scholarly journals GSK-3β/CREB axis mediates IGF-1-induced ECM/adhesion molecule expression, cell cycle progression and monolayer permeability in retinal capillary endothelial cells: Implications for diabetic retinopathy

2011 ◽  
Vol 1812 (9) ◽  
pp. 1080-1088 ◽  
Author(s):  
Takhellambam S. Devi ◽  
Lalit P. Singh ◽  
Ken-Ichi Hosoya ◽  
Tetsuya Terasaki
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
Cell Cycle Progression ◽  
Adhesion Molecule Expression ◽  
Cycle Progression ◽  
Retinal Capillary ◽  
Capillary Endothelial Cells ◽  
Monolayer Permeability ◽  
Gsk 3Β

scholarly journals Protective Effects ofPanax notoginsengSaponins against High Glucose-Induced Oxidative Injury in Rat Retinal Capillary Endothelial Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Yue Fan ◽  
Yuan Qiao ◽  
Jianmei Huang ◽  
Minke Tang
Keyword(s):  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
High Glucose ◽  
Microvascular Dysfunction ◽  
Panax Notoginseng ◽  
Protective Effects ◽  
Pronounced Increase ◽  
Nadph Oxidase 4 ◽  
Retinal Capillary ◽  
Capillary Endothelial Cells

Diabetic retinopathy, a leading cause of visual loss and blindness, is characterized by microvascular dysfunction. Hyperglycemia is considered the major pathogenic factor for diabetic retinopathy and is associated with increased oxidative stress in the retina. In this study, we investigated the potential protective effects ofPanax notoginsengSaponins (PNS) in retinal capillary endothelial cells (RCECs) exposed to high glucose conditions. We found a pronounced increase in cell viability in rat RCECs incubated with both PNS and high glucose (30 mM) for 48 h or 72 h. The increased viability was accompanied by reduced intracellular hydrogen peroxide (H2O2) and superoxide (O2-), decreased mitochondrial reactive oxygen species (ROS), and lowered malondialdehyde (MDA) levels. PNS also increased the activities of total superoxide dismutase (SOD), MnSOD, catalase (CAT), and glutathione peroxidase (GSH-PX). The glutathione (GSH) content also increased after PNS treatment. Furthermore, PNS reduced NADPH oxidase 4 (Nox4) expression. These results indicate that PNS exerts a protective effect against high glucose-induced injury in RCECs, which may be partially attributed to its antioxidative function.

MiR-19b-1 inhibits angiogenesis by blocking cell cycle progression of endothelial cells

2012 ◽  
Vol 417 (2) ◽  
pp. 771-776 ◽  
Author(s):  
Runting Yin ◽  
Weiwei Bao ◽  
Yingying Xing ◽  
Tao Xi ◽  
Shaohua Gou
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Laforin Negatively Regulates Cell Cycle Progression through Glycogen Synthase Kinase 3β-Dependent Mechanisms

2008 ◽  
Vol 28 (23) ◽  
pp. 7236-7244 ◽  
Author(s):  
Runhua Liu ◽  
Lizhong Wang ◽  
Chong Chen ◽  
Yan Liu ◽  
Penghui Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Cyclin D1 ◽  
Tumor Suppression ◽  
Cell Cycle Progression ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3Β ◽  
Cycle Progression ◽  
Gsk 3Β

ABSTRACT Glycogen synthase kinase 3β (GSK-3β) represses cell cycle progression by directly phosphorylating cyclin D1 and indirectly regulating cyclin D1 transcription by inhibiting Wnt signaling. Recently, we reported that the Epm2a-encoded laforin is a GSK-3β phosphatase and a tumor suppressor. The cellular mechanism for its tumor suppression remains unknown. Using ex vivo thymocytes and primary embryonic fibroblasts from Epm2a −/− mice, we show here a general function of laforin in the cell cycle regulation and repression of cyclin D1 expression. Moreover, targeted mutation of Epm2a increased the phosphorylation of Ser9 on GSK-3β while having no effect on the phosphorylation of Ser21 on GSK-3α. In the GSK-3β+/+ but not the GSK-3β−/− cells, Epm2a small interfering RNA significantly enhanced cell growth. Consistent with an increased level of cyclin D1, the phosphorylation of retinoblastoma protein (Rb) and the levels of Rb-E2F-regulated genes cyclin A, cyclin E, MCM3, and PCNA are also elevated. Inhibitors of GSK-3β selectively increased the cell growth of Epm2a +/+ but not of Epm2a −/− cells. Taken together, our data demonstrate that laforin is a selective phosphatase for GSK-3β and regulates cell cycle progression by GSK-3β-dependent mechanisms. These data provide a cellular basis for the tumor suppression activity of laforin.

scholarly journals Hemozoin impairs cell cycle progression and promotes chemokine release in human microvascular endothelial cells

2012 ◽  
Vol 11 (S1) ◽  
Author(s):  
Nicoletta Basilico ◽  
Daniela Girelli ◽  
Sarah D’Alessandro ◽  
Yolanda Corbett ◽  
Mauro Prato ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cell Cycle Progression ◽  
Microvascular Endothelial Cells ◽  
Cycle Progression ◽  
Microvascular Endothelial

scholarly journals Par6 regulates cell cycle progression through enhancement of Akt/PI3K/GSK‐3β signaling pathway activation in glioma

2019 ◽  
Vol 34 (1) ◽  
pp. 1481-1496 ◽  
Author(s):  
Pei Liu ◽  
Chenchen Zhu ◽  
Juanjuan Luo ◽  
Sheng Lan ◽  
Dongsheng Su ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Signaling Pathway ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Pathway Activation ◽  
Gsk 3Β

scholarly journals Silencing Lysine-Specific Histone Demethylase 1 (LSD1) Causes Increased HP1-Positive Chromatin, Stimulation of DNA Repair Processes, and Dysregulation of Proliferation by Chk1 Phosphorylation in Human Endothelial Cells

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1212 ◽  
Author(s):  
Wojtala ◽  
Dąbek ◽  
Rybaczek ◽  
Śliwińska ◽  
Świderska ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Dna Repair ◽  
Cell Cycle Progression ◽  
Cell Model ◽  
Heterochromatin Protein 1 ◽  
Cycle Progression ◽  
Repair Processes ◽  
Lysine Residues ◽  
Stimulation Of

: The methylation of histone lysine residues modifies chromatin conformation and regulates the expression of genes implicated in cell metabolism. Lysine-specific demethylase 1 (LSD1) is a flavin-dependent monoamine oxidase that can demethylate mono- and dimethylated histone lysines 4 and 9 (H3K4 and H3K9). The removal of methyl groups from the lysine residues of histone and non-histone proteins was found to be an important regulatory factor of cell proliferation. However, its role has not been fully elucidated. In this study, we assessed LSD1-mediated cell cycle progression using a human endothelial cell model. The short hairpin RNA knockdown of LSD1 inhibits the G2/M phase of cell cycle progression by checkpoint kinase 1 (Chk1) phosphorylation (S137). We observed elevated DNA damage, which was consistent with the increased detection of double-strand breaks as well as purines and pyrimidines oxidation, which accompanied the activation of ATR/ATRIP signaling by H2AXS139 phosphorylation. The irreversible pharmacological inhibition of LSD1 by 2-phenylcyclopropylamine (2-PCPA) inactivated its enzymatic activity, causing significant changes in heterochromatin and euchromatin conformation assessed by chromatin assembly factor 1 subunit A (CAF1A) and heterochromatin protein 1 isoform α and γ (HP1α/γ) immunofluorescence analysis. We conclude that the knockdown of LSD1 in endothelial cells leads to increased HP1-positive chromatin, the stimulation of DNA repair processes, and the dysregulation of proliferation machinery.

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