Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis

Hua, Wei; Cao, Cong; Wei, Xiaojuan; Meng, Minglv; Wu, Biaoliang; Meng, Lianxin; Wang, Xi; Gu, Shi-Xing; Li, Hong-Mian

doi:10.18632/aging.103478

Cited by 24 publications

(13 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CircVEGFC is a novel circRNA with critical functions in high glucose-induced cell injury. 15 It was reported that…”

Section: Discussionmentioning

confidence: 99%

“…[12][13][14] Circular RNA vascular endothelial growth factor C (circVEGFC) is novel regulator of glucose metabolism. 15 CircVEGFC can promote high glucose-induced injuries of vascular endothelial cells by interacting with the miR-338-3p/HIF-1α/VEGFA axis, 15 while its role in GDM is unknown. This study aimed to detect the expression of circVEGFC in GDM and explore its clinical values.…”

Section: Introductionmentioning

confidence: 99%

“…circVEGFC may interact with the miR-338-3p/HIF-1α/ VEGFA axis to promote the injuries of vascular endothelial cells induced by high glucose. 15 It is well established that high glucose-induced cell injuries contribute to the development of GDM and its complications. 16 Therefore, circVEGFC is likely involved in GDM.…”

mentioning

confidence: 99%

See 2 more Smart Citations

CircRNA circVEGFC is Highly Expressed in Gestational Diabetes Mellitus (GDM) and It is Correlated with Multiple Adverse Events

She¹,

Li²,

Liu³

et al. 2021

DMSO

View full text Add to dashboard Cite

“…CircVEGFC is a novel circRNA with critical functions in high glucose-induced cell injury. 15 It was reported that…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

CircRNA circVEGFC is Highly Expressed in Gestational Diabetes Mellitus (GDM) and It is Correlated with Multiple Adverse Events

She¹,

Li²,

Liu³

et al. 2021

DMSO

View full text Add to dashboard Cite

“…Thus, inhibiting apoptosis-associated endothelial dysfunction may ameliorate dM-induced vascular complications (6)(7)(8). The association between high glucose (HG) stimulation and endothelial apoptosis has been extensively studied (9)(10)(11), as HG is a typical characteristic of dM.…”

Section: Introductionmentioning

confidence: 99%

Isoquercitrin protects HUVECs against high glucose‑induced apoptosis through regulating p53 proteasomal degradation

Liu

Huang

et al. 2021

Int J Mol Med

View full text Add to dashboard Cite

High glucose (HG)-induced endothelial apoptosis serves an important role in the vascular dysfunction associated with diabetes mellitus (dM). It has been reported that isoquercitrin (IQC), a flavonoid glucoside, possesses an anti-DM effect, but the mechanism requires further investigation. The present study investigated the effect of IQc against HG-induced apoptosis in human umbilical vein endothelial cells (HUVEcs) and explored its molecular mechanism. HUVEcs were treated with 5 or 30 mM glucose for 48 h. Endothelial cell viability was monitored using the cell counting Kit-8 assay. Mitochondrial membrane potential was detected by Jc-1 staining. Apoptosis was observed by TUNEL staining and flow cytometry. Western blotting was used for the analysis of apoptosis-associated proteins Bax, Bcl-2, cleaved (c)-caspase3, total-caspase3, p53 and phosphorylated p53. Reverse transcription-quantitative PcR was used to analyze the mRNA expression levels of Bax, Bcl-2 and p53. Immunofluorescence staining was utilized to detect the expression levels and distribution of p53 and ubiquitin specific peptidase 10 (USP10) in HUVEcs. The results revealed that IQC significantly attenuated HG-induced endothelial apoptosis, as shown by decreased apoptotic cells observed by TUNEL, Jc-1 staining and flow cytometry. Moreover, under HG stress, IQc treatment markedly inhibited the increased expression levels of the pro-apoptotic proteins p53, Bax and c-caspase3, and increased the expression levels of the anti-apoptotic protein Bcl-2 in HUVEcs. However, the anti-apoptotic effect of IQc against HG was partially blunted by increasing p53 protein levels in vitro. IQC influenced the mRNA expression levels of Bax and Bcl-2 in response to HG, but it did not affect the transcription of p53. Notably, IQc inhibited the HG-induced phosphorylation of p53 at Ser15 and the nuclear transport of USP10, destabilizing p53 and increasing the proteasomal degradation of the p53 protein. The current findings revealed that IQC exerted a protective effect against the HG-induced apoptosis of endothelial cells by regulating the proteasomal degradation of the p53 protein, suggesting that IQc may be used as a novel therapeutic compound to ameliorate dM-induced vascular complications.

show abstract

“…For example, Cheng et al highlighted that has_circ_0068087 was highly expressed in HG-triggered human umbilical vein endothelial cells (HUVECs) and regulated HG-induced cell dysfunction by acting as an miR-197 sponge ( Cheng et al, 2019 ). Wei et al demonstrated that circRNA vascular endothelial growth factor C (circVEGFC) promoted HG-induced apoptosis in HUVECs through the regulation of miR-338-3p ( Wei et al, 2020 ). Pan et al uncovered that has_circ_0054633 protected HUVECs against HG-induced dysfunction by modulating heme oxygenase-1 (HO-1) expression via sponging miR-218 ( Pan et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Circ_CLASP2 Regulates High Glucose-Induced Dysfunction of Human Endothelial Cells Through Targeting miR-140-5p/FBXW7 Axis

Zhang

Long

et al. 2021

Front. Pharmacol.

View full text Add to dashboard Cite

Hyperglycemia exposure results in the dysfunction of endothelial cells (ECs) and the development of diabetic complications. Circular RNAs (circRNAs) have been demonstrated to play critical roles in EC dysfunction. The current study aimed to explore the role and mechanism of circRNA CLIP–associating protein 2 (circ_CLASP2, hsa_circ_0064772) on HG-induced dysfunction in human umbilical vein endothelial cells (HUVECs). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the levels of circ_CLASP2, miR-140-5p and F-box, and WD repeat domain-containing 7 (FBXW7). The stability of circ_CLASP2 was identified by the actinomycin D and ribonuclease (RNase) R assays. Cell colony formation, proliferation, and apoptosis were measured by a standard colony formation assay, colorimetric 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) assay, and flow cytometry, respectively. Western blot analysis was performed to determine the expression of related proteins. Targeted correlations among circ_CLASP2, miR-140-5p, and FBXW7 were confirmed by dual-luciferase reporter assay. High glucose (HG) exposure downregulated the expression of circ_CLASP2 in HUVECs. Circ_CLASP2 overexpression or miR-140-5p knockdown promoted proliferation and inhibited apoptosis of HUVECs under HG conditions. Circ_CLASP2 directly interacted with miR-140-5p via pairing to miR-140-5p. The regulation of circ_CLASP2 overexpression on HG-induced HUVEC dysfunction was mediated by miR-140-5p. Moreover, FBXW7 was a direct target of miR-140-5p, and miR-140-5p regulated HG-induced HUVEC dysfunction via FBXW7. Furthermore, circ_CLASP2 mediated FBXW7 expression through sponging miR-140-5p. Our current study suggested that the overexpression of circ_CLASP2 protected HUVEC from HG-induced dysfunction at least partly through the regulation of the miR-140-5p/FBXW7 axis, highlighting a novel therapeutic approach for the treatment of diabetic-associated vascular injury.

show abstract

Circular RNA circVEGFC accelerates high glucose-induced vascular endothelial cells apoptosis through miR-338-3p/HIF-1α/VEGFA axis

Cited by 24 publications

References 25 publications

CircRNA circVEGFC is Highly Expressed in Gestational Diabetes Mellitus (GDM) and It is Correlated with Multiple Adverse Events

CircRNA circVEGFC is Highly Expressed in Gestational Diabetes Mellitus (GDM) and It is Correlated with Multiple Adverse Events

Isoquercitrin protects HUVECs against high glucose‑induced apoptosis through regulating p53 proteasomal degradation

Circ_CLASP2 Regulates High Glucose-Induced Dysfunction of Human Endothelial Cells Through Targeting miR-140-5p/FBXW7 Axis

Contact Info

Product

Resources

About