CBP/p300 inhibitor C646 prevents high glucose exposure induced neuroepithelial cell proliferation

2018 ◽  
Vol 110 (14) ◽  
pp. 1118-1128 ◽  
Author(s):  
Baoling Bai ◽  
Qin Zhang ◽  
Chunlei Wan ◽  
Dan Li ◽  
Ting Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
High Glucose ◽  
Neuroepithelial Cell ◽  
Glucose Exposure

OS 02-03 EFFECT OF HIGH GLUCOSE EXPOSURE ON ENDOTHELIAL MICROPARTICLE FORMATION AND COMPOSITION

2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e48 ◽  
Author(s):  
Maddison Turner ◽  
Larissa Reid ◽  
Mercedes Munkonda ◽  
Dylan Burger
Keyword(s):  
High Glucose ◽  
Glucose Exposure ◽  
Microparticle Formation

scholarly journals Upregulation of miRNA-23a-3p rescues high glucose-induced cell apoptosis and proliferation inhibition in cardiomyocytes

2020 ◽  
Vol 56 (10) ◽  
pp. 866-877
Author(s):  
Fang Wu ◽  
Feng Wang ◽  
Qian Yang ◽  
Yawen Zhang ◽  
Ke Cai ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Myocardial Injury ◽  
Proliferation Inhibition ◽  
Cardiomyocyte Proliferation ◽  
Injury Model ◽  
Cell Proliferation Inhibition ◽  
Glucose Treatment

AbstractMaternal hyperglycemia potentially inhibits the development of the fetal heart by suppressing cardiomyocyte proliferation and promoting apoptosis. Different studies have indicated that miRNAs are key regulators of cardiomyocyte proliferation, differentiation, and apoptosis and play a protective role in a variety of cardiovascular diseases. However, the biological function of miRNA-23a in hyperglycemia-related cardiomyocyte injury is not fully understood. The present study investigated the effect of miRNA-23a-3p on cell proliferation and apoptosis in a myocardial injury model induced by high glucose. H9c2 cardiomyocytes were exposed to high glucose to establish an in vitro myocardial injury model and then transfected with miRNA-23a-3p mimics. After miRNA-23a-3p transfection, lens-free microscopy was used to dynamically monitor cell numbers and confluence and calculate the cell cycle duration. CCK-8 and EdU incorporation assays were performed to detect cell proliferation. Flow cytometry was used to measured cell apoptosis. Upregulation of miRNA-23a-3p significantly alleviated high glucose-induced cell apoptosis and cell proliferation inhibition (p < 0.01 and p < 0.0001, respectively). The cell cycle of the miRNA-23a-3p mimics group was significantly shorter than that of the negative control group (p < 0.01). The expression of cell cycle–activating and apoptosis inhibition-associated factors Ccna2, Ccne1, and Bcl-2 was downregulated by high glucose and upregulated by miRNA-23a-3p overexpression in high glucose-injured H9c2 cells. miRNA-23a-3p mimics transfection before high glucose treatment had a significantly greater benefit than transfection after high glucose treatment (p < 0.0001), and the rescue effect of miRNA-23a-3p increased as the concentration increased. This study suggests that miRNA-23a-3p exerted a dose- and time-dependent protective effect on high glucose-induced H9c2 cardiomyocyte injury.

scholarly journals miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42/β-Catenin Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Jing Duan ◽  
Xian-Ling Qian ◽  
Jun Li ◽  
Xing-Hua Xiao ◽  
Xiang-Tong Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
High Glucose ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Glucose Stimulation ◽  
Inhibition Of Proliferation ◽  
Glucose Stimulated Insulin Secretion

Background. Diabetes is a progressive metabolic disease characterized by hyperglycemia. Functional impairment of islet β cells can occur to varying degrees. This impairment can initially be compensated for by proliferation and metabolic changes of β cells. Cell division control protein 42 (Cdc42) and the microRNA (miRNA) miR-29 have important roles in β-cell proliferation and glucose-stimulated insulin secretion (GSIS), which we further explored using the mouse insulinoma cell line MIN6. Methods. Upregulation and downregulation of miR-29a and Cdc42 were accomplished using transient transfection. miR-29a and Cdc42 expression was detected by real-time PCR and western blotting. MIN6 proliferation was detected using a cell counting kit assay. GSIS under high-glucose (20.0 mM) or basal-glucose (5.0 mM) stimulation was detected by enzyme-linked immunosorbent assay. The miR-29a binding site in the Cdc42 mRNA 3′-untranslated region (UTR) was determined using bioinformatics and luciferase reporter assays. Results. miR-29a overexpression inhibited proliferation (P<0.01) and GSIS under high-glucose stimulation (P<0.01). Cdc42 overexpression promoted proliferation (P<0.05) and GSIS under high-glucose stimulation (P<0.05). miR-29a overexpression decreased Cdc42 expression (P<0.01), whereas miR-29a downregulation increased Cdc42 expression (P<0.01). The results showed that the Cdc42 mRNA 3′-UTR is a direct target of miR-29a in vitro. Additionally, Cdc42 reversed miR-29a-mediated inhibition of proliferation and GSIS (P<0.01). Furthermore, miR-29a inhibited β-catenin expression (P<0.01), whereas Cdc42 promoted β-catenin expression (P<0.01). Conclusion. By negatively regulating Cdc42 and the downstream molecule β-catenin, miR-29a inhibits MIN6 proliferation and insulin secretion.

scholarly journals Glucose Regulation of Thrombospondin and Its Role in the Modulation of Smooth Muscle Cell Proliferation

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Laura A. Maile ◽  
Lee B. Allen ◽  
Christopher F. Hanzaker ◽  
Katherine A. Gollahon ◽  
Paul Dunbar ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Smooth Muscle ◽  
High Glucose ◽  
Glucose Regulation ◽  
Molecular Event ◽  
Protein Levels ◽  
Igf I ◽  
Normal Glucose ◽  
The Difference

Smooth muscle cells (SMC) maintained in high glucose are more responsive to IGF-I than those in normal glucose. There is significantly more thrombospondin-1 (TSP-1) in extracellular matrix surrounding SMC grown in 25 mM glucose. In this study we investigated 1) the mechanism by which glucose regulates TSP-1 levels and 2) the mechanism by which TS-1 enhances IGF-I signaling. The addition of TSP-1 to primary SMC was sufficient to enhance IGF-I responsiveness in normal glucose. Reducing TSP-1 protein levels inhibited IGF-I signaling in SMC maintained in high glucose. We determined that TSP-1 protected IAP/CD47 from cleavage and thereby facilitated its association with SHP substrate-1 (SHPS-1). We have shown previously that the hyperglycemia induced protection of IAP from cleavage is an important component of the ability of hyperglycemia to enhance IGF-I signaling. Furthermore we determined that TSP-1 also enhanced phosphorylation of theβ3 subunit of theαVβ3 integrin, another molecular event that we have shown are critical for SMC response to IGF-I in high glucose. Our studies also revealed that the difference in the amount of TSP-1 in the two different glucose conditions was due, at least in part, to a difference in the cellular uptake and degradation of TSP-1.

scholarly journals The effects of high glucose exposure on global gene expression and DNA methylation in human pancreatic islets

2018 ◽  
Vol 472 ◽  
pp. 57-67 ◽  
Author(s):  
Elin Hall ◽  
Marloes Dekker Nitert ◽  
Petr Volkov ◽  
Siri Malmgren ◽  
Hindrik Mulder ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Pancreatic Islets ◽  
High Glucose ◽  
Global Gene Expression ◽  
Human Pancreatic Islets ◽  
Glucose Exposure
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