Inhibitory effects of antithrombin on the expression of secretory group IIA phospholipase A2 in endothelial cells

Tae Hoon Kim; Jong Sup Bae

doi:10.3858/BMBRep.2010.43.9.604

Inhibitory effects of antithrombin on the expression of secretory group IIA phospholipase A₂ in endothelial cells

Tae Hoon Kim, Jong Sup Bae

Daegu Haany University

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Tumor necrosis factor-α (TNF-α) mediates proinflammatory responses in primary human umbilical vein endothelial cells (HUVECs), and it upregulates the expression of secretory group IIA phospholipase A₂ (sPLA₂-IIA). sPLA₂-IIA plays a pivotal role in inflammation, and antithrombin (AT) possesses properties that are beneficial to endothelial cells. Therefore, we investigated the effects of AT on the expression of sPLA₂-IIA in TNF-α-stimulated HUVECs. TNF-α potently upregulated the expression of sPLA₂-IIA, and prior treatment of cells with AT inhibited the expression of sPLA₂-IIA in HUVECs. Also, antibodies or siRNA for syndecan-4 blocked the protective effect of AT. Furthermore, PI3-kinase and the AKT pathway are significantly involved in the AT-mediated inhibition of the expression of sPLA₂-IIA. These results show that AT effectively suppresses the upregulated sPLA₂-IIA expression, which might contribute to the cytoprotective effects of AT in the treatment of severe inflammatory diseases.

Original language	English
Pages (from-to)	604-608
Number of pages	5
Journal	BMB Reports
Volume	43
Issue number	9
DOIs	https://doi.org/10.3858/BMBRep.2010.43.9.604
State	Published - Sep 2010

Keywords

Antithrombin
HUVEC
Inflammation
sPLA-IIA
TNF-α

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.3858/BMBRep.2010.43.9.604

Cite this

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title = "Inhibitory effects of antithrombin on the expression of secretory group IIA phospholipase A2 in endothelial cells",

abstract = "Tumor necrosis factor-α (TNF-α) mediates proinflammatory responses in primary human umbilical vein endothelial cells (HUVECs), and it upregulates the expression of secretory group IIA phospholipase A2 (sPLA2-IIA). sPLA2-IIA plays a pivotal role in inflammation, and antithrombin (AT) possesses properties that are beneficial to endothelial cells. Therefore, we investigated the effects of AT on the expression of sPLA2-IIA in TNF-α-stimulated HUVECs. TNF-α potently upregulated the expression of sPLA2-IIA, and prior treatment of cells with AT inhibited the expression of sPLA2-IIA in HUVECs. Also, antibodies or siRNA for syndecan-4 blocked the protective effect of AT. Furthermore, PI3-kinase and the AKT pathway are significantly involved in the AT-mediated inhibition of the expression of sPLA2-IIA. These results show that AT effectively suppresses the upregulated sPLA2-IIA expression, which might contribute to the cytoprotective effects of AT in the treatment of severe inflammatory diseases.",

keywords = "Antithrombin, HUVEC, Inflammation, sPLA-IIA, TNF-α",

author = "Kim, {Tae Hoon} and Bae, {Jong Sup}",

year = "2010",

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AU - Kim, Tae Hoon

AU - Bae, Jong Sup

PY - 2010/9

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N2 - Tumor necrosis factor-α (TNF-α) mediates proinflammatory responses in primary human umbilical vein endothelial cells (HUVECs), and it upregulates the expression of secretory group IIA phospholipase A2 (sPLA2-IIA). sPLA2-IIA plays a pivotal role in inflammation, and antithrombin (AT) possesses properties that are beneficial to endothelial cells. Therefore, we investigated the effects of AT on the expression of sPLA2-IIA in TNF-α-stimulated HUVECs. TNF-α potently upregulated the expression of sPLA2-IIA, and prior treatment of cells with AT inhibited the expression of sPLA2-IIA in HUVECs. Also, antibodies or siRNA for syndecan-4 blocked the protective effect of AT. Furthermore, PI3-kinase and the AKT pathway are significantly involved in the AT-mediated inhibition of the expression of sPLA2-IIA. These results show that AT effectively suppresses the upregulated sPLA2-IIA expression, which might contribute to the cytoprotective effects of AT in the treatment of severe inflammatory diseases.

AB - Tumor necrosis factor-α (TNF-α) mediates proinflammatory responses in primary human umbilical vein endothelial cells (HUVECs), and it upregulates the expression of secretory group IIA phospholipase A2 (sPLA2-IIA). sPLA2-IIA plays a pivotal role in inflammation, and antithrombin (AT) possesses properties that are beneficial to endothelial cells. Therefore, we investigated the effects of AT on the expression of sPLA2-IIA in TNF-α-stimulated HUVECs. TNF-α potently upregulated the expression of sPLA2-IIA, and prior treatment of cells with AT inhibited the expression of sPLA2-IIA in HUVECs. Also, antibodies or siRNA for syndecan-4 blocked the protective effect of AT. Furthermore, PI3-kinase and the AKT pathway are significantly involved in the AT-mediated inhibition of the expression of sPLA2-IIA. These results show that AT effectively suppresses the upregulated sPLA2-IIA expression, which might contribute to the cytoprotective effects of AT in the treatment of severe inflammatory diseases.

KW - Antithrombin

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