2014
DOI: 10.1007/s10557-014-6533-x
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MiR-132 Inhibits Expression of SIRT1 and Induces Pro-inflammatory Processes of Vascular Endothelial Inflammation through Blockade of the SREBP-1c Metabolic Pathway

Abstract: SIRT1 mRNAs are direct targets of miR-132. miR-132 controls lipogenesis and cholesterogenesis in HUVECs by inhibiting SIRT1 and SREBP-1c expression and their downstream regulated genes, including FASN and HMGCR. Inhibition of SIRT1 by miR-132 was associated with lipid metabolism-dependent pro-inflammatory processes in HUVECs. The newly identified miRNA, miR-132 represents a novel targeting mechanism for AS therapy.

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Cited by 62 publications
(38 citation statements)
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“…The impacts of NGR1 on miRNA expression might be via both genomic (transcriptional) and non-genomic mechanisms of action. Furthermore, we selected miR-132 for use in the follow-up rescue assays, since miR-132 has been reported to promote TNF-α-induced inflammation and cell death of HUVECs [34]. Besides, Kumarswamy and his colleagues have mentioned that deletion of miR-212/132 cluster increased endothelial vasodilatory function [35].…”
Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning
confidence: 99%
“…The impacts of NGR1 on miRNA expression might be via both genomic (transcriptional) and non-genomic mechanisms of action. Furthermore, we selected miR-132 for use in the follow-up rescue assays, since miR-132 has been reported to promote TNF-α-induced inflammation and cell death of HUVECs [34]. Besides, Kumarswamy and his colleagues have mentioned that deletion of miR-212/132 cluster increased endothelial vasodilatory function [35].…”
Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning
confidence: 99%
“…In addition, miR-19b plays a key role in the attenuation of TNF- α -induced EC apoptosis, and this function is closely linked to the Apaf1/caspase-7-dependent pathway [22]. Nevertheless, miR-132 promoted apoptosis of HUVEC induced by TNF- α and inhibited its proliferation, viability, and migration by inhibiting SIRT1 [23]. …”
Section: Mirnas and Vascular Agingmentioning
confidence: 99%
“…miR-214 overexpression resulted in the inhibition of HUVEC migration, sprout formation and tubule formation on Matrigel ® in vitro , whereas anti-miR-214 induced the opposite effects. Interestingly, EC proliferation and viability were not affected by modulating miR-214 levels [77]. …”
Section: Mechanisms Of Mirnas In the Regulation Of Normal Cardiovascumentioning
confidence: 99%
“…Upregulation of miR-132 increases cell migration and viability, proliferation, and induces apoptosis in HUVECs. miR-132 also promotes TNFα-induced proinflammatory processes of ECs [77]. …”
Section: Mechanisms Of Mirnas In the Regulation Of Normal Cardiovascumentioning
confidence: 99%