Apoptotic cell induction of miR-10b in macrophages contributes to advanced atherosclerosis progression in ApoE−/− mice

Wang, Dongliang; Wang, Wenting; Lin, Weiqun; Yang, Wenqi; Zhang, Peiwen; Chen, Ming; Ding, Ding; Liu, Chaoqun; Zheng, Jiakun; Liu, Wenhua

doi:10.1093/cvr/cvy132

Cited by 32 publications

(26 citation statements)

References 49 publications

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“…Macrophages are considered as major inflammatory cells during the formation of AS (27,28). Macrophages can develop into foam cells, and the lipid nucleus is formed after necrosis of foam cells, which is a major component of atherosclerotic plaques (29). In addition, macrophages are also the major inflammatory cellular components in atherosclerotic plaques, and a variety of pro-inflammatory factors secreted by them alter the local environment of plaques and affect the plaque WT group, # P<0.05 vs. ApoE -/group.…”

Section: Discussionmentioning

confidence: 99%

“…WT, C57BL/6 mouse group; ApoE -/-, ApoE -/mouse group; ApoE -/-+ Tac, ApoE -/mouse + tacrolimus intervention group; IL, interleukin; NLRP3, Nod-like receptor protein 3; ROS, reactive oxygen species; DHE, dihydroethidium; ASC, apoptosis-associated speck-like protein containing CARD; Casp-1, caspase-1. stability and disease development (27,29). The collagen fibers produced by smooth muscle cells migrating to plaques are the main source of fibrous caps in plaques, and smooth muscle cells in the fibrous cap are decreased (30,31).…”

Section: Discussionmentioning

confidence: 99%

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Tacrolimus reduces atherosclerotic plaque formation in ApoE-/- mice by inhibiting NLRP3 inflammatory corpuscles

Xiao¹,

Shang²,

Sun³

2019

Exp Ther Med

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Effect of tacrolimus on atherosclerotic plaques and its influence on Nod-like receptor protein 3 (NLRP3) inflammatory pathway were studied by establishing the mouse model of atherosclerosis. The mice were divided into 3 groups: C57BL/6 mouse group (WT group), ApoE-/mouse group (ApoE-/group) and ApoE-/mouse + tacrolimus intervention group (ApoE-/-+ Tac group). The area of atherosclerotic plaques and the pathological morphologic changes were observed. The NLRP3, interleukin-1β (IL-1β), IL-18, NLRP3 inflammatory corpuscles, pro-inflammatory factors IL-1β and IL-18 in the aorta were analyzed. The area of atherosclerotic plaques in ApoE-/mice was increased significantly, and it was significantly reduced after tacrolimus intervention. After tacrolimus intervention, the arterial intima became obviously thinner and no obvious cholesterol crystals were observed. The macrophage infiltration in atherosclerotic plaques was significantly increased, and the content of smooth muscle cells was also increased. The levels of serum IL-1β, IL-18 and NLRP3 in ApoE-/mice were significantly increased, and they remarkably declined after tacrolimus intervention. ROS content in atherosclerotic plaques was increased in ApoE-/mice, and it remarkably declined after tacrolimus intervention. The protein content of NLRP3, ASC, Casp-1, IL-1β and IL-18 in the aorta in ApoE-/mice was remarkably increased, and they were inhibited to some extent after tacrolimus intervention. In conclusion, it is speculated that tacrolimus may reduce the formation of AS through inhibiting ROS in macrophages and activation of NLRP3 inflammatory corpuscles and reducing the release of IL-1β and IL-18.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Tacrolimus reduces atherosclerotic plaque formation in ApoE-/- mice by inhibiting NLRP3 inflammatory corpuscles

Xiao¹,

Shang²,

Sun³

2019

Exp Ther Med

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“…Conversely, miR-10b appears to play a deleterious role in advanced atherosclerosis as human atherosclerotic plaques express higher levels of miR-10b compared to healthy arteries without atherosclerosis 98 . Moreover, inhibition of miR-10b suppressed progression of established aortic and brachiocephalic plaques in Apoe-deficient mice which was associated with increased intra-plaque macrophage ABCA1 expression (and by inference improved cholesterol efflux) and diminished macrophage apoptosis, resulting in plaques with more stable characteristics, however no beneficial effects of miR-10b silencing were observed on atherogenesis within the same model 157 . miR-19: Similarly to miR-10b, miR-19b has been shown to specifically target and down-regulate ABCA1 expression within macrophages and therefore retard cholesterol efflux and drive foam cell formation 158 .…”

Section: Macrophages Mir-10mentioning

confidence: 94%

Non-coding RNAs in cardiovascular cell biology and atherosclerosis

Fasolo

Gregoli

Maegdefessel

et al. 2019

Cardiovascular Research

170

101

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Atherosclerosis underlies the predominant number of cardiovascular diseases and remains a leading cause of morbidity and mortality worldwide. The development, progression and formation of clinically relevant atherosclerotic plaques involves the interaction of distinct and over-lapping mechanisms which dictate the roles and actions of multiple resident and recruited cell types including endothelial cells, vascular smooth muscle cells, and monocyte/macrophages. The discovery of non-coding RNAs (ncRNAs) including microRNAs, long non-coding RNAs, and circular RNAs, and their identification as key mechanistic regulators of mRNA and protein expression has piqued interest in their potential contribution to atherosclerosis. Accruing evidence has revealed ncRNAs regulate pivotal cellular and molecular processes during all stages of atherosclerosis including cell invasion, growth, and survival; cellular uptake and efflux of lipids, expression and release of pro- and anti-inflammatory intermediaries, and proteolytic balance. The expression profile of ncRNAs within atherosclerotic lesions and the circulation have been determined with the aim of identifying individual or clusters of ncRNAs which may be viable therapeutic targets alongside deployment as biomarkers of atherosclerotic plaque progression. Consequently, numerous in vivo studies have been convened to determine the effects of moderating the function or expression of select ncRNAs in well-characterized animal models of atherosclerosis. Together, clinicopathological findings and studies in animal models have elucidated the multifaceted and frequently divergent effects ncRNAs impose both directly and indirectly on the formation and progression of atherosclerosis. From these findings’ potential novel therapeutic targets and strategies have been discovered which may pave the way for further translational studies and possibly taken forward for clinical application.

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“…The upregulation of miR‐24 and its binding to any of the targets, tribbles‐like protein‐3 (Trb3), chitinase 3 Like 1 (Chi3l1) and matrix metallopeptidase 14 (MMP‐14), causes the VSMC phenotype switching and induction of atherosclerosis . Thus, unlike miR‐10b that is active in advanced atherosclerosis progression, miR‐24 is active in the early plaque evolution . In addition, miR‐208 and miR‐17 are pro‐atherosclerosis markers that their expression increase VSMC proliferation by downregulating p21 and very low‐density lipoprotein receptor (VLDLR) targets respectively .…”

Section: Preclinical Studies Of Mirnas In Atherosclerosismentioning

confidence: 99%

Diagnostic and theranostic microRNAs in the pathogenesis of atherosclerosis

Shoeibi

2019

Acta Physiologica

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MicroRNAs (miRNAs) are a group of small single strand and noncoding RNAs that regulate several physiological and molecular signalling pathways. Alterations of miRNA expression profiles may be involved with pathophysiological processes underlying the development of atherosclerosis and cardiovascular diseases, including changes in the functions of the endothelial cells and vascular smooth muscle cells, such as cell proliferation, migration and inflammation, which are involved in angiogenesis, macrophage function and foam cell formation. Thus, miRNAs can be considered to have a crucial role in the progression, modulation and regulation of every stage of atherosclerosis. Such potential biomarkers will enable us to predict therapeutic response and prognosis of cardiovascular diseases and adopt effective preclinical and clinical treatment strategies. In the present review article, the current data regarding the role of miRNAs in atherosclerosis were summarized and the potential miRNAs as prognostic, diagnostic and theranostic biomarkers in preclinical and clinical studies were further discussed. The highlights of this review are expected to present opportunities for future research of clinical therapeutic approaches in vascular diseases resulting from atherosclerosis with an emphasis on miRNAs. K E Y W O R D Satherosclerosis, diagnosis, miRNA, prognosis, therapeutic approaches 2 of 24 | SHOEIBI Because miRNAs have a relatively high stability under the physiological conditions of mammals, they can be used as prognostic and diagnostic markers for diseases, such as atherosclerosis. This review aims to describe and summarize miRNA expression studies in model animal experiments and clinical practices related to atherosclerosis. The expressed pattern of miRNAs contributing to atherosclerosis at different stages of the atherosclerotic process in comparison with healthy arteries is also discussed.

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Apoptotic cell induction of miR-10b in macrophages contributes to advanced atherosclerosis progression in ApoE−/− mice

Abstract: These data suggest that apoptotic cell induction of miR-10b in macrophages is important in advanced atherosclerosis progression.

Cited by 32 publications

References 49 publications

Tacrolimus reduces atherosclerotic plaque formation in ApoE-/- mice by inhibiting NLRP3 inflammatory corpuscles

Tacrolimus reduces atherosclerotic plaque formation in ApoE-/- mice by inhibiting NLRP3 inflammatory corpuscles

Non-coding RNAs in cardiovascular cell biology and atherosclerosis

Diagnostic and theranostic microRNAs in the pathogenesis of atherosclerosis

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