Arsenite inhibits gene expression of perlecan, syndecan-1, -2, -3 and biglycan in cultured vascular endothelial cells

Wu, Dong-pan; Nakano, Tetsuo; Tsuneoka, Yousuke; Takahashi, Tsutomu; Shinoda, Yo; Kaji, Toshiyuki; Fujiwara, Yasuyuki

doi:10.2131/fts.7.77

Cited by 3 publications

(2 citation statements)

References 34 publications

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“…Perlecan and biglycan exhibit anti-thrombin activity through the activation of antithrombin III and heparin cofactor II, respectively [ 54 , 55 ]. We previously showed that arsenite inhibits the expression of both perlecan and biglycan in vascular endothelial cells [ 56 , 57 ]. Thus, exposure to arsenite is thought to promote blood coagulation by inducing vascular endothelial cell dysfunction, including inhibition of the production of both t-PA and proteoglycans [ 56 , 57 ].…”

Section: Discussionmentioning

confidence: 99%

Arsenite Inhibits Tissue-Type Plasminogen Activator Synthesis through NRF2 Activation in Cultured Human Vascular Endothelial EA.hy926 Cells

Nakano

Takahashi

Yamamoto

et al. 2021

IJMS

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Chronic arsenic exposure is known to be related to the progression of atherosclerosis. However, the pathogenic mechanisms of arsenic-induced atherosclerosis have not been fully elucidated. Because disruption of the blood coagulation/fibrinolytic system is involved in the development of arteriosclerosis, we investigated the effect of arsenite on fibrinolytic activity in human vascular endothelial EA.hy926 cells in the present study. Fibrinolysis depends on the balance between tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) secreted from vascular endothelial cells. We found that arsenite reduced fibrinolytic t-PA activity by inhibiting its synthesis without affecting PAI-1 production. The inhibitory effect of arsenite on t-PA expression was partially recovered by the reactive oxygen species (ROS) scavenger Trolox. The nuclear factor erythroid 2 related factor 2 (NRF2) pathway is known to be activated by arsenite via ROS production. We confirmed that arsenite activated the NRF2 pathway, and arsenite-induced inhibition of fibrinolytic t-PA activity was abrogated in NRF2-knockdown EA.hy926 cells. These results suggest that arsenite inhibits the fibrinolytic activity of t-PA by selectively suppressing its synthesis via activation of the NRF2 pathway in vascular endothelial cells.

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Section: Discussionmentioning

confidence: 99%

Arsenite Inhibits Tissue-Type Plasminogen Activator Synthesis through NRF2 Activation in Cultured Human Vascular Endothelial EA.hy926 Cells

Nakano

Takahashi

Yamamoto

et al. 2021

IJMS

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“…Cell culture was performed as described previously (Wu et al, 2020). Briefly, bovine aortic vascular endothelial cells were seeded in six-well culture plates at 2 × 10 4 cells/cm 2 and then cultured for 24, 48, and 72 hr in DMEM supplemented with 10% FBS (10% FBS-DMEM).…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Nucleolin positively regulates spontaneous cell proliferation but is not involved in inhibition of proliferation by lead in cultured bovine aortic endothelial cells

Takahashi

Takagi

Honma

et al. 2020

Fundam. Toxicol. Sci.

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-Nucleolin (NCL) is an abundant DNA-, RNA-, and protein-binding protein that is expressed ubiquitously in eukaryotic cells, implicating it in many cellular functions such as gene silencing, senescence, cytokinesis, and proliferation. NCL is also involved in angiogenesis events including vascular endothelial cell migration and proliferation. We previously found that lead, an environmental pollutant with vascular toxicity, inhibits the repair process of injured vascular endothelium via suppression of cell proliferation as a result of a lower proliferative response of cells to endogenous fibroblast growth factor-2. The present study investigated the expression of NCL in proliferating bovine aortic vascular endothelial cells and the role of NCL in proliferation of the cells in the presence or absence of lead. We found that the expression of NCL protein was independent of cell density. Both siRNA-mediated NCL knockdown and an anti-NCL-neutralizing antibody inhibited the proliferation of vascular endothelial cells without non-specific cell damage, indicating that NCL was involved in endothelial cell proliferation. However, lead significantly inhibited the proliferation of vascular endothelial cells without changing the expression level of NCL. Therefore, NCL may positively regulate spontaneous proliferation, but is not involved in the inhibition of proliferation by lead in vascular endothelial cells.

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Arsenite induces tissue factor synthesis through Nrf2 activation in cultured human aortic smooth muscle cells

et al. 2021

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Arsenite inhibits gene expression of perlecan, syndecan-1, -2, -3 and biglycan in cultured vascular endothelial cells

Cited by 3 publications

References 34 publications

Arsenite Inhibits Tissue-Type Plasminogen Activator Synthesis through NRF2 Activation in Cultured Human Vascular Endothelial EA.hy926 Cells

Arsenite Inhibits Tissue-Type Plasminogen Activator Synthesis through NRF2 Activation in Cultured Human Vascular Endothelial EA.hy926 Cells

Nucleolin positively regulates spontaneous cell proliferation but is not involved in inhibition of proliferation by lead in cultured bovine aortic endothelial cells

Arsenite induces tissue factor synthesis through Nrf2 activation in cultured human aortic smooth muscle cells

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