Potential role for antiangiogenic proteins in the myocardial infarction repair process

Jess L. Thompson, James A. Ryan, Mark L. Barr, Benjamin Franc, Vaughn A. Starnes, Margaret A. Schwarz

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Objective. Although angiogenic proteins have been identified as positive modulators of myocardial revascularization following acute myocardial infarction, little if anything is known regarding the role that antiangiogenic proteins have in myocardial revascularization. We explored the temporospatial distribution of endothelial-monocyte activating polypeptide (EMAP) II to determine whether antiangiogenic proteins have a role in the repair of myocardial tissue following infarction. Methods. A rat model of myocardial infarction was utilized to examine EMAP II distribution (in situ hybridization) and protein expression (Western analysis) over a 6-week period. Results. At baseline, EMAP II protein and mRNA are minimally expressed with transcription products localizing predominately to the perivascular stroma region in the normal rat myocardium. Six hours following myocardial infarction, EMAP II changes its distribution from the perivascular stroma to an invading inflammatory cell population. This is associated with a 2-fold (P < 0.0009) increase in EMAP II protein and its transcription primarily localized to the infarct region. EMAP II protein expression remains elevated throughout the weeks following the infarction with transcription limited to the infarct region and a notable decrease in EMAP II transcription products noted in the viable vasculature surrounding the infarct zone. Six weeks following myocardial infarction, EMAP II protein is elevated above control, changes its location of transcription from the inflammatory cell population to that of the fibroblasts located in the relative avascular scar tissue, and has resumed its perivascular stromal distribution in the viable periinfarct tissue. Conclusion. Thus, the temporospatial distribution of this antiangiogenic protein suggests that negative vascular modulators may have a function in the revascularization process following acute myocardial infarction.

Original languageEnglish (US)
Pages (from-to)156-164
Number of pages9
JournalJournal of Surgical Research
Volume116
Issue number1
DOIs
StatePublished - Jan 2004

Fingerprint

Myocardial Infarction
Proteins
Myocardial Revascularization
Infarction
Angiogenic Proteins
small inducible cytokine subfamily E, member 1
Population
Cicatrix
In Situ Hybridization
Blood Vessels
Myocardium
Fibroblasts
Messenger RNA

Keywords

  • Angiogenesis
  • Antiangiogenic
  • Endothelial-monocyte activating polypeptide II
  • Myocardial infarction

ASJC Scopus subject areas

  • Surgery

Cite this

Thompson, J. L., Ryan, J. A., Barr, M. L., Franc, B., Starnes, V. A., & Schwarz, M. A. (2004). Potential role for antiangiogenic proteins in the myocardial infarction repair process. Journal of Surgical Research, 116(1), 156-164. https://doi.org/10.1016/j.jss.2003.06.001

Potential role for antiangiogenic proteins in the myocardial infarction repair process. / Thompson, Jess L.; Ryan, James A.; Barr, Mark L.; Franc, Benjamin; Starnes, Vaughn A.; Schwarz, Margaret A.

In: Journal of Surgical Research, Vol. 116, No. 1, 01.2004, p. 156-164.

Research output: Contribution to journalArticle

Thompson, JL, Ryan, JA, Barr, ML, Franc, B, Starnes, VA & Schwarz, MA 2004, 'Potential role for antiangiogenic proteins in the myocardial infarction repair process', Journal of Surgical Research, vol. 116, no. 1, pp. 156-164. https://doi.org/10.1016/j.jss.2003.06.001
Thompson, Jess L. ; Ryan, James A. ; Barr, Mark L. ; Franc, Benjamin ; Starnes, Vaughn A. ; Schwarz, Margaret A. / Potential role for antiangiogenic proteins in the myocardial infarction repair process. In: Journal of Surgical Research. 2004 ; Vol. 116, No. 1. pp. 156-164.
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AB - Objective. Although angiogenic proteins have been identified as positive modulators of myocardial revascularization following acute myocardial infarction, little if anything is known regarding the role that antiangiogenic proteins have in myocardial revascularization. We explored the temporospatial distribution of endothelial-monocyte activating polypeptide (EMAP) II to determine whether antiangiogenic proteins have a role in the repair of myocardial tissue following infarction. Methods. A rat model of myocardial infarction was utilized to examine EMAP II distribution (in situ hybridization) and protein expression (Western analysis) over a 6-week period. Results. At baseline, EMAP II protein and mRNA are minimally expressed with transcription products localizing predominately to the perivascular stroma region in the normal rat myocardium. Six hours following myocardial infarction, EMAP II changes its distribution from the perivascular stroma to an invading inflammatory cell population. This is associated with a 2-fold (P < 0.0009) increase in EMAP II protein and its transcription primarily localized to the infarct region. EMAP II protein expression remains elevated throughout the weeks following the infarction with transcription limited to the infarct region and a notable decrease in EMAP II transcription products noted in the viable vasculature surrounding the infarct zone. Six weeks following myocardial infarction, EMAP II protein is elevated above control, changes its location of transcription from the inflammatory cell population to that of the fibroblasts located in the relative avascular scar tissue, and has resumed its perivascular stromal distribution in the viable periinfarct tissue. Conclusion. Thus, the temporospatial distribution of this antiangiogenic protein suggests that negative vascular modulators may have a function in the revascularization process following acute myocardial infarction.

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