LncRNA RNCR3 promotes endothelial cell proliferation and inflammatory cytokine secretion via regulating miR-185-5p/cyclin D2 axis

Qiang, Hong; Lin, Ling; Huang, Wenli; Liu, Yilan; Zhuo, Yafen; Hong, Zhenzhen; Wu, Bing; Zhang, Yi

doi:10.1007/s11356-020-12117-9

Cited by 10 publications

(5 citation statements)

References 30 publications

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“…A previous study has reported that lncRNA RNCR3 facilitates the proliferation and secretion of inflammatory cytokines such as IL-6, IL-1β, and TNF-α in endothelial cells by binding with miR-185-5p to regulate cyclin D2 expression. 25 In our study, we also found that LINC00599 silencing reversed the CSE-induced increase in the secretion of inflammation cytokines, including TNF-α, IL-6 and IL-1β.…”

Section: Discussionsupporting

confidence: 73%

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

Dong

2022

Hum Exp Toxicol

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LINC00599 has been reported to be upregulated in response to cigarette smoking. However, the effect and underlying mechanism of LINC00599 in chronic obstructive pulmonary disease (COPD) are still under exploration. In this study, LINC00599 was upregulated in the COPD patients and was of clinical value to distinguish COPD patients. COPD cell models were established using 16HBE cells under cigarette smoke extract (CSE) treatment. LINC00599 levels were elevated in a dose and time-dependent way in response to CSE stimulation. The effect of LINC00599 on CSE-induced 16HBE cells was explored. The results showed that LINC00599 deficiency reversed the CSE-induced inhibition on cell viability and proliferation, and rescued the CSE-induced enhancement on cell 16HBE cell apoptosis and inflammation response. Moreover, LINC00599 bound with miR-212-5p to upregulate the BASP1 (brain abundant membrane attached signal protein 1) expression. MiR-212-5p was expressed at a low level in the tissue samples of COPD patients, and its levels were upregulated in LINC00599 silenced cells. BASP1 was targeted by miR-212-5p and its upregulation was identified in the tissue samples of COPD patients and cell models. BASP1 levels were downregulated after miR-212-5p overexpression or LINC00599 silencing. Moreover, the rescue assays demonstrated that BASP1 overexpression reversed the effect of silenced LINC00599 on 16HBE cells after CSE treatment, which indicated that LINC00599 promoted the COPD development by regulating BASP1 expression. In conclusion, LINC00599 facilitated CSE-induced cell apoptosis and inflammation response, while inhibiting the cell viability and proliferation in COPD progression via modulating miR-212-5p/BASP1 axis.

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Section: Discussionsupporting

confidence: 73%

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

Dong

2022

Hum Exp Toxicol

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“…Many genes have been identified as the target of miR‐185‐5p including VEGFA, 26 cyclin D2, 27 and cathepsin K 28 . Our previous study has also predicted that CDK6 and DNA methyltransferase 1 (DNMT1) are targets of miR‐185‐5p 9 .…”

Section: Discussionmentioning

confidence: 94%

“…Many genes have been identified as the target of miR‐185‐5p including VEGFA, 26 cyclin D2, 27 and cathepsin K. 28 Our previous study has also predicted that CDK6 and DNA methyltransferase 1 (DNMT1) are targets of miR‐185‐5p. 9 Here, we have further shown that miR‐185‐5p and CDK6 levels are inversely correlated on in lung tissues of hyperoxia‐insulted mice, suggesting a negative regulation of miR‐185‐5p in CDK6.…”

Section: Discussionmentioning

confidence: 99%

Umbilical cord blood–derived exosomes from healthy term pregnancies protect against hyperoxia‐induced lung injury in mice

Zhong

Wang

Chen

et al. 2023

Clinical Translational Sci

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Bronchopulmonary dysplasia (BPD) is a chronic, devastating disease primarily occurring in premature infants. To date, intervention strategies to prevent or treat BPD are limited. We aimed to determine the effects of umbilical cord blood‐derived exosomes (UCB‐EXOs) from healthy term pregnancies on hyperoxia‐induced lung injury and to identify potential targets for BPD intervention. A mouse model of hyperoxia‐induced lung injury was created by exposing neonatal mice to hyperoxia after birth until the 14th day post birth. Age‐matched neonatal mice were exposed to normoxia as the control. Hyperoxia‐induced lung injury mice were intraperitoneally injected with UCB‐EXO or vehicle daily for 3 days, starting on day 4 post birth. Human umbilical vein endothelial cells (HUVECs) were insulted with hyperoxia to establish an in vitro model of BPD to investigate angiogenesis dysfunction. Our results showed that UCB‐EXO alleviated lung injuries in hyperoxia‐insulted mice by reducing histopathological grade and collagen contents in the lung tissues. UCB‐EXO also promoted vascular growth and increased miR‐185‐5p levels in the lungs of hyperoxia‐insulted mice. Additionally, we found that UCB‐EXO elevated miR‐185‐5p levels in HUVECs. MiR‐185‐5p overexpression inhibited cell apoptosis, whereas promoted cell migration in HUVECs exposed to hyperoxia. The luciferase reporter assay results revealed that miR‐185‐5p directly targeted cyclin‐dependent kinase 6 (CDK6), which was downregulated in the lungs of hyperoxia‐insulted mice. Together, these data suggest that UCB‐EXO from healthy term pregnancies protect against hyperoxia‐induced lung injuries via promoting neonatal pulmonary angiogenesis partially by elevating miR‐185‐5p.

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“…23) ECs are an essential structure of vessels, and the anomalous proliferation of ECs may lead to the progression of some vascular disorders, like restenosis. 24) In addition, Wang et al achieved uniform controlled loading of miR-22 by dynamic porous coating and observed that the sustained release of miR-22 conspicuously enhanced the contractile phenotype of SMCs without interfering with EC proliferation and ultimately considerably restrained ISR. 11) Likewise, our study also discovered that miR-22-3p inhibitor had no remarkable influence on the proliferation of HU-VECs.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-22-3p Restrains the Proliferation, Phenotypic Transformation, and Migration of Vascular Smooth Muscle Cells by Manipulating TOMM40

Tan

Yang

Bao³

et al. 2022

Int. Heart J.

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microRNA (miR)-22-3p has been confirmed to be engaged in the phenotype transformation and proliferation of vascular smooth muscle cells (VSMCs), which is intimately correlated with restenosis. The current research set out to explore the detailed mechanism and function of miR-22-3p in VSMC proliferation, phenotype transformation, and migration via the translocase of outer mitochondrial membrane (TOMM40). Peripheral blood samples were acquired from patients with in-stent restenosis (ISR) after percutaneous coronary intervention (PCI), with subsequent quantitative reverse transcription (qRT)-polymerase chain reaction (PCR) and Western blot analyses of miR-22-3p and TOMM40 expression. After miR-22-3p-inhibitor, oe-TOMM40, and sh-TOMM40 were transfected into VSMCs, Cell Counting Kit (CCK)-8 assay, scratch test, and Western blot analysis were implemented to measure the VSMC proliferation, migration, and matrix metallopeptidase 9 (MMP9), α-smooth muscle actin (SMA), smooth muscle-myosin heavy chain (SM-MHC), and osteopontin (OPN) expressions, respectively. In addition, human umbilical vein endothelial cell (HUVEC) proliferation was examined by CCK-8 assay. The binding relationship between miR-22-3p and TOMM40 was assessed by dual luciferase reporter and RNA immunoprecipitation assays. The peripheral blood of patients with ISR after PCI had low expression of miR-22-3p and high expression of TOMM40. The mechanistic analysis reported the negative targeting relationship between miR-22-3p and TOMM40. Down-regulating miR-22-3p or up-regulating TOMM40 elevated the proliferation, migration, and phenotype transformation of VSMCs. miR-22-3p inhibitor had no evident impact on HUVEC proliferation. In addition, rescue assays displayed that TOMM40 silencing annulled miR-22-3p inhibition-enhanced VSMC proliferation, migration, and phenotype transformation. Conclusively, miR-22-3p could repress VSMC proliferation, phenotypic transformation, and migration by targeting TOMM40, which might be a possible treatment candidate for restenosis after PCI in patients with cardiovascular disease.

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LncRNA RNCR3 promotes endothelial cell proliferation and inflammatory cytokine secretion via regulating miR-185-5p/cyclin D2 axis

Cited by 10 publications

References 30 publications

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

Umbilical cord blood–derived exosomes from healthy term pregnancies protect against hyperoxia‐induced lung injury in mice

MicroRNA-22-3p Restrains the Proliferation, Phenotypic Transformation, and Migration of Vascular Smooth Muscle Cells by Manipulating TOMM40

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