The micro<scp>RNA </scp><i>miR‐124</i> inhibits vascular smooth muscle cell proliferation by targeting S100 calcium‐binding protein A4 (S100A4)

Choe, Nakwon; Kwon, Duk-Hwa; Shin, Sera; Kim, Yong Sook; Kim, Young‐Kook; Kim, Jaetaek; Ahn, Youngkeun; Eom, Gwang Hyeon; Kook, Hyun

doi:10.1002/1873-3468.12606

Cited by 41 publications

(35 citation statements)

References 43 publications

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“…These intrinsic differences are the result of adipocyte developmental origin, gene expression patterns, secretory capacity, and lipolytic activity (for review, see [27]). While traditionally AT is subdivided into WAT and BAT, there is evidence that within WAT depots, there is heterogeneity.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic Properties of Brown and White Adipocytes Have Differential Effects on Macrophage Inflammatory Responses

Dowal¹,

Parameswaran²,

Phat³

et al. 2017

Mediators of Inflammation

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Obesity is marked by chronic, low-grade inflammation. Here, we examined whether intrinsic differences between white and brown adipocytes influence the inflammatory status of macrophages. White and brown adipocytes were characterized by transcriptional regulation of UCP-1, PGC1α, PGC1β, and CIDEA and their level of IL-6 secretion. The inflammatory profile of PMA-differentiated U937 and THP-1 macrophages, in resting state and after stimulation with LPS/IFN-gamma and IL-4, was assessed by measuring IL-6 secretion and transcriptional regulation of a panel of inflammatory genes after mono- or indirect coculture with white and brown adipocytes. White adipocyte monocultures show increased IL-6 secretion compared to brown adipocytes. White adipocytes cocultured with U937 and THP-1 macrophages induced a greater increase in IL-6 secretion compared to brown adipocytes cocultured with both macrophages. White adipocytes cocultured with macrophages increased inflammatory gene expression in both types. In contrast, macrophages cocultured with brown adipocytes induced downregulation or no alterations in inflammatory gene expression. The effects of adipocytes on macrophages appear to be independent of stimulation state. Brown adipocytes exhibit an intrinsic ability to dampen inflammatory profile of macrophages, while white adipocytes enhance it. These data suggest that brown adipocytes may be less prone to adipose tissue inflammation that is associated with obesity.

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Section: Discussionmentioning

confidence: 99%

Intrinsic Properties of Brown and White Adipocytes Have Differential Effects on Macrophage Inflammatory Responses

Dowal¹,

Parameswaran²,

Phat³

et al. 2017

Mediators of Inflammation

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“…Until now, only about a dozen microRNAs had been shown to be involved in vascular calcification ( 94 95 ). Our group found that miR-124 inhibits the proliferation of VSMCs by targeting S100 calcium-binding protein A4 (S100A4), which has an important role in the proliferation of VSMCs and correlates with mineralization ( 96 97 ). In addition, our computational prediction suggests that MDM2 could also be a potential target of miR-18a.…”

Section: An Alternative Epigenetic Regulation Of Vascular Calcificatimentioning

confidence: 99%

New Aspects of Vascular Calcification: Histone Deacetylases and Beyond

2017

Self Cite

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Vascular calcification is a pathologic phenomenon in which calcium phosphate is ectopically deposited in the arteries. Previously, calcification was considered to be a passive process in response to metabolic diseases, vascular or valvular diseases, or even aging. However, now calcification is recognized as a highly-regulated consequence, like bone formation, and many clinical trials have been carried out to elucidate the correlation between vascular calcification and cardiovascular events and mortality. As a result, vascular calcification has been implicated as an independent risk factor in cardiovascular diseases. Many molecules are now known to be actively associated with this process. Recently, our laboratory found that posttranslational modification of histone deacetylase (HDAC) 1 is actively involved in the development of vascular calcification. In addition, we found that modulation of the activity of HDAC as well as its protein stability by MDM2, an HDAC1-E3 ligase, may be a therapeutic target in vascular calcification. In the present review, we overview the pathomechanism of vascular calcification and the involvement of posttranslational modification of epigenetic regulators.

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“…The microRNA expression profile in rat vessels was first described by Ji et al 12 ) , and the microRNA expression profile of human PAD was originally described in our previous study 13 – 15 ) . The cellular tropism of microRNA expression and function demonstrates that it could be an ideal potential therapeutic target for ISR 5 , 6 , 16 ) . However, direct evidence as to whether microRNAs are involved in the process of ISR in human arteries with PAD is still missing 16 ) .…”

Section: Introductionmentioning

confidence: 99%

MiR-140-3p is Involved in In-Stent Restenosis by Targeting C-Myb and BCL-2 in Peripheral Artery Disease

Zhu

et al. 2018

J Atheroscler Thromb

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Aim: In-Stent Restenosis (ISR) is the major reason for recurrent ischemia and amputation after endovascular treatment of Peripheral Artery Disease (PAD). Our previous study demonstrated that miR-140-3p is significantly down-regulated in PAD arteries. However, expression and function of miR-140-3p in ISR of human PAD are currently unclear.The aim of this study is to determine the miR-140-3p expression and its regulative role in ISR of PAD.Methods: The RNA level was determined by quantitative real-time polymerase chain Reaction (qRT-PCR) and in situ hybridization. Primary cultured ASMCs were isolated from human femoral arterial of the healthy donors or ISR patients. Cell proliferation was determined by Edu incorporation and CCK-8 assay. Apoptosis was determined by Annexin-V/PI Double-Staining assay and TUNEL assay. A rat carotid artery balloon angioplasty model was used to investigate the effect of miR-140-3p on restenosis.Results: MiR-140-3p was significantly down-regulated in PAD and ISR arteries than normal arteries. Primary cultured ISR ASMCs exhibited elevated proliferation and down-regulated miR-140-3p than normal ASMCs. Transfection of miR-140-3p mimic attenuated PDGF-BB-induced proliferation in cultured ASMCs and induced apoptosis. Luciferase reporter assay indicated that miR-140-3p transfection significantly down-regulated C-Myb and BCL-2 in ISR ASMCs by targeting to their 3′-UTRs. MiR-140-3p transfection induced anti-proliferation and apoptosis in ASMCs, which were ameliorated by over-expression of C-Myb or BCL-2. Moreover, the animal study showed that miR-140-3p can reduce restenosis following angioplasty via targeting C-Myb and BCL-2.Conclusions: The result suggests that miR-140-3p regulates ASMC function via targeting C-Myb and BCL-2 in the process of ISR in PAD. The novel findings may offer a hopeful therapeutic target for human PAD.

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The microRNA miR‐124 inhibits vascular smooth muscle cell proliferation by targeting S100 calcium‐binding protein A4 (S100A4)

Cited by 41 publications

References 43 publications

Intrinsic Properties of Brown and White Adipocytes Have Differential Effects on Macrophage Inflammatory Responses

Intrinsic Properties of Brown and White Adipocytes Have Differential Effects on Macrophage Inflammatory Responses

New Aspects of Vascular Calcification: Histone Deacetylases and Beyond

MiR-140-3p is Involved in In-Stent Restenosis by Targeting C-Myb and BCL-2 in Peripheral Artery Disease

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