scholarly journals DIDS Attenuates Staurosporine-induced Cardiomyocyte Apoptosis by PI3K/Akt Signaling Pathway: Activation of eNOS/NO and Inhibition of Bax Translocation

2008 ◽  
Vol 22 (1-4) ◽  
pp. 177-186 ◽  
Author(s):  
An-Heng Liu ◽  
Ya-Nan Cao ◽  
Hong-Tao Liu ◽  
Wei-Wei Zhang ◽  
Yan Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Cardiomyocyte Apoptosis ◽  
Akt Signaling Pathway ◽  
Pathway Activation

scholarly journals Cisplatin resistance in lung cancer is mediated by MACC1 expression through PI3K/AKT signaling pathway activation

2018 ◽  
Vol 50 (8) ◽  
pp. 748-756 ◽  
Author(s):  
Qiang Zhang ◽  
Bin Zhang ◽  
Leina Sun ◽  
Qingna Yan ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Cisplatin Resistance ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Pathway Activation

Effect of PI3K/Akt Signaling Pathway on PRAS40Thr246 Phosphorylation in Gastric Cancer Cells

2020 ◽  
Author(s):  
Yizhuo LU ◽  
Lianghui LI ◽  
Guoyang WU ◽  
Huiqin ZHUO ◽  
Guoyan LIU ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Cell Group ◽  
Akt Signaling Pathway ◽  
Gastric Cancer Cells ◽  
Pathway Activation ◽  
Related Proteins ◽  
Proliferation And Invasion

Background: We aimed to investigate the effect of PI3K/Akt signaling pathway on PRAS40Thr246 phosphorylation in gastric cancer cells. Methods: The study was conducted from April 2017 to January 2018 in Zhongshan Hospital, Xiamen University, Xiamen, China. Gastric cancer cells were divided into three groups: gastric cancer cell group, LY294002 group and MK-2206 group. Specific tests were conducted accordingly. Results: Inhibition of PI3K/Akt signaling pathway activation and PRAS40Thr246 phosphorylation could inhibit proliferation and invasion and promote apoptosis of gastric cancer cells, and PRAS40Thr246 phosphorylation could activate PI3K/Akt signaling pathway. Conclusion: The levels of PI3K/Akt signaling pathway related proteins and p-PRAS40Thr246 were significantly increased in gastric cancer cells. p-PRAS40-Thr246 was able to reflect the activation of the PI3K/Akt signaling pathway, reflecting the sensitivity of the PI3K/AKT signaling pathway to inhibitors.

scholarly journals Prognostic implications of phosphatidylinositol 3-kinase/AKT signaling pathway activation in gastric carcinomas

2017 ◽  
Vol 6 ◽  
pp. 1262-1268 ◽  
Author(s):  
Paula Blandina Ola Chiappini ◽  
Ivan Ucella Dantas de Medeiros ◽  
Luiz Guilherme Cenaglia Lima ◽  
Jose Humberto Fregnani ◽  
Suely Nonogaki ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Gastric Carcinomas ◽  
Pathway Activation ◽  
Prognostic Implications ◽  
Phosphatidylinositol 3

PSMC6 promotes osteoblast apoptosis through inhibiting PI3K/AKT signaling pathway activation in ovariectomy‐induced osteoporosis mouse model

2020 ◽  
Vol 235 (7-8) ◽  
pp. 5511-5524 ◽  
Author(s):  
Ying Zhang ◽  
Xiangyang Cao ◽  
Peifeng Li ◽  
Yanan Fan ◽  
Leilei Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Pathway Activation ◽  
Osteoblast Apoptosis

scholarly journals PO-163 Aerobic exercise activates myocardial FGF21/FGFR1/PI3K-AKT signaling pathway and inhibits cardiomyocyte apoptosis in post-myocardial infarction rats

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Mingxiao Li ◽  
Zhenjun Tian
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Aerobic Exercise ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Collagen Fibers ◽  
Cardiomyocyte Apoptosis ◽  
Akt Pathway ◽  
Akt Signaling Pathway ◽  
Myocardial Apoptosis

Objective To investigate the effect of aerobic exercise on the expression of fibroblast growth factor 21 (FGF21) and cardiomyocyte apoptosis in Myocardial Infarction (MI) rats. Methods male SD rats were randomly divided into three groups：the sham operation (S), sedentary MI group (MI) and MI with aerobic exercise group (ME). The MI model was established by ligation of the left anterior descending branch of the left coronary artery. ME group were trained four weeks after the operation. LVSP, LVEDP and ±dp/dtmax were used to evaluate cardiac function. H9C2 cardiomyocytes were stimulated by 400 μmol/L H2O2 for 4h to simulate myocardial apoptosis mode. AMPK agonist AICAR and FGF21 receptor inhibitor PD166866 were used to interfere with H9C2. Myocardial collagen volume fraction was calculated by Masson staining and myocardium FGF21, FGFR1, Bax, Bcl-2 and PI3K-AKT pathway by western blotting or RT-Qpcr. Cardiomyocytes apoptosis was evaluated by TUNEL. Results Compared with S, the expression of FGF21, FGFR1, Bax, Bcl-2 and PI3K, AKT increased significantly in MI group, the apoptotic cardiomyocytes and collagen fibers increased significantly, but the cardiac function decreased. Compared to MI, myocardium FGF21, FGFR1 and PI3K, AKT were further increased in ME group, the Bax/Bcl-2 and the apoptotic cardiomyocytes decreased significantly. The percentage of collagen fibers decreased and the cardiac function was improved. Myocardium FGF21 was positively correlated with the inhibition of cardiomyocyte apoptosis and the improvement of cardiac function. Furthermore, the expression of Bax/Bcl-2, TNF-α/IL-10 and the apoptotic cardiomyocytes was significantly increased by PD166866, but PI3K-AKT pathway decreased significantly by PD166866. However, AICAR single intervention or PD166866 simultaneous intervention also can reverse this adverse effects. Conclusions Exercise can increase myocardial FGF21/FGFR1 with MI. The one of the mechanisms is to activate PI3K-AKT pathway to inhibit cardiaomyocyte apoptosis and inflammatory. It indicates that FGF21/FGFR1/PI3K-AKT signaling pathway plays an important role in inhibiting myocardial apoptosis and improving cardiac function.

scholarly journals The Role of PI3K/AKT Pathway and NADPH Oxidase 4 in Host ROS Manipulation by Toxoplasma gondii

2020 ◽  
Vol 58 (3) ◽  
pp. 237-247
Author(s):  
Hei Gwon Choi ◽  
Fei-Fei Gao ◽  
Wei Zhou ◽  
Pu-Reum Sun ◽  
Jae-Min Yuk ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Nadph Oxidase ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Innate Immune ◽  
Akt Pathway ◽  
Akt Signaling Pathway ◽  
Nadph Oxidase 4 ◽  
Pathway Activation

Dendritic cell is one of the first innate immune cell to encounter T. gondii after the parasite crosses the host intestinal epithelium. T. gondii requires intact DC as a carrier to infiltrate into host central nervous system (CNS) without being detected or eliminated by host defense system. The mechanism by which T. gondii avoids innate immune defense of host cell, especially in the dendritic cell is unknown. Therefore, we examined the role of host PI3K/AKT signaling pathway activation by T. gondii in dendritic cell. T. gondii infection or T. gondii excretory/secretory antigen (TgESA) treatment to the murine dendritic cell line DC2.4 induced AKT phosphorylation, and treatment of PI3K inhibitors effectively suppressed the T. gondii proliferation but had no effect on infection rate or invasion rate. Furthermore, it is found that T. gondii or TgESA can reduce H2O2-induced intracellular reactive oxygen species (ROS) as well as host endogenous ROS via PI3K/AKT pathway activation. While searching for the main source of the ROS, we found that NADPH oxidase 4 (NOX4) expression was controlled by T. gondii infection or TgESA treatment, which is in correlation with previous observation of the ROS reduction by identical treatments. These findings suggest that the manipulation of the host PI3K/AKT signaling pathway and NOX4 expression is an essential mechanism for the down-regulation of ROS, and therefore, for the survival and the proliferation of T. gondii.

Sign in / Sign up

Export Citation Format

Share Document