Down-regulation of miR-377 suppresses high glucose and hypoxia-induced angiogenesis and inflammation in human retinal endothelial cells by direct up-regulation of target gene SIRT1

Cui, Chunmei; Li, Yuehua; Liu, Ying

doi:10.1007/s13577-019-00240-w

Cited by 33 publications

(18 citation statements)

References 40 publications

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“…Besides, miR-377 relieves the cerebral inflammation and thereby lessens the ischemic brain injuries [15]. Similar results were observed in renal ischemia-reperfusion injury mice model [16] and retinal endothelial cell model [26]. It would be tempting to explore whether miR-377 was regulated by Mirt2.…”

Section: Discussionsupporting

confidence: 59%

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

Xin

Liang

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: The interaction of long non-coding RNAs (lncRNAs)-microRNAs (miRs) exerts crucial functions in mediating inflammatory reaction. It is still unclear whether myocardial infarction associated transcript 2 (Mirt2)-miR-377 mediates the inflammatory pathogenesis in Sj€ ogren's syndrome (SS). Methods: The inflammatory lesion model was established by stimulating salivary gland epithelial cells (SGECs) by interferon gamma (IFN-c). Mirt2-and/or miR-377-transfected SGECs, as well as their negative controls, were applied to investigate the biological functions in inflammation. Cell viability and apoptosis were examined using commercial kits. Western blot was applied to quantify protein level, and enzyme-linked immuno sorbent assay (ELISA) was used to value the secretion of cytokines. Results: The up-regulation of Mirt2 was observed in IFN-c-treated SGECs. Mirt2 overexpression restored the expression of miR-377 which was repressed by IFN-c. However, miR-377 silence abolished the protective effect on cell viability, inhibitory effect on apoptosis and prohibitive role in pro-inflammatory factors. Mirt2 diminished the phosphorylated expression of crucial regulators while miR-377 silence restored the phosphorylation in IFN-c-treated SGECs. Conclusion: Mirt2 was elevated in IFN-c-treated SGECs and then up-regulated miR-377 in response to inflammatory lesions. Mechanically, in synergy with miR-377 Mirt2 blocked IFN-c-evoked activation of NF-jB and JAK/STAT signalling pathway. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 59%

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

Xin

Liang

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Substantial evidence has demonstrated the critical roles of p65 in the process of GDM, as well as in the related inflammation and angiogenesis processes ( Kuzmicki et al., 2013 ; Cui et al., 2019 ). Consistent with the phenomena observed in previous studies, in our study, we observed an elevated p65 level in peripheral blood subjected to GDM ( Figure 5A ).…”

Section: Resultsmentioning

confidence: 99%

Metformin Ameliorates Gestational Diabetes Mellitus-Induced Endothelial Dysfunction via Downregulation of p65 and Upregulation of Nrf2

et al. 2020

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Gestational diabetes mellitus (GDM) causes oxidative stress in mothers and infants and causes vascular endothelial dysfunction, which is a key factor for maternal and fetal cardiovascular diseases in the later stage of GDM, seriously threatening the life and health of mothers and infants. Nowadays, metformin (MET) has been discovered to improve endothelial function, but studies regarding the mechanism of MET improving endothelial cell function and alleviating endothelial function under hyperglycemia are still extremely limited. We aimed to investigate whether MET exerts its protective role against hyperglycemia-induced endothelial dysfunction through p65 and Nrf2. In our studies, applying cell migration assay and tube formation assay, we observed an obvious improvement of endothelial function under MET-treated, as characterized by that MET accelerated GDM-attenuated migration and angiogenesis of HUVECs. And ELISA assay results uncovered that Nrf2 expression level was decreased in GDM placenta, HVUECs and maternal serum comparing with normal group, however activation Nrf2 largely ameliorated tube formation under hyperglycemic condition. Furthermore, MET elevated the Nrf2 expression level and the level of nuclear Nrf2 accumulation in hyperglycemic HUVECs. Besides, preliminary evidence predicted that Nrf2 expression was modulated by transcription factor p65, which was increased in GDM peripheral blood, placenta and HUVECs, and suppression of p65 could recover GDM-induced suppression of angiogenesis. In addition, we also confirmed MET restores the GDM-induced angiogenesis impairment may via downregulation of p65 and upregulation of Nrf2. Taken together, the endothelial protective effect of MET under GDM (HG) conditions could be partly attributed to its role in downregulating p65 and upregulating Nrf2.

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“…10,11 miR-377, as a multifunctional miRNA which targets many genes, is involved in inflammation, oxidative stress, and angiogenesis and closely related to myocardial regeneration. 12,13 Recent evidence has showed that miR-377 was downmodulated in cerebral ischemic injury, indicating its potential participation in ischemia/reperfusion (I/R). 14 Previous work by researchers has presented that depletion of miR-377 alleviated brain inflammation and heightened angiogenesis in reaction to cerebral ischemia.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-377 Alleviates Myocardial Injury Induced by Hypoxia/Reoxygenation via Downregulating LILRB2 Expression

Xie

et al. 2020

Dose-Response

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Background: miR-377 is closely related to myocardial regeneration. miR-377-adjusted mesenchymal stem cells abducted ischemic cardiac angiogenesis. Nevertheless, there were rarely reports about the impact of miR-377 on myocardial ischemia injury. The purpose of this work is that whether miR-377 can protect against myocardial injury caused by hypoxia/reoxygenation (H/R). Methods: Gene expression omnibus database ( http://www.ncbi.nlm.nih.gov/geo/ ; no. GSE53211) was utilized to study the differential expression of miR-377 in patients with an acute ST-segment elevation myocardial infarction and healthy controls. The luciferase activity was determined utilizing the dual-luciferase reporter system. Quantitative real-time polymerase chain reaction and Western blotting were used to measure the messenger RNA and protein level. Results: Low expression of miR-377 and high expression of leukocyte immunoglobulin-like receptor B2 (LILRB2) were identified in patients with myocardial infarction from analyzing the Gene Expression Omnibus data set. Besides, miR-377 expression was downregulated in cardiomyocyte exposed to H/R. Additionally, overexpression of miR-377 could visibly improve cardiomyocyte injury by regulating cell activity and apoptosis. Conclusions: In short, our findings suggested that miR-377/LILRB2 might regard as a hopeful therapeutic target for myocardial ischemic.

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Down-regulation of miR-377 suppresses high glucose and hypoxia-induced angiogenesis and inflammation in human retinal endothelial cells by direct up-regulation of target gene SIRT1

Cited by 33 publications

References 40 publications

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

RETRACTED ARTICLE: Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome

Metformin Ameliorates Gestational Diabetes Mellitus-Induced Endothelial Dysfunction via Downregulation of p65 and Upregulation of Nrf2

MicroRNA-377 Alleviates Myocardial Injury Induced by Hypoxia/Reoxygenation via Downregulating LILRB2 Expression

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