Coxsackievirus B3 infection induces cyr61 activation via JNK to mediate cell death

Sun Mi Kim, Jung Hyun Park, Sun Ku Chung, Joo Young Kim, Ha Young Hwang, Kwang Chul Chung, Inho Jo, Sang Ick Park, Jae Hwan Nam

Research output: Contribution to journalArticle

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Abstract

Coxsackievirus B3 (CVB3), an enterovirus in the Picornavirus family, is the most common human pathogen associated with myocarditis and idiopathic dilated cardiomyopathy. We found upregulation of the cysteine-rich protein gene (cyr61) after CVB3 infection in HeLa cells with a cDNA microarray approach, which is confirmed by Northern blot analysis. It is also revealed that the extracellular amount of Cyr61 protein was increased after CVB3 infection in HeLa cells, cyr61 is an early-transcribed gene, and the Cyr61 protein is secreted into the extracellular matrix. Its function is related to cell adhesion, migration, and neuronal cell death. Here, we show that activation of the cyr61 promoter by CVB3 infection is dependent on JNK activation induced by CVB3 replication and viral protein expression in infected cells. To explore the role of Cyr61 protein in infected HeLa cells, we transiently overexpressed cyr61 and infected HeLa cells with CVB3. This increased CVB3 growth in the cells and promoted host cell death by viral infection, whereas down-expression of cyr61 with short interfering RNA reduced CVB3 growth and showed resistance to cell death by CVB3 infection. In conclusion, we have demonstrated a new role for cyr61 in HeLa cells infected with CVB3, which is associated with the cell death induced by virus infection. These data thus expand our understanding of the physiological functions of cyr61 in virus-induced cell death and provide new insights into the cellular factors involved.

Original languageEnglish
Pages (from-to)13479-13488
Number of pages10
JournalJournal of Virology
Volume78
Issue number24
DOIs
Publication statusPublished - 2004 Dec 1

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Coxsackievirus Infections
Enterovirus
cell death
Cell Death
HeLa Cells
infection
Virus Diseases
Proteins
Picornaviridae
cells
cell adhesion
Myocarditis
Dilated Cardiomyopathy
Viral Proteins
Growth
Oligonucleotide Array Sequence Analysis
proteins
Cell Adhesion
Northern Blotting
Small Interfering RNA

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Cite this

Kim, S. M., Park, J. H., Chung, S. K., Kim, J. Y., Hwang, H. Y., Chung, K. C., ... Nam, J. H. (2004). Coxsackievirus B3 infection induces cyr61 activation via JNK to mediate cell death. Journal of Virology, 78(24), 13479-13488. https://doi.org/10.1128/JVI.78.24.13479-13488.2004
Kim, Sun Mi ; Park, Jung Hyun ; Chung, Sun Ku ; Kim, Joo Young ; Hwang, Ha Young ; Chung, Kwang Chul ; Jo, Inho ; Park, Sang Ick ; Nam, Jae Hwan. / Coxsackievirus B3 infection induces cyr61 activation via JNK to mediate cell death. In: Journal of Virology. 2004 ; Vol. 78, No. 24. pp. 13479-13488.
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Kim, SM, Park, JH, Chung, SK, Kim, JY, Hwang, HY, Chung, KC, Jo, I, Park, SI & Nam, JH 2004, 'Coxsackievirus B3 infection induces cyr61 activation via JNK to mediate cell death', Journal of Virology, vol. 78, no. 24, pp. 13479-13488. https://doi.org/10.1128/JVI.78.24.13479-13488.2004

Coxsackievirus B3 infection induces cyr61 activation via JNK to mediate cell death. / Kim, Sun Mi; Park, Jung Hyun; Chung, Sun Ku; Kim, Joo Young; Hwang, Ha Young; Chung, Kwang Chul; Jo, Inho; Park, Sang Ick; Nam, Jae Hwan.

In: Journal of Virology, Vol. 78, No. 24, 01.12.2004, p. 13479-13488.

Research output: Contribution to journalArticle

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T1 - Coxsackievirus B3 infection induces cyr61 activation via JNK to mediate cell death

AU - Kim, Sun Mi

AU - Park, Jung Hyun

AU - Chung, Sun Ku

AU - Kim, Joo Young

AU - Hwang, Ha Young

AU - Chung, Kwang Chul

AU - Jo, Inho

AU - Park, Sang Ick

AU - Nam, Jae Hwan

PY - 2004/12/1

Y1 - 2004/12/1

N2 - Coxsackievirus B3 (CVB3), an enterovirus in the Picornavirus family, is the most common human pathogen associated with myocarditis and idiopathic dilated cardiomyopathy. We found upregulation of the cysteine-rich protein gene (cyr61) after CVB3 infection in HeLa cells with a cDNA microarray approach, which is confirmed by Northern blot analysis. It is also revealed that the extracellular amount of Cyr61 protein was increased after CVB3 infection in HeLa cells, cyr61 is an early-transcribed gene, and the Cyr61 protein is secreted into the extracellular matrix. Its function is related to cell adhesion, migration, and neuronal cell death. Here, we show that activation of the cyr61 promoter by CVB3 infection is dependent on JNK activation induced by CVB3 replication and viral protein expression in infected cells. To explore the role of Cyr61 protein in infected HeLa cells, we transiently overexpressed cyr61 and infected HeLa cells with CVB3. This increased CVB3 growth in the cells and promoted host cell death by viral infection, whereas down-expression of cyr61 with short interfering RNA reduced CVB3 growth and showed resistance to cell death by CVB3 infection. In conclusion, we have demonstrated a new role for cyr61 in HeLa cells infected with CVB3, which is associated with the cell death induced by virus infection. These data thus expand our understanding of the physiological functions of cyr61 in virus-induced cell death and provide new insights into the cellular factors involved.

AB - Coxsackievirus B3 (CVB3), an enterovirus in the Picornavirus family, is the most common human pathogen associated with myocarditis and idiopathic dilated cardiomyopathy. We found upregulation of the cysteine-rich protein gene (cyr61) after CVB3 infection in HeLa cells with a cDNA microarray approach, which is confirmed by Northern blot analysis. It is also revealed that the extracellular amount of Cyr61 protein was increased after CVB3 infection in HeLa cells, cyr61 is an early-transcribed gene, and the Cyr61 protein is secreted into the extracellular matrix. Its function is related to cell adhesion, migration, and neuronal cell death. Here, we show that activation of the cyr61 promoter by CVB3 infection is dependent on JNK activation induced by CVB3 replication and viral protein expression in infected cells. To explore the role of Cyr61 protein in infected HeLa cells, we transiently overexpressed cyr61 and infected HeLa cells with CVB3. This increased CVB3 growth in the cells and promoted host cell death by viral infection, whereas down-expression of cyr61 with short interfering RNA reduced CVB3 growth and showed resistance to cell death by CVB3 infection. In conclusion, we have demonstrated a new role for cyr61 in HeLa cells infected with CVB3, which is associated with the cell death induced by virus infection. These data thus expand our understanding of the physiological functions of cyr61 in virus-induced cell death and provide new insights into the cellular factors involved.

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