MiR-106b and MiR-15b Modulate Apoptosis and Angiogenesis in Myocardial Infarction

Liu, Zhihua; Yang, Dan; Xie, Ping; Ren, Guomin; Sun, Guibo; Xu, Zhiai; Sun, Xiaobo

doi:10.1159/000258197

Cited by 85 publications

(59 citation statements)

References 54 publications

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“…MiR-15b has been associated with apoptosis and angiogenesis in myocardial infarction. 42 MiR-27b has been identified as a proangiogenic miRNA, 43 regulating angiogenesis through the angiogenic inhibitor semaphorin 6A. 44 MiR-126 is known to regulate angiogenic signaling and vascular integrity, 45 and miR-16 has been found to play a role in angiogenesis by reducing the proliferation, migration, and angiogenic capacity of endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Differential MicroRNA Expression Profiles in Peripheral Arterial Disease

Stather

Sylvius

Wild

et al. 2013

Circ Cardiovasc Genet

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Background— Peripheral arterial disease (PAD) is a clinical condition caused by an atherosclerotic process affecting the arteries of the limbs. Despite major improvements in surgical endovascular techniques, PAD is still associated with high mortality and morbidity. Recently, microRNAs (miRNAs), a class of short noncoding RNA controlling gene expression, have emerged as major regulators of multiple biological processes. Methods and Results— A whole-miRNA transcriptome profiling was performed in peripheral blood from an initial sample set of patients and controls. A 12-miRNA PAD-specific signature, which includes let 7e, miR-15b, -16, -20b, -25, -26b, -27b, -28-5p, -126, -195, -335, and -363, was further investigated and validated in 2 additional sample sets. Each of these 12 miRNAs exhibited good diagnostic value as evidenced by receiver operating characteristic curve analyses. Pathway enrichment analysis using predicted and validated targets identified several signaling pathways relevant to vascular disorders. Several of these pathways, including cell adhesion molecules, were confirmed by quantifying the expression level of several candidate genes regulating the initial stages of the inflammatory atherosclerotic process. The expression level of 7 of these candidate genes exhibits striking inverse correlation with that of several, if not all, of the miRNAs of the PAD-specific miRNA signature. Conclusions— These results demonstrate the potential of miRNAs for the diagnosis of PAD and provide further insight into the molecular mechanisms leading to the development of PAD, with the potential for future therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Differential MicroRNA Expression Profiles in Peripheral Arterial Disease

Stather

Sylvius

Wild

et al. 2013

Circ Cardiovasc Genet

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“…Other than our previously described candidates, miR-100 7 and miR-214, 10 other already well characterized modulators of blood vessel growth are among the top upregulated and downregulated genes, such as miR-106b, 8 miR-21, 9 miR-378, 21 miR-29c, 22 miR30e, 23 and miR-98 24 , whereby the last 4 named miRNAs are mainly known to modulate tumor angiogenesis. The validity of our screening approach is supported by the fact that Greco et al 25 also identified miR-29c as a downregulated miRNA in a similar setting.…”

Section: Discussionmentioning

confidence: 72%

“…Our hierarchical list of top regulated miRNAs (Tables 1 and 2) included previously described miRNA modulators of neovascularization, such as miRNA-100, 7 miRNA-106b, 8 miRNA-21, 9 and miRNA-214. 10 In addition, our experiment revealed a strong downregulation of miR-155, for which the role in adaptive blood vessel growth was so far unknown.…”

Section: Mirna Expression Profiling Reveals Mir-155 Downregulation Dumentioning

confidence: 99%

MicroRNA-155 Exerts Cell-Specific Antiangiogenic but Proarteriogenic Effects During Adaptive Neovascularization

et al. 2015

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During the course of atherosclerotic vascular disease, the adaptive growth of blood vessels is a naturally occurring process that can partly compensate for the decrease in blood flow after the narrowing or occlusion of a major artery. It includes both the sprouting of new endothelial capillaries (angiogenesis) and the enlargement of pre-existing arteriolar and arterial anastomoses to functional collateral arteries (arteriogenesis).1 During angiogenesis, a drop in tissue oxygen tension results in increased expression of hypoxiainducible transcription factors and cytokines, stimulating endothelial proliferation and sprouting in the ischemic tissue, improving distribution and use of the remaining blood flow. On the other hand, arteriogenesis is characterized by a well-orchestrated inflammatory response that is not restricted to the endothelial cell (EC) layer but facilitated by the perivascular infiltration of bone marrow-derived cell populations, mediating the proliferation of both endothelial and vascular smooth muscle cells. During the past decade, monocytes and macrophages were especially demonstrated to exert an important stimulatory function in the regulation of collateral artery growth.2 Although our knowledge about these contributing cell populations in the different forms of vascular growth steadily increases, our understanding of the basic regulatory principles controlling these processes is still limited. Other than canonical mediators of blood vessel growth, such as growth factors and their receptors, an additional functional group of regulators has recently emerged: microRNAs (miRNAs). These short (17-24 nucleotides), single-stranded regulatory RNA sequences are transcribed as precursor hairpin structures from intergenic or intronic regions of the genome that undergo several nuclear and cytoplasmatic processing steps to the mature miRNA.3 Together with Argonaute proteins, they form the RNA-induced silencing complex and recognize specific sequences mostly located in the 3′ untranslated region of their target mRNA, resulting either in inhibition of translation or degradation of Background-Adaptive neovascularization after arterial occlusion is an important compensatory mechanism in cardiovascular disease and includes both the remodeling of pre-existing vessels to collateral arteries (arteriogenesis) and angiogenic capillary growth. We now aimed to identify regulatory microRNAs involved in the modulation of neovascularization after femoral artery occlusion in mice. Methods and Results-Using microRNA-transcriptome analysis, we identified miR-155 as a downregulated microRNA during hindlimb ischemia. Correspondingly, inhibition of miR-155 in endothelial cells had a stimulatory effect on proliferation and angiogenic tube formation via derepression of its direct target gene angiotensin II type 1 receptor. Surprisingly, miR-155-deficient mice showed an unexpected phenotype in vivo, with a strong reduction of blood flow recovery after femoral artery ligation (arteriogenesis) dependent on the attenuation of leuko...

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“…By highlighting miRNA-gene networks, overall relationships between miRNAs and gene targets were discovered, particularly in apoptosis and angiogenesis. Experimental data identified miR-106b as an anti-apoptotic modulator through inhibition of p21 expression and miR-15b as an anti-angiogenic miRNA with the possible targets vascular endothelial growth factor and Ang2 (angiopoietin 2) [30] . All miRNAs with suggested role in angiogenesis in MI are summarized in Figure 2.…”

Section: Mirna In Myocardial Infarctionmentioning

confidence: 99%

miRNome in myocardial infarction: Future directions and perspective

Boštjančič

Glavač

2014

WJC

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MicroRNAs (miRNAs), which are small and non-coding RNAs, are genome encoded from viruses to humans. They contribute to various developmental, physiological and pathological processes in living organisms. A huge amount of research results revealed that miRNAs regulate these processes also in the heart. miRNAs may have cell-type-specific or tissue-specific expression patterns or may be expressed ubiquitously. Primary studies of miRNA involvement in hypertrophy, heart failure and myocardial infarction analyzed miRNAs that are enriched in or specific for cardiomyocytes; however, growing evidence suggest that other miRNAs, not cardiac or muscle-specific, play a significant role in cardiovascular disease. Abnormal miRNA regulation has been shown to be involved in cardiac diseases, suggesting that miRNAs might affect cardiac structure and function. In this review, we focus on miRNAs that have been found to contribute to the pathogenesis of myocardial infarction (MI) and the response post-MI and characterized as diagnostic, prognostic and therapeutic targets. The majority of these studies were performed using mouse and rat models of MI, with a focus on the identification of basic cellular and molecular pathways involved in MI and in the response post-MI. Much research has also been performed on animal and human plasma samples from MI individuals to identify miRNAs that are possible prognostic and/or diagnostic targets of MI and other MI-related diseases. A large proportion of research is focused on miRNAs as promising therapeutic targets and biomarkers of drug responses and/or stem cell treatment approaches. However, only a few studies have described miRNA expression in human heart tissue following MI.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: MicroRNAs; Myocardial infarction; Human; Animal models; Biomarkers and targets Core tip: MicroRNAs (miRNAs) contribute to various developmental, physiological and pathological processes in the heart. Cardiac diseases show abnormal miRNA regulation. Primary studies of miRNA involvement in cardiac disease analyzed mainly miRNAs that enriched in or specific for cardiomyocytes; however, growing evidence suggests that other cell-type-specific or ubiquitously expressed miRNAs are also involved in cardiovascular disease. miRNAs were found to contribute to the pathogenesis of myocardial infarction (MI) and post-MI. The majority of studies focused on miRNAs in animal models of MI, in human and animal plasma samples of MI (prognostic and diagnostic targets), and on miRNAs as promising therapeutic targets.Boštjančič E, Glavač D. miRNome in myocardial infarction: Future directions and perspective. World J Cardiol 2014; 6(9): 939-958 Available from:

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MiR-106b and MiR-15b Modulate Apoptosis and Angiogenesis in Myocardial Infarction

Cited by 85 publications

References 54 publications

Differential MicroRNA Expression Profiles in Peripheral Arterial Disease

Differential MicroRNA Expression Profiles in Peripheral Arterial Disease

MicroRNA-155 Exerts Cell-Specific Antiangiogenic but Proarteriogenic Effects During Adaptive Neovascularization

miRNome in myocardial infarction: Future directions and perspective

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