2017
DOI: 10.1253/circj.cj-16-1165
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MicroRNA-182 Promotes Lipoprotein Lipase Expression and Atherogenesisby Targeting Histone Deacetylase 9 in Apolipoprotein E-Knockout Mice

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Cited by 21 publications
(13 citation statements)
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“…qPCR analysis was performed as described previously. 28 Cells total RNA was extracted using TRIzol reagent (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's introduction. Reverse transcription was conducted by a High-Capacity cDNA reverse transcription kit (Takara).…”
Section: Real-time Quantitative Pcr (Qpcr) Analysismentioning
confidence: 99%
See 1 more Smart Citation
“…qPCR analysis was performed as described previously. 28 Cells total RNA was extracted using TRIzol reagent (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's introduction. Reverse transcription was conducted by a High-Capacity cDNA reverse transcription kit (Takara).…”
Section: Real-time Quantitative Pcr (Qpcr) Analysismentioning
confidence: 99%
“…Western Blot Analysis Cells were lysed in RIPA buffer (Sigma, St Louis, MO, USA) on ice for protein extraction, as described previously. 19,28 The protein content was assayed by BCA protein assay reagent (Pierce, USA). A sample of 50 µg protein was loaded to SDS-PAGE, and then transferred to the polyvinylidene difluoride (PVDF) (Millipore Corporation, USA) membranes.…”
mentioning
confidence: 99%
“…Because miR‐92a has anti‐angiogenic activity, it might be used as an atheroprotective miRNA and indicator of endothelial cell migration and the progression of atherosclerosis. MiR‐182 may promote lipid accumulation and increase apoptosis of Ox‐LDL‐induced vascular endothelial cells and inflammation in atherosclerotic lesions like miR‐92a . However, a recent study showed that miR‐182 has a significant role in inhibiting oxidative stress and apoptosis via targeting TLR‐4 in vitro (Figure C).…”
Section: Preclinical Studies Of Mirnas In Atherosclerosismentioning
confidence: 99%
“…Moreover, HDAC9 repressed cholesterol efflux by downregulating ABCA1, ABCG1, and PPARγ and alternatively promoted macrophage activation in AS (Cao et al, 2014). On the contrary, it was demonstrated that reduced expression of HDAC9 induced by miR-182 was implicated in increased levels of cholesterol, lipoprotein lipase, and proinflammatory cytokines in oxLDL-treated human THP-1 macrophages, which the author suggested might mediate the lipid accumulation in atherosclerotic lesions and thus promoted atherogenesis in ApoE −/− mice administered with miR-182 agomir (Cheng et al, 2017). Moreover, it was found that HDAC1/2/3/4/6/11 were all upregulated in atherosclerotic carotid arteries and aortas from human and ApoE −/− mice, respectively (Manea et al, 2020).…”
Section: Hdacs Regulate Atherosclerosis In Human and Animalsmentioning
confidence: 99%