Transient receptor potential vanilloid type 1 is vital for (−)‐epigallocatechin‐3‐gallate mediated activation of endothelial nitric oxide synthase

Guo, Bei-Chia; Wei, Jeng; Su, Kuo‐Hui; Chiang, An-Na; Zhao, Jin‐Feng; Chen, Hsiang-Ying; Shyue, Song Kun; Lee, Tzong‐Shyuan

doi:10.1002/mnfr.201400699

Cited by 25 publications

(25 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the released ectodomain portion of TNFR1 may bind to TNF-α in the extracellular space and neutralize its activity [20]. Although the mechanisms are not completely elucidated, EGCG also increases cytosolic Ca 2+ in vascular smooth muscle cells and endothelial cells by extracellular Ca 2+ influx or release from endoplasmic reticulum (ER) storage Ca 2+ [21][22][23]. Thus, we hypothesized that EGCG may have anti-TNF-α effects by causing ectodomain shedding of TNFR1 through Ca 2+ -dependent activation of ADAM10.…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Attenuates the Effects of TNF-α in Vascular Endothelial Cells by Causing Ectodomain Shedding of TNF Receptor 1

Yang

Moon²,

Lee

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: We investigated the mechanism underlying anti-tumor necrosis factor-α (TNF-α) effects of epigallocatechin-3-gallate (EGCG) in human aortic endothelial cells. Methods: Tumor necrosis factor receptor 1 (TNFR1) was assessed by Western blot analysis. Cytosolic Ca²⁺ was measured using Fluo-4 AM. A disintegrin and metalloprotease 10 (ADAM10) was localized by immunofluorescence staining. Results: EGCG caused ectodomain shedding of TNFR1 within 30 min and attenuated TNF-α-induced endothelin-1 (ET-1) expression. EGCG-induced TNFR1 ectodomain shedding was prevented by BAPTA-AM (intracellular Ca²⁺ chelator), but not by the absence of extracellular Ca²⁺. In physiologic extracellular Ca²⁺ concentration, EGCG markedly increased cytosolic Ca²⁺. Even in the absence of extracellular Ca²⁺, EGCG raised cytosolic Ca²⁺, though less potently. siRNA depletion of ADAM10 prevented EGCG-induced ectodomain shedding of TNFR1 and also diminished the inhibitory effect of EGCG on TNF-α-induced ET-1 expression. EGCG caused translocation of ADAM10 to the plasma membrane, and this effect was prevented by BAPTA-AM. Besides extracellular Ca²⁺ influx, release of intracellular stored Ca²⁺ caused ADAM10-dependent ectodomain shedding of TNFR1. Conclusion: EGCG decreases the responsiveness of cells to TNF-α by causing ADAM10-dependent ectodomain shedding of TNFR1. This effect was attributed to its property to increase cytosolic Ca²⁺ through both extracellular Ca²⁺ influx and release of stored Ca²⁺.

show abstract

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Attenuates the Effects of TNF-α in Vascular Endothelial Cells by Causing Ectodomain Shedding of TNF Receptor 1

Yang

Moon²,

Lee

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…NO plays a key role in maintaining circulatory balance by modulating vascular tension [22,23]. Some herbs, such as epigallocatechin-3-gallate and nuciferine, have been shown to activate TRPV-1-Ca 2+ signaling, which leads to the phosphorylation of Akt, AMPK, and CaMKII, resulting in eNOS activation, NO production, and ultimately, angiogenesis in endothelial cells [24,25]. These data suggest that the endothelial Ca 2+ -eNOS signaling pathway plays the most important role in regulating vascular tone.…”

Section: Introductionmentioning

confidence: 99%

Nobiletin Relaxes Isolated Mesenteric Arteries by Activating the Endothelial Ca<sup>2+</sup>-eNOS Pathway in Rats

Yang

Lin

et al. 2016

J Vasc Res

View full text Add to dashboard Cite

Aims: Nobiletin, a natural polymethoxylated flavonoid compound, has various beneficial properties, such as anticancer, anti-inflammatory, and antioxidant effects, and it also improves memory. Therefore, we investigated the effects and mechanisms of nobiletin on rat isolated mesenteric arteries (MAs). Methods: We examined vasodilation induced by nobiletin on rat isolated MA rings with a tension study, the expression and activity of endothelial nitric oxide synthase (eNOS) with Western blotting, NO production with DAF- FMDA fluorescence, and intracellular Ca²⁺ concentration ([Ca²⁺]i) with Fluo-3AM. Results and Conclusion: Our study showed that nobiletin elicited a dose-dependent vasodilation in phenylephrine precontracted MA rings, but it did not elicit the same response in pulmonary artery rings. Vasodilation was related to endothelium and activated partly by eNOS. Vasodilation was inhibited by denudation of the endothelium or inhibition of eNOS activity. Nobiletin increased NO production by promoting the phosphorylation of eNOS at Ser-1177 without changing the level of eNOS expression in rat mesenteric artery endothelial cells (RMAECs). Nobiletin increased the concentration of endothelial [Ca²⁺]i, which enhances eNOS activity in RMAECs. In summary, vasodilation induced by nobiletin was dependent on the endothelium and partly on eNOS activation, which is mediated by high endothelial [Ca²⁺]i. Results suggest nobiletin may offer a therapeutic benefit and could potentially be used as a vasodilator for the treatment of hypertension.

show abstract

“…Simvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase blocker that is employed to treat hypercholesterolaemia and cardiovascular disorders, stimulated in vivo angiogenesis by promoting NO release through the assembly of the TRPV1-Akt-CaMKII-AMPK-eNOS complex described above (Su et al, 2014b). The same signaling pathway is recruited to promote tube formation in vitro and vascular development in vivo by erythropoietin (Yu et al, 2017) and epigallocatechin-3-gallate, the main catechin present in the green tea (Guo et al, 2015). Finally, pharmacological (with capsazepine) and genetic (with a selective siRNA) inhibition of TRPV1 prevented 14,15-EET-induced Ca 2+ influx, NO release, in vitro tube formation and in vivo angiogenesis in HMECs (Su et al, 2014a).…”

Section: Trpv1 In Angiogenesismentioning

confidence: 99%

Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular Ca2 + Entry for Angiogenesis, Arteriogenesis and Vasculogenesis

et al. 2020

View full text Add to dashboard Cite

Vasculogenesis, angiogenesis and arteriogenesis represent three crucial mechanisms involved in the formation and maintenance of the vascular network in embryonal and post-natal life. It has long been known that endothelial Ca 2+ signals are key players in vascular remodeling; indeed, multiple pro-angiogenic factors, including vascular endothelial growth factor, regulate endothelial cell fate through an increase in intracellular Ca 2+ concentration. Transient Receptor Potential (TRP) channel consist in a superfamily of non-selective cation channels that are widely expressed within vascular endothelial cells. In addition, TRP channels are present in the two main endothelial progenitor cell (EPC) populations, i.e., myeloid angiogenic cells (MACs) and endothelial colony forming cells (ECFCs). TRP channels are polymodal channels that can assemble in homo-and heteromeric complexes and may be sensitive to both pro-angiogenic cues and subtle changes in local microenvironment. These features render TRP channels the most versatile Ca 2+ entry pathway in vascular endothelial cells and in EPCs. Herein, we describe how endothelial TRP channels stimulate vascular remodeling by promoting angiogenesis, arteriogenesis and vasculogenesis through the integration of multiple environmental, e.g., extracellular growth factors and chemokines, and intracellular, e.g., reactive oxygen species, a decrease in Mg 2+ levels, or hypercholesterolemia, stimuli. In addition, we illustrate how endothelial TRP channels induce neovascularization in response to synthetic agonists and small molecule drugs. We focus the attention on TRPC1, TRPC3, TRPC4, TRPC5, TRPC6, TRPV1, TRPV4, TRPM2, TRPM4, TRPM7, TRPA1, that were shown to be involved in angiogenesis, arteriogenesis and vasculogenesis. Finally, we discuss the role of endothelial TRP channels in aberrant tumor vascularization by focusing on TRPC1, TRPC3, TRPV2, TRPV4, TRPM8, and TRPA1. These observations suggest that endothelial TRP channels represent potential therapeutic targets in multiple disorders featured by abnormal vascularization, including cancer, ischemic disorders, retinal degeneration and neurodegeneration.

show abstract

Transient receptor potential vanilloid type 1 is vital for (−)‐epigallocatechin‐3‐gallate mediated activation of endothelial nitric oxide synthase

Abstract: EGCG may trigger activation of TRPV1-Ca(2+) signaling, which leads to phosphorylation of Akt, AMPK, and CaMKII; eNOS activation; NO production; and, ultimately, angiogenesis in ECs.

Cited by 25 publications

References 50 publications

Epigallocatechin-3-Gallate Attenuates the Effects of TNF-α in Vascular Endothelial Cells by Causing Ectodomain Shedding of TNF Receptor 1

Epigallocatechin-3-Gallate Attenuates the Effects of TNF-α in Vascular Endothelial Cells by Causing Ectodomain Shedding of TNF Receptor 1

Nobiletin Relaxes Isolated Mesenteric Arteries by Activating the Endothelial Ca<sup>2+</sup>-eNOS Pathway in Rats

Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular Ca2 + Entry for Angiogenesis, Arteriogenesis and Vasculogenesis

Contact Info

Product

Resources

About