Streptococcus sanguinis and the sera of patients with Behçet's disease stimulate membrane expression of α-enolase in human dermal microvascular endothelial cells

Suhyun Cho, Zhenlong Zheng, Sung Bin Cho, Min Ju Choi, Kwanghoon Lee, Dongsik Bang

Research output: Contribution to journalArticle

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Abstract

The glycolytic enzyme α-enolase is a plasminogen-binding protein that is generally found in the cytosolic compartment. However, α-enolase can also be expressed on cell surfaces following an inflammatory stimulus via an unknown mechanism. We investigated the effects of Streptococcus sanguinis (S. sanguinis) and the sera of patients with Behçet's disease (BD) on the expression and distribution of α-enolase in human dermal microvascular endothelial cells (HDMECs). HDMECs were stimulated with cultured S. sanguinis and the sera of active BD patients. HDMECs incubated for 6, 12 or 24 h were harvested, and the membrane and cytoplasmic fractions of proteins were extracted. The expression and distribution of α-enolase were analyzed using subcellular fractionation and immunoblotting. Subcellular localization of α-enolase was also assessed by immunocytochemistry. S. sanguinis stimulated the expression of α-enolase in the membranous compartment of HDMECs in a dose-dependent manner. This pattern was also observed in HDMECs incubated with BD patients' sera. Although incubation of HDMECs with sera from healthy controls increased membrane expression of α-enolase, incubation with BD sera resulted in earlier and higher expression of this glycoprotein in the cellular membrane of HDMECs. Immunocytochemistry revealed strong immunostaining of α-enolase in the cytoplasm and cytoplasmic membrane of HDMECs incubated with S. sanguinis or BD patients' sera. In conclusions, these results indicate that S. sanguinis infection and the sera of BD patients with active disease are inflammatory stimuli that can induce membranous α-enolase expression in endothelial cells. Membrane-expressed α-enolase could potentially react with anti-α-enolase antibodies in BD patients' sera, resulting in increased inflammation.

Original languageEnglish
Pages (from-to)223-232
Number of pages10
JournalArchives of Dermatological Research
Volume305
Issue number3
DOIs
Publication statusPublished - 2013 Apr 1

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Phosphopyruvate Hydratase
Streptococcus
Endothelial Cells
Skin
Membranes
Serum
Immunohistochemistry
Cell Membrane
Plasminogen
Immunoblotting
Anti-Idiotypic Antibodies
Glycoproteins
Carrier Proteins
Cytoplasm
Inflammation

All Science Journal Classification (ASJC) codes

  • Dermatology

Cite this

@article{6585134ce04940e08dfee3e627d2a91a,
title = "Streptococcus sanguinis and the sera of patients with Beh{\cc}et's disease stimulate membrane expression of α-enolase in human dermal microvascular endothelial cells",
abstract = "The glycolytic enzyme α-enolase is a plasminogen-binding protein that is generally found in the cytosolic compartment. However, α-enolase can also be expressed on cell surfaces following an inflammatory stimulus via an unknown mechanism. We investigated the effects of Streptococcus sanguinis (S. sanguinis) and the sera of patients with Beh{\cc}et's disease (BD) on the expression and distribution of α-enolase in human dermal microvascular endothelial cells (HDMECs). HDMECs were stimulated with cultured S. sanguinis and the sera of active BD patients. HDMECs incubated for 6, 12 or 24 h were harvested, and the membrane and cytoplasmic fractions of proteins were extracted. The expression and distribution of α-enolase were analyzed using subcellular fractionation and immunoblotting. Subcellular localization of α-enolase was also assessed by immunocytochemistry. S. sanguinis stimulated the expression of α-enolase in the membranous compartment of HDMECs in a dose-dependent manner. This pattern was also observed in HDMECs incubated with BD patients' sera. Although incubation of HDMECs with sera from healthy controls increased membrane expression of α-enolase, incubation with BD sera resulted in earlier and higher expression of this glycoprotein in the cellular membrane of HDMECs. Immunocytochemistry revealed strong immunostaining of α-enolase in the cytoplasm and cytoplasmic membrane of HDMECs incubated with S. sanguinis or BD patients' sera. In conclusions, these results indicate that S. sanguinis infection and the sera of BD patients with active disease are inflammatory stimuli that can induce membranous α-enolase expression in endothelial cells. Membrane-expressed α-enolase could potentially react with anti-α-enolase antibodies in BD patients' sera, resulting in increased inflammation.",
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Streptococcus sanguinis and the sera of patients with Behçet's disease stimulate membrane expression of α-enolase in human dermal microvascular endothelial cells. / Cho, Suhyun; Zheng, Zhenlong; Cho, Sung Bin; Choi, Min Ju; Lee, Kwanghoon; Bang, Dongsik.

In: Archives of Dermatological Research, Vol. 305, No. 3, 01.04.2013, p. 223-232.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Streptococcus sanguinis and the sera of patients with Behçet's disease stimulate membrane expression of α-enolase in human dermal microvascular endothelial cells

AU - Cho, Suhyun

AU - Zheng, Zhenlong

AU - Cho, Sung Bin

AU - Choi, Min Ju

AU - Lee, Kwanghoon

AU - Bang, Dongsik

PY - 2013/4/1

Y1 - 2013/4/1

N2 - The glycolytic enzyme α-enolase is a plasminogen-binding protein that is generally found in the cytosolic compartment. However, α-enolase can also be expressed on cell surfaces following an inflammatory stimulus via an unknown mechanism. We investigated the effects of Streptococcus sanguinis (S. sanguinis) and the sera of patients with Behçet's disease (BD) on the expression and distribution of α-enolase in human dermal microvascular endothelial cells (HDMECs). HDMECs were stimulated with cultured S. sanguinis and the sera of active BD patients. HDMECs incubated for 6, 12 or 24 h were harvested, and the membrane and cytoplasmic fractions of proteins were extracted. The expression and distribution of α-enolase were analyzed using subcellular fractionation and immunoblotting. Subcellular localization of α-enolase was also assessed by immunocytochemistry. S. sanguinis stimulated the expression of α-enolase in the membranous compartment of HDMECs in a dose-dependent manner. This pattern was also observed in HDMECs incubated with BD patients' sera. Although incubation of HDMECs with sera from healthy controls increased membrane expression of α-enolase, incubation with BD sera resulted in earlier and higher expression of this glycoprotein in the cellular membrane of HDMECs. Immunocytochemistry revealed strong immunostaining of α-enolase in the cytoplasm and cytoplasmic membrane of HDMECs incubated with S. sanguinis or BD patients' sera. In conclusions, these results indicate that S. sanguinis infection and the sera of BD patients with active disease are inflammatory stimuli that can induce membranous α-enolase expression in endothelial cells. Membrane-expressed α-enolase could potentially react with anti-α-enolase antibodies in BD patients' sera, resulting in increased inflammation.

AB - The glycolytic enzyme α-enolase is a plasminogen-binding protein that is generally found in the cytosolic compartment. However, α-enolase can also be expressed on cell surfaces following an inflammatory stimulus via an unknown mechanism. We investigated the effects of Streptococcus sanguinis (S. sanguinis) and the sera of patients with Behçet's disease (BD) on the expression and distribution of α-enolase in human dermal microvascular endothelial cells (HDMECs). HDMECs were stimulated with cultured S. sanguinis and the sera of active BD patients. HDMECs incubated for 6, 12 or 24 h were harvested, and the membrane and cytoplasmic fractions of proteins were extracted. The expression and distribution of α-enolase were analyzed using subcellular fractionation and immunoblotting. Subcellular localization of α-enolase was also assessed by immunocytochemistry. S. sanguinis stimulated the expression of α-enolase in the membranous compartment of HDMECs in a dose-dependent manner. This pattern was also observed in HDMECs incubated with BD patients' sera. Although incubation of HDMECs with sera from healthy controls increased membrane expression of α-enolase, incubation with BD sera resulted in earlier and higher expression of this glycoprotein in the cellular membrane of HDMECs. Immunocytochemistry revealed strong immunostaining of α-enolase in the cytoplasm and cytoplasmic membrane of HDMECs incubated with S. sanguinis or BD patients' sera. In conclusions, these results indicate that S. sanguinis infection and the sera of BD patients with active disease are inflammatory stimuli that can induce membranous α-enolase expression in endothelial cells. Membrane-expressed α-enolase could potentially react with anti-α-enolase antibodies in BD patients' sera, resulting in increased inflammation.

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