Activation Of TLR4 Induces VEGF Expression Via Akt Pathway In Nasal Polyps

Cho, Jung-Sun; Kang, Ju-Hyung; Han, In-Hye; Um, Ji Young; Park, Il Ho; Lee, Heung‐Man

doi:10.1016/j.jaci.2013.12.605

Cited by 5 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, it is not clear how the Akt‐mTOR signaling was activated in NP tissues. Although Akt has been shown to be activated in NP‐derived fibroblasts stimulated with lipopolysaccharide (LPS), whether activation of Akt requires certain inflammation inducers such as LPS in the microenvironment of nasal mucosa has yet to be elucidated. Moreover, it has been demonstrated that phosphorylation of mTOR, a known downstream target of Akt, is significantly elevated and is associated with T regulatory cell (Treg) insufficiency in NPs .…”

Section: Discussionmentioning

confidence: 99%

Autophagy is deficient in nasal polyps: implications for the pathogenesis of the disease

Chen

Hour

Yang

et al. 2014

Int Forum Allergy Rhinol

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Autophagy is deficient in nasal polyps: implications for the pathogenesis of the disease

Chen

Hour

Yang

et al. 2014

Int Forum Allergy Rhinol

View full text Add to dashboard Cite

show abstract

“…Numerous studies have shown that the TLR4/NF-κB signaling pathway plays an important role in regulating the activity of VeGF (25,28,38). The proteasomal degradation of iκB-α is an important event in the canonical pathway of nF-κB activation.…”

Section: Discussionmentioning

confidence: 99%

“…VeGF is an important pro-angiogenic regulator of APL (25). Numerous studies have shown that the TLR4/nF-κB signaling pathway plays an important role in regulating the activity of VeGF (26)(27)(28). Therefore, the effects of dFMG on the TLR4/nF-κB signaling pathway and VeGF in Hl-60 cells were examined by WB and rT-qPcr.…”

Section: Dfmg Inhibits the Tlr4/nf-κb Signaling Pathway And Reduces Tmentioning

confidence: 99%

7‑Difluoromethyl‑5,4'‑dimethoxygenistein exerts anti‑angiogenic effects on acute promyelocytic leukemia HL‑60 cells by inhibiting the TLR4/NF‑κB signaling pathway

Xiang

et al. 2020

Mol Med Report

View full text Add to dashboard Cite

angiogenesis plays an important role in the development and metastasis of tumors, and anti-angiogenesis agents are used to treat tumors. For example, the acute promyelocytic leukemia (aPl) may be treated with arsenic trioxide. angiogenesis in aPl is a multi-step dynamic equilibrium process coordinated by various angiogenic stimulators and inhibitors, which play key roles in the occurrence, progression and chemosensitivity of this disease. our research group previously synthesized 7-difluoromethyl-5,4'-dimethoxygenistein (dFMG), and found that it inhibits angiogenesis during atherosclerotic plaque formation. in the present study, the effect and mechanism of dFMG in angiogenesis induced by aPl Hl-60 cells was investigated using a chick embryo chorioallantoic membrane model and Matrigel tubule formation assays. The results obtained revealed an anti-angiogenesis effect of dFMG towards Hl-60 cells. When the Toll-like receptor 4/nuclear factor-κB (TLR4/nF-κB) signaling pathway was inhibited, the anti-angiogenic effect of dFMG was further enhanced. However, when the TLR4/nF-κB signaling pathway was activated, the anti-angiogenic effect of dFMG was attenuated. These results demonstrated that dFMG inhibits angiogenesis induced by aPl Hl-60 cells, and provides insights into the mechanism by which dFMG inhibits the TLR4/nF-κB signaling pathway. in conclusion, in the present study, the anti-angiogenesis effect of dFMG on aPl has been reported, and the mechanism by which dFMG induced the anti-angiogenesis effect was explored. These findings have provided a potential new drug candidate for the treatment of patients with aPl.

show abstract

“…VEGF, acting through VEGFR2, converges on the PI3K/Akt pathway to increase mTOR signaling, and mTOR activation enhances VEGF transcription (Liu, Chen, Cheng, Chen, & Qian, ). Moreover, studies in non‐neuronal tissues have reported a causal association between TLR4 activation and increases in VEGF expression (Botero, Shelburne, Holland, Hanks, & Nor, ; Cho, Kang, Han, Um, & Lee, ). These studies highlight the highly interconnected molecular signaling between VEGF, mTOR, and TLR4 pathways and their convergence on various aspects of post‐traumatic cellular and synaptic responses.…”

Section: Neuroimmune Interactions In Brain Injurymentioning

confidence: 99%

Converging early responses to brain injury pave the road to epileptogenesis

Neuberger

Gupta

Subramanian

et al. 2017

J of Neuroscience Research

View full text Add to dashboard Cite

Epilepsy, characterized by recurrent seizures and abnormal electrical activity in the brain, is one of the most prevalent brain disorders. Over two million people in the United States have been diagnosed with epilepsy and 3% of the general population will be diagnosed with it at some point in their lives. While most developmental epilepsies occur due to genetic predisposition, a class of "acquired" epilepsies results from a variety of brain insults. A leading etiological factor for epilepsy that is currently on the rise is traumatic brain injury (TBI), which accounts for up to 20% of all symptomatic epilepsies. Remarkably, the presence of an identified early insult that constitutes a risk for development of epilepsy provides a therapeutic window in which the pathological processes associated with brain injury can be manipulated to limit the subsequent development of recurrent seizure activity and epilepsy. Recent studies have revealed diverse pathologies, including enhanced excitability, activated immune signaling, cell death, and enhanced neurogenesis within a week after injury, suggesting a period of heightened adaptive and maladaptive plasticity. An integrated understanding of these processes and their cellular and molecular underpinnings could lead to novel targets to arrest epileptogenesis after trauma. This review attempts to highlight and relate the diverse early changes after trauma and their role in development of epilepsy and suggests potential strategies to limit neurological complications in the injured brain.

show abstract

Activation Of TLR4 Induces VEGF Expression Via Akt Pathway In Nasal Polyps

Cited by 5 publications

References 0 publications

Autophagy is deficient in nasal polyps: implications for the pathogenesis of the disease

Autophagy is deficient in nasal polyps: implications for the pathogenesis of the disease

7‑Difluoromethyl‑5,4'‑dimethoxygenistein exerts anti‑angiogenic effects on acute promyelocytic leukemia HL‑60 cells by inhibiting the TLR4/NF‑κB signaling pathway

Converging early responses to brain injury pave the road to epileptogenesis

Contact Info

Product

Resources

About