NF‑κB and JNK signaling pathways

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