New Insights Into miR-17–92 Cluster Regulation and Angiogenesis

Fiedler, Jan; Thum, Thomas

doi:10.1161/circresaha.115.307935

Cited by 26 publications

(20 citation statements)

References 15 publications

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“…MicroRNAs have been widely investigated to regulate vascularization through various signaling [33,34]. MiR-17, a potential inhibitor of VEGF, has been reported to be associated with periodontal regeneration [21,22,24] and tissue angiogenesis [23].…”

Section: Discussionmentioning

confidence: 99%

“…Numerous micro-RNAs (miRNAs) were investigated to play significant roles in dental tissues [20]. MiR-17, an inhibitor of VEGF, is a crucial microRNA associated with bone remodeling and angiogenesis [21][22][23][24]. Our previous study demonstrated that miR-17 regulated periodontal tissue regeneration via PDLSCs-mediated pathway in chronic periodontitis [21,22,24].…”

Section: Ivyspringmentioning

confidence: 99%

See 1 more Smart Citation

PDLSCs Regulate Angiogenesis of Periodontal Ligaments via VEGF Transferred by Exosomes in Periodontitis

Zhang

Zhou

et al. 2020

Int. J. Med. Sci.

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Abnormal angiogenesis is one of the significant features in periodontitis leading to progressive inflammation, but angiogenic changes of periodontal ligaments under inflammatory condition were rarely reported. Periodontal ligament stem cells (PDLSCs) were a kind of dental stem cells associated with vascularization. Here we investigated the alteration of angiogenesis of periodontal ligament in periodontitis, and revealed an exosome-mediated pathway to support the effect of PDLSCs on angiogenic improvement. Vascular specific marker CD31 and VEGFA were found to be highly expressed in periodontal ligaments of periodontitis. The VEGFA expression was up-regulated in inflamed PDLSCs compared to control, meanwhile the tube formation of HUVECs was improved when co-cultured with inflamed PDLSCs. Exosomes secretion of PDSLCs was augmented by inflammation, and promoted angiogenesis of HUVECs, whereas blocking secretion of exosomes led to degenerated angiogenesis of HUVECs. Exosome-trasferred VEGFA was proven to be the crucial communicator between PDLSCs and HUVECs. Inflammation inhibited miR-17-5p expression of PDLSCs and relieved its target VEGFA. However, overexpression of miR-17-5p blocked the pro-angiogenic ability of inflamed PDLSCs. In conclusion, the findings indicated that vascularization of periodontal ligaments was enhanced, and inflammatory micro-environment of periodontitis facilitated pro-angiogenesis of PDLSCs through regulating exosome-mediated transfer of VEGFA, which was targeted by miR-17-5p.

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Section: Discussionmentioning

confidence: 99%

Section: Ivyspringmentioning

confidence: 99%

PDLSCs Regulate Angiogenesis of Periodontal Ligaments via VEGF Transferred by Exosomes in Periodontitis

Zhang

Zhou

et al. 2020

Int. J. Med. Sci.

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“…Since then, this view has become widely accepted as the way in which miRNAs regulate gene expression for the last 20 years. miRNAs are found to be involved in numerous biological processes and diverse disease pathogenesis, such as cell differentiation and development, cell cycle and state, immune response, tumorigenesis, neurological disorders, and metabolic diseases [3] , [4] , [5] , [6] , [7] , [8] , [9] , [10] . Therefore, profound understanding of miRNA regulation in all these biological activities and diseases would undoubtedly facilitate unraveling the underlying mechanisms and developing new therapeutic methods for diseases.…”

Section: Mirnas and Their Functionsmentioning

confidence: 99%

Steering Against Wind: A New Network of NamiRNAs and Enhancers

Zou

2017

Genomics, Proteomics &Amp; Bioinformatics

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MicroRNAs (miRNAs) are a class of endogenous non-coding RNAs with regulatory functions. Traditionally, miRNAs are thought to play a negative regulatory role in the cytoplasm by binding to the 3′UTR of target genes to degrade mRNA or inhibit translation. However, it remains a challenge to interpret the potential function of many miRNAs located in the nucleus. Recently, we reported a new type of miRNAs present in the nucleus, which can activate gene expression by binding to the enhancer, and named them nuclear activating miRNAs (NamiRNAs). The discovery of NamiRNAs showcases a complementary regulatory mechanism of miRNA, demonstrating their differential roles in the nucleus and cytoplasm. Here, we reviewed miRNAs in nucleus to better understand the function of NamiRNAs in their interactions with the enhancers. Accordingly, we propose a NamiRNA–enhancer–target gene activation network model to better understand the crosstalk between NamiRNAs and enhancers in regulating gene transcription. Moreover, we hypothesize that NamiRNAs may be involved in cell identity or cell fate determination during development, although further study is needed to elucidate the underlying mechanisms in detail.

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“…Researches of miRNAs in angiogenesis and thrombosis have been paid widespread attention [9]. The miR-17-92 cluster (miR-17, miR-18a, miR-19a/b, miR-20a, and miR-92a) is highly expressed in endothelial cells, which regulate vascular endothelial function [10][11][12]. miR-92a can promote atherosclerosis by upregulating proinflammatory signaling in endothelial cells [13].…”

Section: Introductionmentioning

confidence: 99%

Role of miR-92a-3p, oxidative stress, and p38MAPK/NF-κB pathway in rats with central venous catheter related thrombosis

Gan

Zhao

Yan

et al. 2020

BMC Cardiovasc Disord

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Background: miR-92a-3p and oxidative stress are reportedly associated with venous thrombosis. However, the role of miR-92a-3p and oxidative stress in catheter-related thrombosis (CRT) remains ambiguous. Herein, we studied the roles of miR-92a-3p, oxidative stress, and p38-mitogen-activated protein kinase/nuclear factor kappa-B (MAPK/NF-κB) pathway in CRT. Methods: Forty-five male rats were randomly and equally divided into control, sham operation, and CRT groups. The rats were sacrificed after 10 days. Reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) levels in the serum were determined by enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-92a-3p, heme oxygenase-1 (HO-1), NF-κB p65, and p38 MAPK in the venous tissues were detected with quantitative polymerase chain reaction (qPCR) and Western blot. Results: Thrombosis was observed only in the CRT group. Compared with the levels in the control and sham operation groups, ROS and MDA significantly increased in the CRT group, but SOD significantly decreased. qPCR and Western blot results showed that miR-92a-3p, HO-1, p38 MAPK, and NF-κB p65 expression was significantly upregulated in the venous tissues of the CRT group. Moreover, miR-92a-3p was positively correlated with HO-1, which was positively correlated with p38 MAPK and NF-κB p65. Conclusion: miR-92a-3p was correlated with oxidative stress in CRT. miR-92a-3p and oxidative stress contributed to endothelial dysfunction and simultaneously was associated with CRT.

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New Insights Into miR-17–92 Cluster Regulation and Angiogenesis

Cited by 26 publications

References 15 publications

PDLSCs Regulate Angiogenesis of Periodontal Ligaments via VEGF Transferred by Exosomes in Periodontitis

PDLSCs Regulate Angiogenesis of Periodontal Ligaments via VEGF Transferred by Exosomes in Periodontitis

Steering Against Wind: A New Network of NamiRNAs and Enhancers

Role of miR-92a-3p, oxidative stress, and p38MAPK/NF-κB pathway in rats with central venous catheter related thrombosis

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