MicroRNA-9 is an activation-induced regulator of PDGFR-beta expression in cardiomyocytes

Jian-hu, Zhang; Chintalgattu, Vishnu; Shih, Tiffany; Ai, Di; Xia, Ying; Khakoo, Aarif Y.

doi:10.1016/j.yjmcc.2011.05.019

Cited by 33 publications

(19 citation statements)

References 33 publications

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“…Although bioinformatics reveal over 1,000 target genes with predicted miR-9 seed sites in their 3 0 -UTR, the presence of a conserved seed is not sufficient to indicate a true biologic interaction between miR-9 and putative target genes (40). In this study, our experimental evidence showed that MMP-14 was a target of miR-9.…”

Section: Discussionmentioning

confidence: 67%

microRNA-9 Targets Matrix Metalloproteinase 14 to Inhibit Invasion, Metastasis, and Angiogenesis of Neuroblastoma Cells

Zhang

et al. 2012

Molecular Cancer Therapeutics

139

156

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Matrix metalloproteinase (MMP)-14 is the only membrane-anchored MMP that plays a critical role in tumor metastasis and angiogenesis. However, the mechanisms underlying MMP-14 expression in tumors still remain largely unknown. In this study, MMP-14 immunostaining was identified in 29/42 neuroblastoma tissues, which was correlated with clinicopathologic features and shorter patients' survival. In subtotal 20 neuroblastoma cases, microRNA 9 (miR-9) was downregulated and inversely correlated with MMP-14 expression. Bioinformatics analysis revealed a putative miR-9-binding site in the 3 0 -untranslated region (3 0 -UTR) of MMP-14 mRNA. Overexpression or knockdown of miR-9 responsively altered both the mRNA and protein levels of MMP-14 and its downstream gene, vascular endothelial growth factor, in cultured neuroblastoma cell lines SH-SY5Y and SK-N-SH. In an MMP-14 3 0 -UTR luciferase reporter system, miR-9 downregulated the luciferase activity, and these effects were abolished by a mutation in the putative miR-9-binding site. Overexpression of miR-9 suppressed the invasion, metastasis, and angiogenesis of SH-SY5Y and SK-N-SH cells in vitro and in vivo. In addition, the effects of miR-9 on MMP-14 expression, adhesion, migration, invasion, and angiogenesis were rescued by overexpression of MMP-14 in these cells. Furthermore, anti-miR-9 inhibitor or knockdown of MMP-14 respectively increased or inhibited the migration, invasion, and angiogenesis of neuroblastoma cells. These data indicate that miR-9 suppresses MMP-14 expression via the binding site in the 3 0 -UTR, thus inhibiting the invasion, metastasis, and angiogenesis of neuroblastoma.

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Section: Discussionmentioning

confidence: 67%

microRNA-9 Targets Matrix Metalloproteinase 14 to Inhibit Invasion, Metastasis, and Angiogenesis of Neuroblastoma Cells

Zhang

et al. 2012

Molecular Cancer Therapeutics

139

156

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“…Previous studies in inflammation revealed the importance of miR-9 in LPS mediated release of proinflammatory cytokines, and its progressive role in cancer metastasis [29–31]. Recent studies have implicated MiR-9 in cardiac hypertrophy [32, 33]. However, the role of miR-9 in DCM or HG induced inflammation and cardiac pyroptosis and its effect on cardiovascular diseases is very limited.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1

Jeyabal

Thandavarayan

Joladarashi

et al. 2016

Biochemical and Biophysical Research Communications

134

106

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Diabetic cardiomyopathy is a common complication in patients with diabetes and is associated with underlying chronic inflammation and cardiac cell death, subsequently leading to heart failure (HF). ELAV-like protein 1 (ELAVL1) plays a critical role in the progression of inflammation and HF. However the role of ELAVL-1 in inflammation induced cardiac cell death (pyroptosis) under hyper glycemic condition remains elusive. Our data demonstrates that ELAVL1 expression augmented with a concomitant increase in caspase-1 and IL-1 beta expression in human hearts and human ventricular cardiomyocytes under hyperglycemic condition. Furthermore, ELAVL1 knockdown abrogates TNF-α induced canonical pyroptosis via NLRP3, caspase-1 and IL-1beta suppression. Bioinformatics analysis and target validation assays showed that miR-9 directly targets ELAVL1. Interestingly, miRNA-9 expression significantly reduced in high glucose treated cardiomyocytes and in human diabetic hearts. Inhibition of miR-9 upregulates ELAVL1 expression and activates caspase-1. Alternatively, treatment with miR-9 mimics attenuates hyperglycemia-induced ELAVL1 and inhibits cardiomyocyte pyroptosis. Taken together our study highlights the potential therapeutic implications of targeting miR-9/ELAVL1 in preventing cardiomyocyte cell loss during HF in diabetics.

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“…50 This miRNA has also been implicated in regulating cancer cell proliferation and metastasis and has been associated with cardiotoxicity through regulation of platelet-derived growth factor receptor b expression. [51][52][53] Recently, miR-9 expression was shown to be induced by high-dose (100 ng/mL) LPS in primary human polymorphonuclear neutrophils and monocytes in a myeloid differentiation primary response gene 88-and nuclear factor kB-dependent manner. 54 Furthermore, miR-9-dependent inhibition of NFKB1 transcription suggests that the rapid induction of miR-9 operates as a feedback control of nuclear factor kB-dependent responses in these cells.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-9 regulates steroid-resistant airway hyperresponsiveness by reducing protein phosphatase 2A activity

Tay

Maltby

et al. 2015

Journal of Allergy and Clinical Immunology

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MicroRNA-9 is an activation-induced regulator of PDGFR-beta expression in cardiomyocytes

Cited by 33 publications

References 33 publications

microRNA-9 Targets Matrix Metalloproteinase 14 to Inhibit Invasion, Metastasis, and Angiogenesis of Neuroblastoma Cells

microRNA-9 Targets Matrix Metalloproteinase 14 to Inhibit Invasion, Metastasis, and Angiogenesis of Neuroblastoma Cells

MicroRNA-9 inhibits hyperglycemia-induced pyroptosis in human ventricular cardiomyocytes by targeting ELAVL1

MicroRNA-9 regulates steroid-resistant airway hyperresponsiveness by reducing protein phosphatase 2A activity

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