Decreased cultured endothelial cell proliferation in high glucose medium is reversed by antioxidants: New insights on the pathophysiological mechanisms of diabetic vascular complications

1992 ◽  
Vol 28 (11-12) ◽  
pp. 787-790 ◽  
Author(s):  
Francesco Curcio ◽  
Antonio Ceriello
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
High Glucose ◽  
Vascular Complications ◽  
Endothelial Cell Proliferation ◽  
Glucose Medium ◽  
Pathophysiological Mechanisms ◽  
Diabetic Vascular Complications ◽  
High Glucose Medium

Toxicity features of high glucose on endothelial cell cycle and protection by Dan Gua-Fang (丹瓜方) in ECV-304 in high glucose medium

2012 ◽  
Vol 19 (8) ◽  
pp. 596-602 ◽  
Author(s):  
Xian-pei Heng ◽  
Ke-ji Chen ◽  
Zhen-feng Hong ◽  
Wei-dong He ◽  
Ke-dan Chu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endothelial Cell ◽  
High Glucose ◽  
Glucose Medium ◽  
High Glucose Medium

scholarly journals Autoantibodies Targeting AT1- and ETA-Receptors Link Endothelial Proliferation and Coagulation via Ets-1 Transcription Factor

2021 ◽  
Vol 23 (1) ◽  
pp. 244
Author(s):  
Rusan Catar ◽  
Melanie Herse-Naether ◽  
Nan Zhu ◽  
Philine Wagner ◽  
Oskar Wischnewski ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcription Factor ◽  
Endothelial Cell ◽  
Intracellular Signaling ◽  
Mapk Pathway ◽  
Vascular Complications ◽  
Receptor Activation ◽  
Endothelial Cell Proliferation ◽  
Scleroderma Renal Crisis ◽  
Endothelial Proliferation

Scleroderma renal crisis (SRC) is an acute life-threatening manifestation of systemic sclerosis (SSc) caused by obliterative vasculopathy and thrombotic microangiopathy. Evidence suggests a pathogenic role of immunoglobulin G (IgG) targeting G-protein coupled receptors (GPCR). We therefore dissected SRC-associated vascular obliteration and investigated the specific effects of patient-derived IgG directed against angiotensin II type 1 (AT1R) and endothelin-1 type A receptors (ETAR) on downstream signaling events and endothelial cell proliferation. SRC-IgG triggered endothelial cell proliferation via activation of the mitogen-activated protein kinase (MAPK) pathway and subsequent activation of the E26 transformation-specific-1 transcription factor (Ets-1). Either AT1R or ETAR receptor inhibitors/shRNA abrogated endothelial proliferation, confirming receptor activation and Ets-1 signaling involvement. Binding of Ets-1 to the tissue factor (TF) promoter exclusively induced TF. In addition, TF inhibition prevented endothelial cell proliferation. Thus, our data revealed a thus far unknown link between SRC-IgG-induced intracellular signaling, endothelial cell proliferation and active coagulation in the context of obliterative vasculopathy and SRC. Patients’ autoantibodies and their molecular effectors represent new therapeutic targets to address severe vascular complications in SSc.

scholarly journals High glucose promotes breast cancer proliferation and metastasis by impairing angiotensinogen expression

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Shichao Sun ◽  
Yao Sun ◽  
Xiaoping Rong ◽  
Lei Bai
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
High Glucose ◽  
Breast Cancer Cells ◽  
Glucose Medium ◽  
Cancer Proliferation ◽  
High Glucose Medium ◽  
Proliferation And Metastasis

Abstract A number of investigations have addressed the importance of high glucose in breast cancer, however, the involvement of angiotensinogen (AGT) in this scenario is yet to be defined. Here we set out to analyze the potential pro-tumor effects of high glucose in breast cancer, and understand the underlying molecular mechanism. We demonstrated that high glucose promoted cell proliferation, viability, and anchorage-independent growth of breast cancer cells. In addition, the migrative and invasive capacities were significantly enhanced by high glucose medium. Mechanistically, AGT expression was inhibited by high glucose at both transcriptional and translational levels. High AGT remarkably suppressed proliferation, inhibited viability, and compromised migration/invasion of breast cancer cells. Most importantly, ectopic introduction of AGT almost completely abrogated pro-tumor effects of high glucose. Our study has characterized the pro-tumor properties of high glucose in breast cancer cells, which is predominantly attributed to the suppression of AGT.

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