Epidermal growth factor and insulin inhibit cell death in pancreatic beta cells by activation of PI3-kinase/AKT signaling pathway under oxidative stress

2004 ◽  
Vol 36 (4) ◽  
pp. 1163-1165 ◽  
Author(s):  
H Maeda ◽  
K Gopalrao Rajesh ◽  
H Maeda ◽  
R Suzuki ◽  
S Sasaguri
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Signaling Pathway ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Epidermal Growth

scholarly journals MicroRNA-126 modulates angiogenesis and tube formation through enhancing epidermal growth factor-like domain 7 expression and phosphorylating PI3K/AKT signaling pathway

2021 ◽  
Author(s):  
Qiang Li ◽  
Zhong-ming Wang ◽  
Ai-yue Wang ◽  
Qiong-Guan Xu ◽  
Zhou-feng Fu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Tube Formation ◽  
Luciferase Assay ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Invasive Ability ◽  
Epidermal Growth

IntroductionDysregulated angiogenesis is a critical characteristic for endothelial dysfunction disorders. This study aimed to determine functions of microRNA-126 in formation of tube and investigated the potential mechanisms.Material and methodsThe synthesized microRNA-126 control and microRNA-126 inhibitor plasmids were transfected into human umbilical-vein endothelial cells (HUVECs) using lipofectamine 2000 reagent. Cell counting kit-8 (CCK-8) was employed to measure proliferative capability of HUVECs. Transwell analysis was used to evaluate HUVECs invasive ability. Real time PCR (RT-PCR) was utilized to access epidermal growth factor-like domain 7 (EGFL7) and microRNA-126 mRNA transcription. Tube-forming capability in HUVECs was determined. Dual-luciferase assay and linear-regression analysis were conducted to measure interaction between EGFL7 and microRNA-126 molecule. Phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling pathway associated molecules were evaluated using western blot assay.ResultsSilencing of microRNA-126 significantly enhanced proliferative capability and invasive ability of HUVECs compared to those of microRNA-126 control group (p<0.05). microRNA-126 silencing remarkably promoted tube formation and significantly up-regulated EGFL7 compared to those of microRNA-126 control group (p<0.05). microRNA-126 could interact with EGFL7 molecule. microRNA-126 was also negatively correlated with EGFL7 molecule in HUVECs (p<0.05). Silencing of microRNA-126 significantly enhanced p-PI3K/PI3K ratio compared to that of microRNA-126 control group (p<0.05). microRNA-126 silencing also remarkably increased p-AKT/AKT ratio compared to that of microRNA-126 control group (p<0.05).ConclusionsmicroRNA-126 modulated angiogenesis and tube formation through increasing EGFL7 expression and phosphorylating PI3K/AKT signaling pathway.

scholarly journals YM155 inhibits retinal pigment epithelium cell survival through EGFR/MAPK signaling pathway

2021 ◽  
Vol 14 (4) ◽  
pp. 489-496
Author(s):  
Teng Li ◽  
◽  
Jia-Min Meng ◽  
Bo Yuan ◽  
Wen-Juan Lin ◽  
...  
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Retinal Pigment Epithelium ◽  
Epidermal Growth Factor ◽  
Cell Survival ◽  
Signaling Pathway ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Mapk Signaling ◽  
Epidermal Growth

AIM: To investigate YM155's effect on retinal pigment epithelium (RPE) cells' viability and the potential regulatory mechanisms. METHODS: Human immortalized RPE cell lines (ARPE-19 cell line) were processed with YM155 and epidermal growth factor (EGF). ARPE-19 cell viability was detected by methyl thiazolyl tetrazolium assay, and apoptosis was tested by flow cytometry assay. ARPE-19 cell proliferation was assessed with bromodeoxyuridine tagged incorporation assay, and migration ability was evaluated via a wound-healing assay. Epidermal growth factor receptor (EGFR)/MAPK pathway proteins were tested via immunoblotting. EGFR localization was examined by immunofluorescence assay. RESULTS: YM155 suppressed ARPE-19 cells' viability in a time and concentration-dependent manner. A high dose of YM155 caused a small amount of ARPE-19 cell death. YM155 significantly diminished the ARPE-19 cells' proliferative and migrative capacity. YM155 down-regulated total EGFR and phosphorylated external signal-regulated protein kinase (ERK), and it up-regulated the phosphorylation of P38MAPK and c-Jun N-terminal kinase (JNK). YM155 induced endocytosis of EGFR in ARPE-19 cell. YM155 also attenuated EGF-induced ARPE-19 cells' proliferative and migrative capacity. Moreover, YM155 significantly decreased the expression of phosphorylated EGFR and ERK after treated by EGF. CONCLUSION: YM155 inhibits RPE cell survival, the cell proliferative and migrative capacity, and it effectuates a small amount of cell death through the EGFR/MAPK signaling pathway. YM155 might, therefore, be an agent to prevent and treat abnormal RPE cell survival in proliferative vitreoretinopathy.

scholarly journals Maresin 1 protects the liver against ischemia/reperfusion injury via the ALXR/Akt signaling pathway

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Da Tang ◽  
Guang Fu ◽  
Wenbo Li ◽  
Ping Sun ◽  
Patricia A. Loughran ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Serum Aminotransferase ◽  
Primary Mouse ◽  
Maresin 1

Abstract Background Hepatic ischemia/reperfusion (I/R) injury can be a major complication following liver surgery contributing to post-operative liver dysfunction. Maresin 1 (MaR1), a pro-resolving lipid mediator, has been shown to suppress I/R injury. However, the mechanisms that account for the protective effects of MaR1 in I/R injury remain unknown. Methods WT (C57BL/6J) mice were subjected to partial hepatic warm ischemia for 60mins followed by reperfusion. Mice were treated with MaR1 (5-20 ng/mouse), Boc2 (Lipoxin A4 receptor antagonist), LY294002 (Akt inhibitor) or corresponding controls just prior to liver I/R or at the beginning of reperfusion. Blood and liver samples were collected at 6 h post-reperfusion. Serum aminotransferase, histopathologic changes, inflammatory cytokines, and oxidative stress were analyzed to evaluate liver injury. Signaling pathways were also investigated in vitro using primary mouse hepatocyte (HC) cultures to identify underlying mechanisms for MaR1 in liver I/R injury. Results MaR1 treatment significantly reduced ALT and AST levels, diminished necrotic areas, suppressed inflammatory responses, attenuated oxidative stress and decreased hepatocyte apoptosis in liver after I/R. Akt signaling was significantly increased in the MaR1-treated liver I/R group compared with controls. The protective effect of MaR1 was abrogated by pretreatment with Boc2, which together with MaR1-induced Akt activation. MaR1-mediated liver protection was reversed by inhibition of Akt. Conclusions MaR1 protects the liver against hepatic I/R injury via an ALXR/Akt signaling pathway. MaR1 may represent a novel therapeutic agent to mitigate the detrimental effects of I/R-induced liver injury.

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