Morphological characteristics of the microvasculature in healing myocardial infarcts

Guofeng Ren, Lloyd H. Michael, Mark L. Entman, Nikolaos G. Frangogiannis

Research output: Contribution to journalArticle

117 Citations (Scopus)

Abstract

Myocardial infarction (MI) is associated with an angiogenic response, critical for healing and cardiac repair. Using a canine model of myocardial ischemia and reperfusion, we examined the structural characteristics of the evolving microvasculature in healing MI. After 7 days of reperfusion, the infarcted territory was rich in capillaries and contained enlarged, pericyte-poor "mother vessels" and endothelial bridges. During scar maturation arteriolar density in the infarct increased, and a higher percentage of microvessels acquired a pericyte coat (60.4 ± 6.94% after 28 days of reperfusion vs 30.17 ± 3.65% after 7 days of reperfusion; p<0.05). The microvascular endothelium in the early stages of healing showed intense CD31/PECAM-1 and CD146/MeI-CAM immunoreactivity but weak staining with the Griffonia simplicifolia lectin I (GS-I). In contrast, after 28 days of reperfusion, most infarct microvessels demonstrated significant lectin binding. Our findings suggest that the infarct microvasculature undergoes a transition from an early phase of intense angiogenic activity to a maturation stage associated with pericyte recruitment and formation of a muscular coat. In addition, in the endothelium of infarct microvessels CD31 and CD146 expression appears to precede that of the specific sugar groups that bind the GS-I lectin. Understanding of the mechanisms underlying the formation and remodeling of the microvasculature after MI may be important in designing therapeutic interventions to optimize cardiac repair.

Original languageEnglish (US)
Pages (from-to)71-79
Number of pages9
JournalJournal of Histochemistry and Cytochemistry
Volume50
Issue number1
StatePublished - 2002
Externally publishedYes

Fingerprint

Microvessels
Myocardial Infarction
Pericytes
Reperfusion
Lectins
Endothelium
CD31 Antigens
Myocardial Reperfusion
Phase Transition
Cicatrix
Myocardial Ischemia
Canidae
Staining and Labeling

Keywords

  • α-smooth muscle actin
  • Angiogenesis
  • CD146
  • CD31
  • Endothelium
  • Healing
  • Lectin
  • Myocardial infarction
  • Pericyte

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology

Cite this

Morphological characteristics of the microvasculature in healing myocardial infarcts. / Ren, Guofeng; Michael, Lloyd H.; Entman, Mark L.; Frangogiannis, Nikolaos G.

In: Journal of Histochemistry and Cytochemistry, Vol. 50, No. 1, 2002, p. 71-79.

Research output: Contribution to journalArticle

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AB - Myocardial infarction (MI) is associated with an angiogenic response, critical for healing and cardiac repair. Using a canine model of myocardial ischemia and reperfusion, we examined the structural characteristics of the evolving microvasculature in healing MI. After 7 days of reperfusion, the infarcted territory was rich in capillaries and contained enlarged, pericyte-poor "mother vessels" and endothelial bridges. During scar maturation arteriolar density in the infarct increased, and a higher percentage of microvessels acquired a pericyte coat (60.4 ± 6.94% after 28 days of reperfusion vs 30.17 ± 3.65% after 7 days of reperfusion; p<0.05). The microvascular endothelium in the early stages of healing showed intense CD31/PECAM-1 and CD146/MeI-CAM immunoreactivity but weak staining with the Griffonia simplicifolia lectin I (GS-I). In contrast, after 28 days of reperfusion, most infarct microvessels demonstrated significant lectin binding. Our findings suggest that the infarct microvasculature undergoes a transition from an early phase of intense angiogenic activity to a maturation stage associated with pericyte recruitment and formation of a muscular coat. In addition, in the endothelium of infarct microvessels CD31 and CD146 expression appears to precede that of the specific sugar groups that bind the GS-I lectin. Understanding of the mechanisms underlying the formation and remodeling of the microvasculature after MI may be important in designing therapeutic interventions to optimize cardiac repair.

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