Viscolin reduces VCAM-1 expression in TNF-α-treated endothelial cells via the JNK/NF-κB and ROS pathway

Liang, Chan Jung; Wang, Shu‐Huei; Chen, Yung‐Hsiang; Chang, Shih‐Sheng; Hwang, Tsong‐Long; Leu, Yann Lii; Tseng, Ying Chih; Li, Chi Yuan; Chen, Yuh‐Lien

doi:10.1016/j.freeradbiomed.2011.06.023

Cited by 48 publications

(55 citation statements)

References 29 publications

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“…Leukocyte adhesion is primarily mediated by endothelial surface expression of adhesion molecules, ie, VCAM-1. Although the levels of VCAM-1 expression have been suggested to be associated with the levels of ROS generation, 27 in the current study we find that blocking S303-4 phosphorylation inhibits O 2 .2 production, but has no significant effect on endothelial VCAM-1 expression. The pathophysiological relevance of this is that increased O 2 .2 production is not a prerequisite for p47 phox to mediate TNF signaling, VCAM-1 expression, and acute inflammation, which may imply that nonspecific antioxidant therapy is not effective in those conditions.…”

Section: Discussioncontrasting

confidence: 92%

Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Teng

Fan

Meijles

et al. 2012

ATVB

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Section: Discussioncontrasting

confidence: 92%

Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Teng

Fan

Meijles

et al. 2012

ATVB

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“…Kamioka et al [21] also reported that olmesartan inhibited ROS production by advanced glycation end products via inhibition of NADPH oxidase activity. TNF-α-induced ROS production is also mediated by NADPH oxidase acitivation [22]. As shown in figure 2c, RNH-6270 inhibited TNF-α-induced NADPH oxidase activity in HGECs.…”

Section: Discussionmentioning

confidence: 79%

Angiotensin II Receptor Blocker Improves Tumor Necrosis Factor-a-Induced Cytotoxicity via Antioxidative Effect in Human Glomerular Endothelial Cells

Izawa‐Ishizawa¹,

Ishizawa

Sakurada³

et al. 2012

Pharmacology

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Background/Aims: Tumor necrosis factor-α (TNF-α) is known to involve the progression of renal dysfunction through its cytotoxicity and proinflammatory effects such as the induction of intercellular adhesion molecule (ICAM)-1 expression in vascular endothelial cells (ECs). Olmesartan, one of the angiotensin II type 1 receptor blockers (ARBs), has been reported to show protective effects on injured ECs by some causal factors of renal disorder other than angiotensin II. However, the effects of olmesartan on TNF-α-induced glomerular EC damage have not been investigated. In the present study, we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Methods: Cultured HGECs were stimulated by TNF-α, and then cell viability and cytotoxicity were measured by MTT assay and lactate dehydrogenase release assay, respectively. TNF-α-induced oxidative stress was estimated by dihydroethidium assay and lucigenin chemiluminescence assay. ICAM-1 expression and the phosphorylations of mitogen-activated protein kinases were measured using Western blotting assay. Results: RNH-6270 suppressed cell death and the increase in ICAM-1 expression induced by TNF-α via the inhibition of reactive oxygen species in HGECs. Conclusion: Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction.

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“…It was reported in vascular ECs that TNF-␣-induced ROS production was inhibited by NADPH oxidase (NOX) inhibitors, diphenylene iodonium and apocynin (22). In the same report, it was demonstrated that diphenylene iodonium and apocynin inhibited TNF-␣-induced phosphorylation of JNK and NF-B as well as VCAM-1 expression and monocyte adhesion.…”

Section: Discussionmentioning

confidence: 91%

Eukaryotic elongation factor 2 kinase regulates the development of hypertension through oxidative stress-dependent vascular inflammation

Usui

Okada

Hara

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Eukaryotic elongation factor 2 kinase (eEF2K) is a Ca2+/calmodulin-dependent protein kinase. We recently demonstrated that eEF2K protein increases in mesenteric artery from spontaneously hypertensive rats (SHR). Pathogenesis of hypertension is regulated in part by vascular inflammation. We tested the hypothesis whether eEF2K mediates vascular inflammatory responses and development of hypertension. In vascular endothelial cells, small interfering RNA (siRNA) against eEF2K inhibited induction of VCAM-1 and endothelial-selectin as well as monocyte adhesion by TNF-α (10 ng/ml). eEF2K siRNA inhibited phosphorylation of JNK and NF-κB p65 as well as reactive oxygen species (ROS) production by TNF-α. In vascular smooth muscle cells, eEF2K siRNA also inhibited VCAM-1 induction and phosphorylation of JNK and NF-κB by TNF-α. In vivo, increased blood pressure in SHR and ROS production, induction of inflammatory molecules, and hypertrophy in SHR superior mesenteric artery were reduced by an eEF2K inhibitor NH125 (500 μg·kg(-1)·day(-1)). In SHR superior mesenteric artery, impairment of ACh-induced relaxation was normalized by NH125. The present results for the first time demonstrate that eEF2K mediates TNF-α-induced vascular inflammation via ROS-dependent mechanism, which is at least partly responsible for the development of hypertension in SHR.

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Viscolin reduces VCAM-1 expression in TNF-α-treated endothelial cells via the JNK/NF-κB and ROS pathway

Cited by 48 publications

References 29 publications

Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Angiotensin II Receptor Blocker Improves Tumor Necrosis Factor-a-Induced Cytotoxicity via Antioxidative Effect in Human Glomerular Endothelial Cells

Eukaryotic elongation factor 2 kinase regulates the development of hypertension through oxidative stress-dependent vascular inflammation

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Viscolin reduces VCAM-1 expression in TNF-α-treated endothelial cells via the JNK/NF-κB and ROS pathway

Cited by 48 publications

References 29 publications

Divergent Effects of p47 phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Divergent Effects of p47 phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Angiotensin II Receptor Blocker Improves Tumor Necrosis Factor-a-Induced Cytotoxicity via Antioxidative Effect in Human Glomerular Endothelial Cells

Eukaryotic elongation factor 2 kinase regulates the development of hypertension through oxidative stress-dependent vascular inflammation

Contact Info

Product

Resources

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Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells