Ghrelin inhibits high glucose-induced 16HBE cells apoptosis by regulating Wnt/β-catenin pathway

Liu, Xiaoyan; Chen, Dilong; Wu, Zhongjun; Li, Jing; Li, Jianqiang; Zhao, Hui; Liu, Tanzhen

doi:10.1016/j.bbrc.2016.06.156

Cited by 11 publications

(11 citation statements)

References 30 publications

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“…Consistent with a previous study (15), it was demonstrated that high glucose elicited cell death of HUVECs. Apoptosis of HUVECs occurs following high glucose treatment (22,23). Kinase signaling pathways are important in the regulation of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effects of reduced β2 glycoprotein I on high glucose-induced cell death in HUVECs

Zhang

et al. 2017

Molecular Medicine Reports

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Reduced β2 glycoprotein I (β2GPI) has been demonstrated to exhibit a beneficial effect in diabetic atherosclerosis and retinal neovascularization. However, the effect of reduced β2GPI on vascular disorders in diabetic mellitus (DM) remains to be elucidated. The present study established a high glucose‑induced injury model using human umbilical cords veins (HUVECs) and evaluated the protective effects of reduced β2GPI against the injury. The data demonstrated that a low concentration of reduced β2GPI (0.5 µM) mitigated high glucose‑induced cell loss, decreased nitric oxide (NO) production and resulted in calcium overloading. Mechanically, reduced β2GPI additionally reversed high glucose‑induced phosphatase and tensin homolog (PTEN) accumulation, decrease of protein kinase B phosphorylation and nitric oxide synthase activity, and increase of cyclooxygenase‑2 activity. It was further confirmed that PTEN inhibitor‑bpV (1 µM) exhibited similar effects to those resulting from reduced β2GPI. Overall, the data revealed that reduced β2GPI exerts protective effects from glucose‑induced injury in HUVECs, potentially via decreasing PTEN levels. The present study suggests reduced β2GPI may act as a novel therapeutic strategy for the treatment of vascular disorders in DM.

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Section: Discussionmentioning

confidence: 99%

Effects of reduced β2 glycoprotein I on high glucose-induced cell death in HUVECs

Zhang

et al. 2017

Molecular Medicine Reports

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“…Extensive research has shown that various factors play an important role in endothelial dysfunction in T2DM, including aging, obesity, hypertension, hyperlipidemia, hyperglycemia, low-grade inflammation, and insulin resistance 4–6. The most recent investigations have been focused on effective approaches to prevent hyperglycemia-induced endothelial cell injury 7–9. However, lowering glucose levels is not enough to turn off the oxidative damage in vascular endothelial cells induced by high glucose 10.…”

Section: Introductionmentioning

confidence: 99%

<p>mRNAs expression profiles of high glucose-induced memory in human umbilical vein endothelial cells</p>

Jin¹,

Wang²,

Pei³

et al. 2019

DMSO

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Purpose: A long-term "memory" of hyperglycemic stress, even when glycemia is normalized, has been previously reported in endothelial cells. However, the molecular mechanism of "metabolic memory" (MM) remains unknown. In this report, we sought to screen at the whole transcriptome level the genes that participate in MM. Methods: In the present research, RNA sequencing was used to determine the proteincoding mRNA expression profiles of human umbilical vein endothelial cells (HUVECs) under normal-glucose concentration (LG), high-glucose concentration (HG), and MM. A series of bioinformatic analyses was performed. HG-induced MM-involved up-regulated genes (up-HGMMGs) and HG-induced MM-involved down-regulated genes (down-HGMMGs) were identified. Afterward, based on up-HGMMGs and down-HGMMGs, the biological functions and signaling pathways were analyzed using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). In addition, several of the identified genes were validated by RT-qPCR. Results: A total of 726 HGMMGs were identified, including 210 down-and 516 up-HGMMGs, which were enriched in the cell cycle (hsa04110), oocyte meiosis (hsa04114), p53 signaling pathway (hsa04115), and oxidative phosphorylation (hsa00190), among others. The protein-protein-interaction (PPI) network consisted of 462 nodes and 2656 connections, and four main modules were identified by MCODE. The cell cycle (hsa04110), oocyte meiosis (hsa04114), p53 signaling pathway (hsa04115), and oxidative phosphorylation (hsa00190), among others, could be potential therapeutic targets of HG-induced MM in endothelial cells. The real-time PCR results validated the RNA-seq data. Conclusion: This study identified crucial mRNAs related to MM-persistent injury in endothelial cells even after switching the cells from high-glucose to normal glucose levels. Further research focusing on these mRNA may unravel new ways to modify MM in diabetes.

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“…Extensive studies have revealed that various factors, including aging, obesity, hypertension, hyperlipidemia, hyperglycemia, low‐grade inflammation, and insulin resistance, play a significant role in endothelial dysfunction in T2DM . Since vascular endothelial cells play a major role in maintaining cardiovascular homeostasis, more investigations are now focused on effective approaches to prevent hyperglycemia‐induced endothelial cell injury .…”

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confidence: 99%

Profiling and functional analysis of differentially expressed circular RNAs in high glucose‐induced human umbilical vein endothelial cells

Jin

Wang

et al. 2019

FEBS Open Bio

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Dysfunction of vascular endothelial cells often results in diabetic vascular complications. Circular RNAs (circRNAs) have been implicated in the pathogenesis of various diseases, including diabetes and many vascular diseases. This study aimed to explore the roles of circRNAs in high glucose‐induced human umbilical vein endothelial cells (HUVECs) to elucidate the contributions of circRNAs to diabetic vascular complications. We subjected control and high glucose‐induced HUVECs to RNA sequencing and identified 214 differentially expressed circRNAs (versus control HUVECs, fold change ≥ 2.0, P < 0.05). We then validated seven of these differentially expressed circRNAs by qPCR ( hsa_circ_0008360 , hsa_circ_0005741 , hsa_circ_0003250 , hsa_circ_0045462 , hsa_circ_0064772 , hsa_circ_0007976 , and hsa_circ_0005263 ). A representative circRNA–microRNA (miRNA) network was constructed using the three most up‐regulated circRNAs ( hsa_circ_0008360 , hsa_circ_0000109 , and hsa_circ_0002317 ) and their putative miRNA. Bioinformatic analysis indicated that these circRNAs regulate the expressions of genes involved in vascular endothelial function and angiogenesis through targeting miRNAs. Our work highlights the potential regulatory mechanisms of three crucial circRNAs in diabetes‐associated endothelial dysfunction.

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Ghrelin inhibits high glucose-induced 16HBE cells apoptosis by regulating Wnt/β-catenin pathway

Cited by 11 publications

References 30 publications

Effects of reduced β2 glycoprotein I on high glucose-induced cell death in HUVECs

Effects of reduced β2 glycoprotein I on high glucose-induced cell death in HUVECs

<p>mRNAs expression profiles of high glucose-induced memory in human umbilical vein endothelial cells</p>

Profiling and functional analysis of differentially expressed circular RNAs in high glucose‐induced human umbilical vein endothelial cells

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