Post-Translational Modification of Adiponectin Affects Lipid Accumulation, Proliferation and Migration of Vascular Smooth Muscle Cells

Chen, Xinzhong; Yuan, Yanhong; Wang, Qin; Xie, Fei; Xia, Dongsheng; Wang, Xianguo; Wei, Yongzhong; Xie, Ting

doi:10.1159/000480336

Cited by 9 publications

(4 citation statements)

References 22 publications

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“…Adiponectin ( ADIPOQ ) is a kind of adipocytokine mainly secreted by adipose tissue. Through the action of ADIPOR1 and ADIPOR2 , it can activate the signaling pathway of AMPK and PPAR α and inhibit lipid synthesis 31 , 32 . Recently, researchers also found that some factors (such as ATGL and HSL ) can act downstream of AMPK and mediate the lipid-lowering effect of ADIPOQ 33 .…”

Section: Discussionmentioning

confidence: 99%

Different expression of lipid metabolism-related genes in Shandong black cattle and Luxi cattle based on transcriptome analysis

Liu

Bai

et al. 2020

Sci Rep

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To provide new ideas for improving meat quality and generating new breeds of cattle, the important candidate genes affecting fat deposition in two kinds of cattle were identified. Eighteen months Shandong black cattle (n = 3) and Luxi cattle (n = 3) were randomly assigned into two environmental. The longissimus dorsi muscles of Shandong Black Cattle and Luxi Cattle were collected and analyzed by fatty acid determination, high-throughput sequencing transcriptomics, qRT-PCR expression profile and western blot. The ratio of unsaturated fatty acids to saturated fatty acids was 1.37:1 and 1.24:1 in the muscle tissues of Shandong black cattle and Luxi cattle, respectively. The results of RNA-Seq analysis revealed 1320 DEGs between the longissimus dorsi of Shandong black cattle and Luxi cattle. A total of 867 genes were upregulated, and the other 453 genes were downregulated. With GO enrichment analysis, it was found that the identified DEGs were significantly enriched in regulation of the Wnt signaling pathway, negative regulation of the Wnt signaling pathway, cAMP metabolic process, fat cell differentiation and among other functions. We found that regulation of lipolysis in adipocytes was the significant enrichment pathway of upregulated genes and downregulated genes, PPAR signaling pathway and AMPK signaling pathway are highly representative pathways of lipid metabolism in Shandong black cattle. Network analysis showed that PPARGC1A, ADCY4, ANKRD6, COL1A1, FABP4, ADIPOQ, PLIN1, PLIN2, and LIPE genes were correlated with key loci genes in multiple metabolic pathways. Meanwhile we found that FABP4 and ADIPOQ had 7 common regulatory factors in different genes, which were PLIN1, PLIN2, PPARGC1A, RXRA, PCK1, LEPR, LEP. These genes were involved in regulation of lipolysis in adipocytes, adipocytokine signaling pathway, PPAR signaling pathway. FABP4 and ADIPOQ were selected as important candidate marker genes for fat deposition based on the results.

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Section: Discussionmentioning

confidence: 99%

Different expression of lipid metabolism-related genes in Shandong black cattle and Luxi cattle based on transcriptome analysis

Liu

Bai

et al. 2020

Sci Rep

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“… 141 Adiponectin also inhibits growth factor- and oxidized low-density lipoprotein-stimulated VSMC proliferation and migration. 142 , 143 Notably, an orally administered adiponectin receptor agonist decreased intimal hyperplasia in mice and inhibited PDGF-induced VSMC proliferation. 144 In models of restenosis and atherosclerosis, recombinant adiponectin decreased inflammation, oxidative stress, and apoptosis.…”

Section: Potential New Avenues For Therapeutic Modulation Of Smc Phenotype In Intimal Hyperplasiamentioning

confidence: 99%

Targeting smooth muscle cell phenotypic switching in vascular disease

Chakraborty

Chatterjee

Dave

et al. 2021

JVS-Vascular Science

102

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Objective The phenotypic plasticity of vascular smooth muscle cells (VSMCs) is central to vessel growth and remodeling, but also contributes to cardiovascular pathologies. New technologies including fate mapping, single cell transcriptomics, and genetic and pharmacologic inhibitors have provided fundamental new insights into the biology of VSMC. The goal of this review is to summarize the mechanisms underlying VSMC phenotypic modulation and how these might be targeted for therapeutic benefit. Methods We summarize findings from extensive literature searches to highlight recent discoveries in the mechanisms underlying VSMC phenotypic switching with particular relevance to intimal hyperplasia. PubMed was searched for publications between January 2001 and December 2020. Search terms included VSMCs, restenosis, intimal hyperplasia, phenotypic switching or modulation, and drug-eluting stents. We sought to highlight druggable pathways as well as recent landmark studies in phenotypic modulation. Results Lineage tracing methods have determined that a small number of mature VSMCs dedifferentiate to give rise to oligoclonal lesions in intimal hyperplasia and atherosclerosis. In atherosclerosis and aneurysm, single cell transcriptomics reveal a striking diversity of phenotypes that can arise from these VSMCs. Mechanistic studies continue to identify new pathways that influence VSMC phenotypic plasticity. We review the mechanisms by which the current drug-eluting stent agents prevent restenosis and note remaining challenges in peripheral and diabetic revascularization for which new approaches would be beneficial. We summarize findings on new epigenetic (DNA methylation/TET methylcytosine dioxygenase 2, histone deacetylation, bromodomain proteins), transcriptional (Hippo/Yes-associated protein, peroxisome proliferator-activity receptor-gamma, Notch), and β3-integrin-mediated mechanisms that influence VSMC phenotypic modulation. Pharmacologic and genetic targeting of these pathways with agents including ascorbic acid, histone deacetylase or bromodomain inhibitors, thiazolidinediones, and integrin inhibitors suggests potential therapeutic value in the setting of intimal hyperplasia. Conclusions Understanding the molecular mechanisms that underlie the remarkable plasticity of VSMCs may lead to novel approaches to treat and prevent cardiovascular disease and restenosis.

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“…It also suppresses the proliferation of HASMCs by decreasing the phosphorylation of RAF1, ERK1/2, and NF-κB as well as increasing AMPK expression [10] . Osmotin exerts the same suppressive effects of adiponectin and AdipoRon on the migration and proliferation of VSMCs [42][43][44] .…”

Section: Preventive Effects Of Osmotin On the Migration And Proliferamentioning

confidence: 97%

Therapeutic properties of the new phytochemical osmotin for preventing atherosclerosis

Watanabe¹

2020

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Post-Translational Modification of Adiponectin Affects Lipid Accumulation, Proliferation and Migration of Vascular Smooth Muscle Cells

Cited by 9 publications

References 22 publications

Different expression of lipid metabolism-related genes in Shandong black cattle and Luxi cattle based on transcriptome analysis

Different expression of lipid metabolism-related genes in Shandong black cattle and Luxi cattle based on transcriptome analysis

Targeting smooth muscle cell phenotypic switching in vascular disease

Therapeutic properties of the new phytochemical osmotin for preventing atherosclerosis

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