scholarly journals Effect of Fermented Platycodon grandiflorum Extract on Cell Proliferation and Migration in Bovine Aortic Endothelial Cells

2016 ◽  
Vol 26 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Woosoung Choi ◽  
Jina Song ◽  
Mi-Hyeon Park ◽  
Heui Jong Yu ◽  
Heonyong Park
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Aortic Endothelial Cells ◽  
Platycodon Grandiflorum ◽  
Cell Proliferation And Migration ◽  
Bovine Aortic Endothelial Cells ◽  
And Migration ◽  
Proliferation And Migration ◽  
Aortic Endothelial

Angiopoietin-1 promotes endothelial cell proliferation and migration through AP-1–dependent autocrine production of interleukin-8

Blood ◽  
2008 ◽  
Vol 111 (8) ◽  
pp. 4145-4154 ◽  
Author(s):  
Nelly A. Abdel-Malak ◽  
Coimbatore B. Srikant ◽  
Arnold S. Kristof ◽  
Sheldon A. Magder ◽  
John A. Di Battista ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Interleukin 8 ◽  
Endothelial Cell Migration ◽  
Endothelial Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration ◽  
Angiopoietin 1

Abstract Angiopoietin-1 (Ang-1), ligand for the endothelial cell–specific Tie-2 receptors, promotes migration and proliferation of endothelial cells, however, whether these effects are promoted through the release of a secondary mediator remains unclear. In this study, we assessed whether Ang-1 promotes endothelial cell migration and proliferation through the release of interleukin-8 (IL-8). Ang-1 elicited in human umbilical vein endothelial cells (HUVECs) a dose- and time-dependent increase in IL-8 production as a result of induction of mRNA and enhanced mRNA stability of IL-8 transcripts. IL-8 production is also elevated in HUVECs transduced with retroviruses expressing Ang-1. Neutralization of IL-8 in these cells with a specific antibody significantly attenuated proliferation and migration and induced caspase-3 activation. Exposure to Ang-1 triggered a significant increase in DNA binding of activator protein-1 (AP-1) to a relatively short fragment of IL-8 promoter. Upstream from the AP-1 complex, up-regulation of IL-8 transcription by Ang-1 was mediated through the Erk1/2, SAPK/JNK, and PI-3 kinase pathways, which triggered c-Jun phosphorylation on Ser63 and Ser73. These results suggest that promotion of endothelial migration and proliferation by Ang-1 is mediated, in part, through the production of IL-8, which acts in an autocrine fashion to suppress apoptosis and facilitate cell proliferation and migration.

Abstract 633: Protein Kinase D Regulates VEGFR-2 Transcriptional Activity in Endothelial Cells Through AP-2β

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Luke H Hoeppner ◽  
Resham Bhattacharya ◽  
Ying Wang ◽  
Ramcharan Singh Angom ◽  
Enfeng Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Heart Disease ◽  
Binding Sites ◽  
Transcriptional Activity ◽  
Endothelial Cell Proliferation ◽  
Protein Kinase D ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Vascular endothelial growth factor A (VEGF) signals primarily through its cognate receptor VEGFR-2 to control vasculogenesis and angiogenesis. Dysregulation of these physiological processes contributes to the pathologies of heart disease, stroke, and cancer. Protein kinase D (PKD) plays a crucial role in the regulation of angiogenesis by modulating endothelial cell proliferation and migration. In human umbilical vein endothelial cells (HUVEC) and human blood outgrowth endothelial cells (BOEC), knockdown of PKD-1 or PKD-2 downregulates VEGFR-2 and significantly inhibits VEGF-induced endothelial cell proliferation and migration. We sought to determine the molecular mechanism through which PKD modulates VEGFR-2 expression. Based on bioinformatics data, activating enhancer binding protein 2 (AP2) binding sites exist within the VEGFR-2 promoter. Thus, we hypothesized PKD may downregulate VEGFR-2 through AP2-mediated transcriptional repression of the VEGFR-2 promoter. Indeed, AP2β binds the VEGFR-2 promoter upon PKD knockdown in HUVEC as evident by chromatin immunoprecipitation assay. Luciferase reporter assays using serial deletions of AP2β binding sites within the VEGFR-2 promoter revealed transcriptional activity negatively correlated with the number of AP2β binding sites, thus confirming negative regulation of VEGFR-2 transcription by AP2β. Next, using siRNA, we demonstrated that upregulation of AP2β decreased VEGFR-2 expression and loss of AP2β enhanced VEGFR-2 expression. In vivo studies confirmed this finding as we observed increased VEGFR-2 immunostaining in the dorsal horn of the spinal cord of embryonic day 13 AP2β knockout mice. We hypothesize that PKD directly regulates AP2β function by serine phosphorylation and ongoing studies are being conducted to determine phosphorylation sites in AP2β directly regulated by PKD. Taken together, we demonstrate AP2β negatively regulates VEGFR-2 transcription and VEGFR-2 is a major downstream target of PKD. Our findings describing how PKD regulates angiogenesis may contribute to the development of therapies to improve the clinical outcome of patients afflicted by heart disease, stroke, and cancer.

scholarly journals 3,4-Di-O-Caffeoylquinic Acid Inhibits Angiotensin-II-Induced Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating the JNK and PI3K/Akt Signaling Pathways

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Wen-Fei Chiou ◽  
Chien-Chih Chen ◽  
Bai-Luh Wei
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Ang Ii ◽  
Caffeoylquinic Acid ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

We previously reported 3,4-di-O-caffeoylquinic acid (CQC) protected vascular endothelial cells against oxidative stress and restored impaired endothelium-dependent vasodilatation. Here, we further investigated its anti-atherosclerotic effect against angiotensin II (Ang II) evoked proliferation and migration of cultured rat vascular smooth muscle cells (rVSMC). The results showed CQC (1–20μM) clearly inhibited Ang-II-stimulated BrdU incorporation and cell migration of rVSMC in a concentration-dependent manner but without significant cytotoxicity. Western blot analysis revealed Ang II increased the phosphorylation levels of Akt and mitogen-activated protein kinases (MAPKs;p38, ERK1/2 and JNK) in rVSMC. In the presence of phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin and three individual MAPK inhibitors SB203580, PD98059 and SP600125, both Ang-II-induced cell proliferation and migration were significantly attenuated, although to differing extents, suggesting the PI3K and MAPK signal pathways all participated in regulating rVSMC proliferation and migration. Also, the CQC pretreatment markedly suppressed Ang-II-induced phosphorylation of Akt and JNK rather than ERK1/2, although it failed to affect p38 phosphorylation. In conclusion, our data demonstrate CQC may act by down-regulating Akt, JNK and part of the ERK1/2 pathways to inhibit Ang-II-induced rVSMC proliferation and migration. The anti-atherosclerotic effect of CQC is achieved either by endothelial cells protection or by VSMC proliferation/migration inhibition, suggesting this compound may be useful in preventing vascular diseases.

scholarly journals Dysregulation of miR-637 is involved in the development of retinopathy in hypertension patients and serves a regulatory role in retinol endothelial cell proliferation

2021 ◽  
Author(s):  
Weiguang Yang ◽  
Manxia Su ◽  
Yanli Yu ◽  
Qingxin Fang ◽  
Yusheng Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Logistic Regression ◽  
Regression Analysis ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Retinal Endothelial Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Background: MicroRNAs (miRNAs) play an important role in the proliferation and migration of retinal endothelial cells in patients with hypertension and hypertensive retinopathy (HR). This study aimed to investigate the clinical value of miR-637 in HR and its role in retinal endothelial cell proliferation and migration. Methods: A total of 126 subjects were recruited for the study, including 42 patients with hypertension (male/female 25/17), 42 healthy individuals (male/female 20/22), and 42 cases with HR (male/female 20/22). Except SBP and DBP, there was no significant difference in other indexes among the three groups. qRT-PCR was used to detect the expression of miR-637. The receiver operating curve (ROC) was used for diagnosis value analysis. Logistic regression analysis was used to evaluate the relationship between miR-637 and HR. CCK-8 and Transwell were used to detect the effect of miR-637 on the proliferation and migration of HUVECs. Results: Compared with hypertensive patients, HR patients had the lowest expression of miR-637. The area under the curve (AUC) of miR-637 detected by the ROC curve method is 0.892, which has the ability to distinguish hypertension and HR patients. Logistic regression analysis showed that miR-637 was an independent influence factor in HR. Cell experiment results showed that overexpression of miR-637 significantly inhibited cell proliferation and migration, while downregulation of miR-637 had the opposite effect. Luciferase analysis showed that STAT3 was the target gene of miR-637. Conclusion: Our data indicate that miR-637 is a potential non-invasive marker for patients with HR. The action of miR-637 on STAT3 may inhibit the proliferation and migration of retinal endothelial cells, providing a possible target for the treatment of HR.

Epalrestat induces cell proliferation and migration in endothelial cells via mTOR activation through PI3/Akt signaling

2013 ◽  
Vol 5 (2) ◽  
pp. 105-111
Author(s):  
Kunihiro Suzuki ◽  
Seiichi Tanaka ◽  
Kazunori Yanagi ◽  
Tosie Iijima ◽  
Mai Niitani ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Akt Signaling ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Silver nanoparticles inhibit VEGF induced cell proliferation and migration in bovine retinal endothelial cells

2009 ◽  
Vol 73 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Kalimuthu Kalishwaralal ◽  
Elayappan Banumathi ◽  
SureshBabu Ram Kumar Pandian ◽  
Venkataraman Deepak ◽  
Jeyaraj Muniyandi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Silver Nanoparticles ◽  
Endothelial Cells ◽  
Retinal Endothelial Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration
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