Caffeoylserotonin suppresses THP-1 monocyte adhesion and migration via inhibition of the integrin β1/FAK/Akt signalling pathway

Yoon, Ji-Hae; Kim, Hye-Eun; Choi, Jang-Yeol; Bae, Hyeun‐Jong; Lee, Seong-Gene

doi:10.1016/j.fitote.2012.04.025

Cited by 5 publications

(3 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a previous study, we demonstrated that CaS has strong radical scavenging activity and antioxidant activity in HepG2 and HaCaT cells, based on its ability to reduce intracellular ROS generation, lipid peroxidation, oxidative stress‐induced cell death, and phosphorylation of histone H2AX, a marker of DNA damage (Choi et al ., ). Recently, we reported the anti‐inflammatory activity of CaS, which acted to prevent THP‐1 monocyte adhesion and migration via inhibition of the integrin β1/focal adhesion kinase/Akt signaling pathway (Yoon et al ., ). However, the molecular mechanism of CaS activity against ROS‐induced cell death has not been clarified.…”

Section: Introductionmentioning

confidence: 97%

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H₂O₂‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway

Nguyen

Kim

Lee

2013

Phytotherapy Research

Self Cite

View full text Add to dashboard Cite

Caffeoylserotonin (CaS) has strong radical scavenging activity as well as antioxidant activities, protecting cells from lipid peroxidation, intracellular reactive oxygen species generation, DNA damage, and cell death. The molecular mechanism by which CaS protects against oxidative stress is not well understood. Here, we analyzed the cytoprotective activity of CaS in hydrogen peroxide (H2 O2 )-treated keratinocyte HaCaT cells. H2 O2 induced apoptosis in the cells through activation of pro-apoptotic p21, Bax, and caspase-3. Pretreatment with CaS inhibited apoptotic gene expression and activated the anti-apoptotic gene, Bcl-xL. Although CaS did not directly affect heme oxygenase-1 (HO-1) expression, pretreatment with CaS augmented HO-1 expression through an increase in NF-E2-related factor (Nrf2) stability and stimulation of Nrf2 translocation to the nucleus upon H2 O2 exposure. H2 O2 also induced the phosphorylation and subsequent activation of ERK, p38 MAPK, and Akt. Analysis using specific inhibitors of p38 MAPK and Akt demonstrated that only Akt activation was involved in HO-1 and Nrf2 expressions. In addition, PI3K and PKC inhibitors suppressed HO-1/Nrf2 expression and Akt phosphorylation. These results demonstrate that CaS protects against oxidative stress-induced keratinocyte cell death in part through the activation of Nrf2-mediated HO-1 induction via the PI3K/Akt and/or PKC pathways, but not MAPK signaling.

show abstract

Section: Introductionmentioning

confidence: 97%

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H₂O₂‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway

Nguyen

Kim

Lee

2013

Phytotherapy Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…Focal adhesion kinase (FAK), a non-receptor tyrosine kinase, makes a crucial contribution to focal adhesion (FA) assembly by accelerating cytoskeleton dynamics and regulating cell motility (12). Caffeoylserotonin inhibits THP-1 monocyte migration and adhesion via suppressing the integrin β1/FAK/Akt signalling pathway (13). After traumatic brain injury in rats, milk fat globule-EGF factor-8 (MFG-E8) inhibits neuronal apoptosis and offers neuroprotection via the regulation of integrin-β3/FAK/ PI3K/AKT signaling (14).…”

Section: Introductionmentioning

confidence: 99%

Artesunate alleviates myocardial ischemia/reperfusion-induced myocardial necrosis in rats and hypoxia/reoxygenation-induced apoptosis in H9C2 cells via regulating the FAK/PI3K/Akt pathway

Fan¹,

Zhang²,

Liu³

et al. 2020

Ann Transl Med

View full text Add to dashboard Cite

Background: The various anti-inflammatory, anti-apoptotic, and antioxidant effects of Artesunate (Art) have been explored in numerous studies. This study aimed to evaluate the function of Art on myocardial necrosis in apoptotic cardiomyocytes in vivo and in vitro.Methods: Sprague Dawley (SD) rats were randomly divided into groups: a control group, a myocardial ischemia reperfusion (MI/R) group, and MI/R+ Art groups. To establish a MI/R model, rats were subjected to left anterior descending artery ischemia for 45 minutes, and then reperfusion for 2 hours. Hypoxia was induced in H9C2 cells by subjecting them to hypoxic conditions at 37 ℃ for 4 hours, before placing them in a normoxic chamber for 2 hours. The test methods were used in this test, such as echocardiography, enzyme-linked immunosorbent assay (ELISA), HE staining, TUNEL staining, immunohistochemistry, flow cytometry, western blot, and CCK-8 assay. Results: Art improved myocardial systolic function caused by MI/R injury in vivo. Simultaneously, Art reduced the levels of cardiac troponin I (cTnl), creatine kinase-MB (CK-MB) and myohemoglobin (Mb) in vivo and in vitro. Moreover, Art inhibited cardiomyocyte apoptosis in vivo and in vitro. The focal adhesion kinase (FAK)/phosphatidylinositide-3 kinases (PI3K)/AKT signaling pathway was also activated by Art in vivo and in vitro. Furthermore, after inhibitor PF573228 was added, Art inhibited apoptosis in H9C2 cells via activation of the FAK/PI3K/AKT signaling pathway in vitro.Conclusions: This study confirms that Art alleviated MI/R injury and inhibited cardiomyocyte apoptosis in vivo and in vitro. Art exerted an inhibitory effect on cardiomyocyte apoptosis by activating the FAK/PI3K/ AKT signaling pathway. Therefore, Art may serve as an alternative treatment for MI/R injury.

show abstract

“…Activated FAK binds to cell membrane integrins with the assistance of other proteins, such as paxillin and vinculin, contributing to FA formation, cell adhesion, and cell migration [ 13 , 14 ]. Considerable evidence indicates that the FAK pathway promotes the migration and adhesion of many types of cells, such as THP-1 monocytes, macrophages, and lung cancer cells [ 15 – 17 ]. Moreover, the activation of FAK is known to promote the growth and differentiation of skeletal muscle cells in culture via the translocation of FAK to costameres [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Focal adhesion kinase and paxillin promote migration and adhesion to fibronectin by swine skeletal muscle satellite cells

et al. 2016

View full text Add to dashboard Cite

The focal adhesion kinase (FAK) signaling pathway contributes to the cell migration and adhesion that is critical for wound healing and regeneration of damaged muscle, but its function in skeletal muscle satellite cells (SCs) is less clear. We compared the migration and adhesion of SCs derived from two species of pig (Lantang and Landrace) in vitro, and explored how FAK signaling modulates the two processes. The results showed that Lantang SCs had greater ability to migrate and adhere to fibronection (P < 0.05) than Landrace SCs. Compared to Landrace SCs, Lantang SCs expressed many more focal adhesion (FA) sites, which were indicated by the presence of p-paxillin (Tyr118), and exhibited less F-actin reorganization 24 h after seeding onto fibronectin. Levels of p-FAK (Tyr397) and p-paxillin (Tyr118) were greater (P < 0.05) in Lantang SCs than Landrace SCs after migration for 24 h. Similarly, Lantang SCs showed much higher levels of p-FAK (Tyr397), p-paxillin (Tyr118) and p-Akt (Ser473) than Landrace SCs 2 h after adhesion. Treatment with the FAK inhibitor PF-573228 (5 or 10 μmol/L) inhibited Lantang SC migration and adhesion to fibronectin (P < 0.05), decreased levels of p-paxillin (Tyr118) and p-Akt (Ser473) (P < 0.05), and suppressed the formation of FA sites on migrating SCs. Thus FAK appears to play a key role in the regulation of SC migration and adhesion necessary for muscle regeneration.

show abstract

Caffeoylserotonin suppresses THP-1 monocyte adhesion and migration via inhibition of the integrin β1/FAK/Akt signalling pathway

Cited by 5 publications

References 28 publications

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H₂O₂‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H₂O₂‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway

Artesunate alleviates myocardial ischemia/reperfusion-induced myocardial necrosis in rats and hypoxia/reoxygenation-induced apoptosis in H9C2 cells via regulating the FAK/PI3K/Akt pathway

Focal adhesion kinase and paxillin promote migration and adhesion to fibronectin by swine skeletal muscle satellite cells

Contact Info

Product

Resources

About

Caffeoylserotonin suppresses THP-1 monocyte adhesion and migration via inhibition of the integrin β1/FAK/Akt signalling pathway

Cited by 5 publications

References 28 publications

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H2O2‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H2O2‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway

Artesunate alleviates myocardial ischemia/reperfusion-induced myocardial necrosis in rats and hypoxia/reoxygenation-induced apoptosis in H9C2 cells via regulating the FAK/PI3K/Akt pathway

Focal adhesion kinase and paxillin promote migration and adhesion to fibronectin by swine skeletal muscle satellite cells

Contact Info

Product

Resources

About

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H₂O₂‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway

Caffeoylserotonin Protects Human Keratinocyte HaCaT Cells against H₂O₂‐Induced Oxidative Stress and Apoptosis through Upregulation of HO‐1 Expression via Activation of the PI3K/Akt/Nrf2 Pathway