MicroRNA-101 overexpression by IL-6 and TNF-α inhibits cholesterol efflux by suppressing ATP-binding cassette transporter A1 expression

Zhang, Nan; Lei, Jiayan; Lv, Han; Ruan, Xiongzhong; Liu, Qing; Chen, Yaxi; Huang, Wei

doi:10.1016/j.yexcr.2015.05.023

Cited by 64 publications

(34 citation statements)

References 35 publications

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“…IL-6 and TNF-α inhibit cholesterol efflux by suppressing ABCA1 expression (23). IL-1β has been demonstrated to promote lipid accumulation and inhibit cholesterol efflux in human mesangial cells by dysregulating the expression of lipoprotein receptors, thus inhibiting cholesterol efflux through the PPAR-LXRα-ABCA1 pathway (24).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux

Dong²,

Feng

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Interleukin-32 (IL-32) is a pro-inflammatory cytokine and its effects in various inflammatory diseases have been investigated. However, the role of IL-32 on atherosclerosis, an inflammatory disease, remains unknown. The present study examined the use of IL-32α, the most abundant transcript of IL-32, in the treatment of oxidized low-density lipoprotein (ox-LDL)-stimulated THP-1 macrophages for 24 h, which simulates a foam cell formation model. The effect of IL-32α (20, 50 and 100 ng/ml) on lipid deposition in the macrophages was analyzed using Oil Red O staining, while the cholesterol efflux on apolipoprotein A-I was also measured. The mRNA and protein expression levels of peroxisome proliferator-activated receptor γ (PPARγ), liver X receptor α (LXRα), ATP-binding cassette transporter A1 (ABCA1) and ABCG1 were quantified by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. The results indicated that IL-32α exposure enhanced the lipid deposition and attenuated the cholesterol efflux from ox-LDL-stimulated THP-1 macrophages in a dose-dependent manner. Furthermore, the expression levels of ABCA1, LXRα and PPARγ were dose-dependently decreased by IL-32α at the mRNA and protein levels. Addition of the PPARγ agonist 15d-PGJ2 or overexpression of PPARγ in THP-1 macrophages abrogated the IL-32α-mediated inhibition of cholesterol efflux and reversed the IL-32α-mediated downregulation of ABCA1 and LXRα. In conclusion, IL-32α enhances lipid accumulation and inhibits cholesterol efflux from ox-LDL-exposed THP-1 macrophages by regulating the PPARγ-LXRα-ABCA1 pathway.

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Section: Discussionmentioning

confidence: 99%

Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux

Dong²,

Feng

et al. 2017

Experimental and Therapeutic Medicine

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“…These include miR-758 (42), miR-26 (43), miR-106b (44), miR-10b (45), miR-144 (46,47), and miR-101 (48). We propose that studies are now warranted to address whether these microRNAs exert similar ABCA1-dependent actions on proinflammatory cytokine induction by TLRs.…”

Section: Mir-33 Regulates the Innate Immune Responsementioning

confidence: 99%

MicroRNA-33 Regulates the Innate Immune Response via ATP Binding Cassette Transporter-mediated Remodeling of Membrane Microdomains

Lai

Azzam

Lin

et al. 2016

Journal of Biological Chemistry

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MicroRNAs (miRNAs) 3 are small (ϳ22-nucleotide) noncoding RNAs that regulate gene expression by binding to partially complementary sites in the 3Ј-untranslated regions (UTRs) of specific mRNAs, thereby promoting degradation and/or repressing translation of target mRNAs. The human genome contains Ͼ2500 unique mature miRNAs (1). Because individual miRNAs typically have multiple targets, it is thought that Ͼ60% of all human genes may be subject to regulation by miRNAs (2). The promiscuity of miRNAs for target RNAs is expected to represent a fundamental mechanism of cross-talk and coordination among signaling networks in development, health, and disease.Among the signaling networks that have been shown in recent years to be regulated by miRNAs are the Toll-like receptors (TLRs) of the innate immune system. Multiple TLRs up-regulate miRNAs, including miR-155, miR-146, miR-21, miR-147, and miR-9, whereas activation of TLR4 by lipopolysaccharide (LPS) down-regulates a distinct set of miRNAs (3, 4). In turn, miRNAs "fine tune" the proinflammatory signaling output of TLR cascades by controlling the expression of TLR pathway members (3, 4). Thus, miR-146 suppresses signaling by multiple TLRs via targeting the common signaling hubs IL-1 receptor-associated kinase 1 and TNF receptor-associated factor 6 (5), whereas miR-155 has complex effects, repressing the TLR adaptor myeloid differentiation primary response 88 (MyD88) (6, 7) and TAK1-binding protein 2 (8), an upstream activator of the mitogen-activated protein kinases, but also promoting cytokine expression through actions on other targets (3). Although virtually all known examples of TLR regulation by miRNAs operate through direct targeting of TLR pathway components, it is expected that miRNAs may also indirectly impact the innate immune response by regulating other networks that cross-talk with TLRs.miR-33a and miR-33b (present in primates but absent in rodents and lower species in which miR-33a is simply referred to as "miR-33") are now known to be master regulators of cho-

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“…Apart from the miRNAs discussed above, numerous other miRNAs including miR-19b, miR-106b, miR-93, miR-101 have been described to have an impact on ABCA1 expression and HDL-C metabolism under different physiological stimuli 68–72 . Interestingly, gut microbiota metabolism of anthocyanin modulates RCT by modifying miR-10b expression.…”

Section: Other Mirnas That Regulate Hdl-c Metabolismmentioning

confidence: 99%

Micro-RNAs and High-Density Lipoprotein Metabolism

Canfrán‐Duque

Lin

Goedeke

et al. 2016

ATVB

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Improved prevention and treatment of cardiovascular diseases (CVD) is one of the challenges in Western societies, where ischemic heart disease and stroke are the leading cause of death. Early epidemiological studies have shown an inverse correlation between circulating high-density lipoprotein cholesterol (HDL-C) and cardiovascular disease (CVD). The cardioprotective effect of HDL is due to its ability to remove cholesterol from plaques in the artery wall to the liver for excretion by a process known as reverse cholesterol transport (RCT). Numerous studies have reported the role that microRNAs (miRNAs) play in the regulation of the different steps in RCT, including HDL biogenesis, cholesterol efflux, cholesterol uptake in the liver and bile acid synthesis and secretion. Due to their ability to control different aspects of HDL metabolism and function, miRNAs have emerged as potential therapeutic targets to combat CVDs. In this review, we summarize the recent advances in the miRNA-mediated control of HDL metabolism. We also discuss how HDL particles serve as carriers of miRNAs and the potential use of HDL-containing miRNAs as CVD biomarkers.

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MicroRNA-101 overexpression by IL-6 and TNF-α inhibits cholesterol efflux by suppressing ATP-binding cassette transporter A1 expression

Cited by 64 publications

References 35 publications

Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux

Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux

MicroRNA-33 Regulates the Innate Immune Response via ATP Binding Cassette Transporter-mediated Remodeling of Membrane Microdomains

Micro-RNAs and High-Density Lipoprotein Metabolism

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