Acarbose inhibits the proliferation and migration of vascular smooth muscle cells via targeting Ras signaling

Yu, Meng-Hsun; Lin, Ming‐Cheng; Huang, Chien‐Ning; Chan, Kuei-Chuan; Wang, Chau‐Jong

doi:10.1016/j.vph.2018.02.001

Cited by 22 publications

(22 citation statements)

References 41 publications

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“…Therefore, the changes imposed by acarbose treatment are also affected by the starting gut communities in the animals, which then restrict the potential changes that are observed. Recently, acarbose therapy was evaluated in animal models for the treatment of a variety of other conditions, including cardiovascular disease and cognition (62, 63). As we learn more about how human disease is affected by the intestinal bacterial community, the interplay between medications such as acarbose and the diet will become increasingly important to evaluate.…”

Section: Discussionmentioning

confidence: 99%

The Glucoamylase Inhibitor Acarbose Has a Diet-Dependent and Reversible Effect on the Murine Gut Microbiome

Baxter

Lesniak

Sinani

et al. 2019

mSphere

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The gut microbial community has a profound influence on host physiology in both health and disease. In diabetic individuals, the gut microbiota can affect the course of disease, and some medications for diabetes, including metformin, seem to elicit some of their benefits via an interaction with the microbiota. Here, we report that acarbose, a glucoamylase inhibitor for type 2 diabetes, changes the murine gut bacterial community structure in a reversible and diet-dependent manner. In both high-starch and high-fiber diet backgrounds, acarbose treatment results in increased short-chain fatty acids, particularly butyrate, as measured in stool samples. As we learn more about how human disease is affected by the intestinal bacterial community, the interplay between medications such as acarbose and the diet will become increasingly important to evaluate.

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Section: Discussionmentioning

confidence: 99%

The Glucoamylase Inhibitor Acarbose Has a Diet-Dependent and Reversible Effect on the Murine Gut Microbiome

Baxter

Lesniak

Sinani

et al. 2019

mSphere

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“…A study demonstrated FAK-mediated monocyte adhesion to endothelial cells by up-regulating VCAM-1 induced by ox-LDL (Yurdagul et al, 2016), which is consistent with our experimental results, the expression of VCAM-1 and ICAM-1, and activation of FAK were increased in HUVECs under ox-LDL stimulation in vitro, pretreated with Rg3 in ox-LDL stimulated HUVECs significantly suppressed FAK activation and VCAM-1 and ICAM-1 expression in a dose-dependent manner, indicating that Rg3 may play a role in protecting endothelial function by repressing FAK activation. Furthermore, FAK is highly conserved during evolution and widely expressed in different cells, FAK protein levels are increased in adipocytes of insulin-resistant mice which relate to adipose tissue expansion, leading to obese (Luk et al, 2017), FAK also can be activated by TNF-a in vascular smooth muscle cells which is involved in the process of atherosclerosis restenosis (Yu et al, 2018), suggesting that activation of FAK may increase not only in abnormal vascular endothelial cells and smooth muscle cells, but also in whole aorta of atherosclerotic ApoE −/− mice (Chen et al, 2018). In this study, activation of FAK was remarkable increased in gross aorta of ApoE −/− mice, while the ICAM-1 and VCAM-1 expression were increased mainly derived from vascular endothelium, and study confirmed that ICAM-1 and VCAM-1 were the endothelial-derived ligands may recruit monocytes, dendritic cells, T cells by binding to the integrin very late antigen-4 and lymphocyte function-associated antigen-1 expressed in these immune cells (Wu et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE−/− Mice by Regulating PPARγ/FAK Signaling Pathway

Geng

et al. 2020

Front. Pharmacol.

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The initiation of atherosclerosis (AS) induced by dyslipidemia is accompanied by endothelial dysfunction, including decreased healing ability and increased recruitment of monocytes. Studies showed ginsenoside Rg3 has potential to treat diseases associated with endothelial dysfunction which can protects against antineoplastic drugs induced cardiotoxicity by repairing endothelial function, while the effect and mechanism of Rg3 on dyslipidemia induced endothelial dysfunction and AS are not clear. Therefore, we investigated the effects of Rg3 on oxidized low-density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) dysfunction and high-fat diets (HFD) induced atherosclerosis in ApoE −/− mice, as well as the mechanism. For in vitro assay, Rg3 enhanced healing of HUVECs and inhibited human monocytes (THP-1) adhesion to HUVECs disturbed by ox-LDL, down-regulated focal adhesion kinase (FAK)-mediated expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1); restrained the FAK-mediated non-adherent dependent pathway containing matrix metalloproteinase (MMP)-2/9 expression, activation of nuclear factorkappa B (NF-kB), high mRNA levels of monocyte chemotactic protein 1 (MCP-1) and interleukin 6 (IL-6), besides Rg3 up-regulated peroxisome proliferators-activated receptor g (PPARg) in ox-LDL-stimulated HUVECs. GW9662, the PPARg-specific inhibitor, can repressed the effects of Rg3 on ox-LDL-stimulated HUVECs. For in vivo assay, Rg3 significantly reduced atherosclerotic pathological changes in ApoE −/− mice fed with HFD, up-regulated PPARg, and inhibited activation FAK in aorta, thus inhibited expression of VCAM-1, ICAM-1 in intima. We conclude that Rg3 may protect endothelial cells and inhibit atherosclerosis by up-regulating PPARg via repressing FAK-mediated pathways, indicating that Rg3 have good potential in preventing dyslipidemia induced atherosclerosis.

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“…4, among the these speci c genes and pathways, previous studies showed that MMP-14, ICAM-1, TLR4, and Ras signaling pathway, AMPK signaling pathway play important roles in the development and progression of atherosclerosis, (i.e. proliferation and migration of vascular smooth cells), while modulating vascular remodeling and in ammation [31][32][33][34][35]. Hence, the miRNA-gene-GO network and miRNA-gene-KEGG network diagram provide novel avenue for searching for potential diagnostic biomarkers, and also provide a novel direction for assessing the mechanism of these miRNAs in ISR.…”

Section: Discussionmentioning

confidence: 99%

MicroRNAs Expression Profiles in Platelet-Derived Exosomes From Coronary In-Stent Restenosis and the Potential Markers

Hua¹,

Qiao²,

Li³

et al. 2021

Preprint

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Background: We conducted this study was to identify any difference in platelet-derived exosome micro-RNA (microRNA) profile between patients with in-stent restenosis and patients without restenosis using gene sequencing.Method: Platelet-derived exosomes(PDEs) were isolated through ultracentrifugation and validated by Western blotting, transmission electron microscope and NanoSight analysis. The platelet-derived exosome microRNA expression profile was identified by Illumina Hiseq2000/2500 sequencing, and validated by qRT-PCR. Finally, the potential functions of microRNAs were predicted using miRNA-gene-GO network and miRNA-gene-KEGG network. Result: We identified several differentially expressed platelet-derived exosome microRNAs. In particular, we found that the microRNA PC-3p-75179_24 was up-regulated, while hsa-miR-133a-3p_R+1 and hsa-miR-589-5p_R-1 were down-regulated in patients with in-stent restenosis which were further validated by qRT-PCR results. Our results also showed their potential miRNA-gene-GO and miRNA-gene-KEGG interaction.Conclusion: In summary, our study reveals for the first time microRNA expression is altered, in platelet-derived exosomes in patients with in-stent restenosis, with specific up-regulation of microRNA PC-3p-75179_24 and down-regulation of hsa-miR-133a-3p_R+1 and hsa-miR-589-5p_R-1. Our findings supports the need to explore the potential of these microRNAs as biomarkers and the pathological effects on in-stent restenosis.

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Acarbose inhibits the proliferation and migration of vascular smooth muscle cells via targeting Ras signaling

Cited by 22 publications

References 41 publications

The Glucoamylase Inhibitor Acarbose Has a Diet-Dependent and Reversible Effect on the Murine Gut Microbiome

The Glucoamylase Inhibitor Acarbose Has a Diet-Dependent and Reversible Effect on the Murine Gut Microbiome

Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE−/− Mice by Regulating PPARγ/FAK Signaling Pathway

MicroRNAs Expression Profiles in Platelet-Derived Exosomes From Coronary In-Stent Restenosis and the Potential Markers

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