Gene expression in giant cell myocarditis

Altered expression of immune response genes

Michelle M. Kittleson, Khalid M. Minhas, Rafael A. Irizarry, Shui Q. Ye, Gina Edness, Elayne Breton, John V. Conte, Gordon Tomaselli, Joe GN Garcia, Joshua M. Hare

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Background: Giant cell myocarditis is a rapidly progressive and often fatal condition without a clear etiology or treatment. A better understanding of giant cell myocarditis pathogenesis is critical to developing treatments to prevent progression and reverse damage. We compared the gene expression of giant cell myocarditis with that of nonfailing hearts. Methods: Left ventricular samples from two giant cell myocarditis patients harvested during ventricular assist device placement and six unused donor hearts were examined using Affymetrix U133A microarrays. Differential gene expression was defined with a Bonferroni-adjusted p value ≤ 0.05 from a Student's t-test and an absolute fold change ≥ 2.0. Select gene expression was confirmed with quantitative PCR. Results: Of 115 differentially expressed genes, most were upregulated in giant cell myocarditis and involved in immune response, transcriptional regulation, and metabolism. T-cell activation genes included chemokine receptor 4; chemokine ligands 5, 9, 13, and 18; interleukin-10 receptor alpha; and beta-2 integrin. Conclusions: Gene expression analysis of giant cell myocarditis offers novel insights into its pathogenesis, namely the role of T-cell activators of the Th1 subset and immune response genes previously implicated in heart failure. This forms the basis for future work aimed at defining novel therapeutic targets for giant cell myocarditis.

Original languageEnglish (US)
Pages (from-to)333-340
Number of pages8
JournalInternational Journal of Cardiology
Volume102
Issue number2
DOIs
StatePublished - Jul 10 2005
Externally publishedYes

Fingerprint

Myocarditis
Giant Cells
Gene Expression
Genes
Interleukin-10 Receptors
Integrin beta Chains
T-Lymphocytes
Heart-Assist Devices
Chemokine Receptors
Chemokines
Transcriptional Activation
Therapeutics
Heart Failure
Tissue Donors
Students
Ligands
Polymerase Chain Reaction

Keywords

  • Cardiomyopathy
  • Gene expression
  • Giant cell myocarditis
  • Microarray

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Kittleson, M. M., Minhas, K. M., Irizarry, R. A., Ye, S. Q., Edness, G., Breton, E., ... Hare, J. M. (2005). Gene expression in giant cell myocarditis: Altered expression of immune response genes. International Journal of Cardiology, 102(2), 333-340. https://doi.org/10.1016/j.ijcard.2005.03.075

Gene expression in giant cell myocarditis : Altered expression of immune response genes. / Kittleson, Michelle M.; Minhas, Khalid M.; Irizarry, Rafael A.; Ye, Shui Q.; Edness, Gina; Breton, Elayne; Conte, John V.; Tomaselli, Gordon; Garcia, Joe GN; Hare, Joshua M.

In: International Journal of Cardiology, Vol. 102, No. 2, 10.07.2005, p. 333-340.

Research output: Contribution to journalArticle

Kittleson, MM, Minhas, KM, Irizarry, RA, Ye, SQ, Edness, G, Breton, E, Conte, JV, Tomaselli, G, Garcia, JGN & Hare, JM 2005, 'Gene expression in giant cell myocarditis: Altered expression of immune response genes', International Journal of Cardiology, vol. 102, no. 2, pp. 333-340. https://doi.org/10.1016/j.ijcard.2005.03.075
Kittleson, Michelle M. ; Minhas, Khalid M. ; Irizarry, Rafael A. ; Ye, Shui Q. ; Edness, Gina ; Breton, Elayne ; Conte, John V. ; Tomaselli, Gordon ; Garcia, Joe GN ; Hare, Joshua M. / Gene expression in giant cell myocarditis : Altered expression of immune response genes. In: International Journal of Cardiology. 2005 ; Vol. 102, No. 2. pp. 333-340.
@article{23640dce6eed403f99aaf6138e8673f9,
title = "Gene expression in giant cell myocarditis: Altered expression of immune response genes",
abstract = "Background: Giant cell myocarditis is a rapidly progressive and often fatal condition without a clear etiology or treatment. A better understanding of giant cell myocarditis pathogenesis is critical to developing treatments to prevent progression and reverse damage. We compared the gene expression of giant cell myocarditis with that of nonfailing hearts. Methods: Left ventricular samples from two giant cell myocarditis patients harvested during ventricular assist device placement and six unused donor hearts were examined using Affymetrix U133A microarrays. Differential gene expression was defined with a Bonferroni-adjusted p value ≤ 0.05 from a Student's t-test and an absolute fold change ≥ 2.0. Select gene expression was confirmed with quantitative PCR. Results: Of 115 differentially expressed genes, most were upregulated in giant cell myocarditis and involved in immune response, transcriptional regulation, and metabolism. T-cell activation genes included chemokine receptor 4; chemokine ligands 5, 9, 13, and 18; interleukin-10 receptor alpha; and beta-2 integrin. Conclusions: Gene expression analysis of giant cell myocarditis offers novel insights into its pathogenesis, namely the role of T-cell activators of the Th1 subset and immune response genes previously implicated in heart failure. This forms the basis for future work aimed at defining novel therapeutic targets for giant cell myocarditis.",
keywords = "Cardiomyopathy, Gene expression, Giant cell myocarditis, Microarray",
author = "Kittleson, {Michelle M.} and Minhas, {Khalid M.} and Irizarry, {Rafael A.} and Ye, {Shui Q.} and Gina Edness and Elayne Breton and Conte, {John V.} and Gordon Tomaselli and Garcia, {Joe GN} and Hare, {Joshua M.}",
year = "2005",
month = "7",
day = "10",
doi = "10.1016/j.ijcard.2005.03.075",
language = "English (US)",
volume = "102",
pages = "333--340",
journal = "International Journal of Cardiology",
issn = "0167-5273",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

TY - JOUR

T1 - Gene expression in giant cell myocarditis

T2 - Altered expression of immune response genes

AU - Kittleson, Michelle M.

AU - Minhas, Khalid M.

AU - Irizarry, Rafael A.

AU - Ye, Shui Q.

AU - Edness, Gina

AU - Breton, Elayne

AU - Conte, John V.

AU - Tomaselli, Gordon

AU - Garcia, Joe GN

AU - Hare, Joshua M.

PY - 2005/7/10

Y1 - 2005/7/10

N2 - Background: Giant cell myocarditis is a rapidly progressive and often fatal condition without a clear etiology or treatment. A better understanding of giant cell myocarditis pathogenesis is critical to developing treatments to prevent progression and reverse damage. We compared the gene expression of giant cell myocarditis with that of nonfailing hearts. Methods: Left ventricular samples from two giant cell myocarditis patients harvested during ventricular assist device placement and six unused donor hearts were examined using Affymetrix U133A microarrays. Differential gene expression was defined with a Bonferroni-adjusted p value ≤ 0.05 from a Student's t-test and an absolute fold change ≥ 2.0. Select gene expression was confirmed with quantitative PCR. Results: Of 115 differentially expressed genes, most were upregulated in giant cell myocarditis and involved in immune response, transcriptional regulation, and metabolism. T-cell activation genes included chemokine receptor 4; chemokine ligands 5, 9, 13, and 18; interleukin-10 receptor alpha; and beta-2 integrin. Conclusions: Gene expression analysis of giant cell myocarditis offers novel insights into its pathogenesis, namely the role of T-cell activators of the Th1 subset and immune response genes previously implicated in heart failure. This forms the basis for future work aimed at defining novel therapeutic targets for giant cell myocarditis.

AB - Background: Giant cell myocarditis is a rapidly progressive and often fatal condition without a clear etiology or treatment. A better understanding of giant cell myocarditis pathogenesis is critical to developing treatments to prevent progression and reverse damage. We compared the gene expression of giant cell myocarditis with that of nonfailing hearts. Methods: Left ventricular samples from two giant cell myocarditis patients harvested during ventricular assist device placement and six unused donor hearts were examined using Affymetrix U133A microarrays. Differential gene expression was defined with a Bonferroni-adjusted p value ≤ 0.05 from a Student's t-test and an absolute fold change ≥ 2.0. Select gene expression was confirmed with quantitative PCR. Results: Of 115 differentially expressed genes, most were upregulated in giant cell myocarditis and involved in immune response, transcriptional regulation, and metabolism. T-cell activation genes included chemokine receptor 4; chemokine ligands 5, 9, 13, and 18; interleukin-10 receptor alpha; and beta-2 integrin. Conclusions: Gene expression analysis of giant cell myocarditis offers novel insights into its pathogenesis, namely the role of T-cell activators of the Th1 subset and immune response genes previously implicated in heart failure. This forms the basis for future work aimed at defining novel therapeutic targets for giant cell myocarditis.

KW - Cardiomyopathy

KW - Gene expression

KW - Giant cell myocarditis

KW - Microarray

UR - http://www.scopus.com/inward/record.url?scp=20744435933&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=20744435933&partnerID=8YFLogxK

U2 - 10.1016/j.ijcard.2005.03.075

DO - 10.1016/j.ijcard.2005.03.075

M3 - Article

VL - 102

SP - 333

EP - 340

JO - International Journal of Cardiology

JF - International Journal of Cardiology

SN - 0167-5273

IS - 2

ER -