HCMV infection attenuates hydrogen peroxide induced endothelial apoptosis - involvement of ERK pathway

Jing Wang; Ying H. Shen; Budi Utama; Jian Wang; Scott A. LeMaire; Joseph S. Coselli; Greg M. Vercellotti; Xing Li Wang

doi:10.1016/j.febslet.2006.04.041

HCMV infection attenuates hydrogen peroxide induced endothelial apoptosis - involvement of ERK pathway

Jing Wang, Ying H. Shen, Budi Utama, Jian Wang, Scott A. LeMaire, Joseph S. Coselli, Greg M. Vercellotti, Xing Li Wang

Medicine - Hematology, Oncology, Transplant

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

22 Scopus citations

Abstract

Human cytomegalovirus (HCMV) exerts anti-apoptotic effect during early stage of infection, which provides HCMV time for propagation. We investigated pathways mediating the resistance to H₂O₂-induced cell death - a self-defense mechanism to remove infected cells. We found that human aortic endothelial cells (HAECs) infected with VHL/E strain of HCMV during first 3 days were resistant to H₂O₂ (0-2 mM) induced apoptosis. This anti-apoptotic effect may be mediated by the upregulation of Bcl-2, an anti-apoptotic protein through the activation pro-survival pathway extracellular signal regulated kinase (ERK). Through this mechanism, HCMV is able to propagate and causes endothelial dysfunction, hence vascular disease.

Original language	English (US)
Pages (from-to)	2779-2787
Number of pages	9
Journal	FEBS Letters
Volume	580
Issue number	11
DOIs	https://doi.org/10.1016/j.febslet.2006.04.041
State	Published - May 15 2006

Bibliographical note

Funding Information:
This project is supported by Grant NIH R01-HL071608 to X.L.W. Dr. Xing Li Wang is an AHA Established Investigator.

Keywords

Apoptosis
Cytomegalovirus
Endothelium
Hydrogen peroxide

UN SDGs

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

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10.1016/j.febslet.2006.04.041

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title = "HCMV infection attenuates hydrogen peroxide induced endothelial apoptosis - involvement of ERK pathway",

abstract = "Human cytomegalovirus (HCMV) exerts anti-apoptotic effect during early stage of infection, which provides HCMV time for propagation. We investigated pathways mediating the resistance to H2O2-induced cell death - a self-defense mechanism to remove infected cells. We found that human aortic endothelial cells (HAECs) infected with VHL/E strain of HCMV during first 3 days were resistant to H2O2 (0-2 mM) induced apoptosis. This anti-apoptotic effect may be mediated by the upregulation of Bcl-2, an anti-apoptotic protein through the activation pro-survival pathway extracellular signal regulated kinase (ERK). Through this mechanism, HCMV is able to propagate and causes endothelial dysfunction, hence vascular disease.",

keywords = "Apoptosis, Cytomegalovirus, Endothelium, Hydrogen peroxide",

author = "Jing Wang and Shen, {Ying H.} and Budi Utama and Jian Wang and LeMaire, {Scott A.} and Coselli, {Joseph S.} and Vercellotti, {Greg M.} and Wang, {Xing Li}",

note = "Funding Information: This project is supported by Grant NIH R01-HL071608 to X.L.W. Dr. Xing Li Wang is an AHA Established Investigator.",

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T1 - HCMV infection attenuates hydrogen peroxide induced endothelial apoptosis - involvement of ERK pathway

AU - Wang, Jing

AU - Shen, Ying H.

AU - Utama, Budi

AU - Wang, Jian

AU - LeMaire, Scott A.

AU - Coselli, Joseph S.

AU - Vercellotti, Greg M.

AU - Wang, Xing Li

N1 - Funding Information: This project is supported by Grant NIH R01-HL071608 to X.L.W. Dr. Xing Li Wang is an AHA Established Investigator.

PY - 2006/5/15

Y1 - 2006/5/15

N2 - Human cytomegalovirus (HCMV) exerts anti-apoptotic effect during early stage of infection, which provides HCMV time for propagation. We investigated pathways mediating the resistance to H2O2-induced cell death - a self-defense mechanism to remove infected cells. We found that human aortic endothelial cells (HAECs) infected with VHL/E strain of HCMV during first 3 days were resistant to H2O2 (0-2 mM) induced apoptosis. This anti-apoptotic effect may be mediated by the upregulation of Bcl-2, an anti-apoptotic protein through the activation pro-survival pathway extracellular signal regulated kinase (ERK). Through this mechanism, HCMV is able to propagate and causes endothelial dysfunction, hence vascular disease.

AB - Human cytomegalovirus (HCMV) exerts anti-apoptotic effect during early stage of infection, which provides HCMV time for propagation. We investigated pathways mediating the resistance to H2O2-induced cell death - a self-defense mechanism to remove infected cells. We found that human aortic endothelial cells (HAECs) infected with VHL/E strain of HCMV during first 3 days were resistant to H2O2 (0-2 mM) induced apoptosis. This anti-apoptotic effect may be mediated by the upregulation of Bcl-2, an anti-apoptotic protein through the activation pro-survival pathway extracellular signal regulated kinase (ERK). Through this mechanism, HCMV is able to propagate and causes endothelial dysfunction, hence vascular disease.

KW - Apoptosis

KW - Cytomegalovirus

KW - Endothelium

KW - Hydrogen peroxide

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JO - FEBS Letters

JF - FEBS Letters

IS - 11

ER -

HCMV infection attenuates hydrogen peroxide induced endothelial apoptosis - involvement of ERK pathway

Abstract

Bibliographical note

Keywords

UN SDGs

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