Grafting an Acellular 3-Dimensional Collagen Scaffold Onto a Non-transmural Infarcted Myocardium Induces Neo-angiogenesis and Reduces Cardiac Remodeling

Mohamed A. Gaballa, Julia N E Sunkomat, Hoang Thai, Eugene Morkin, Gordon Ewy, Steven Goldman

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Background: This study was designed to determine whether tissue engineering could be used to reduce ventricular remodeling in a rat model of non-transmural, non-ST-elevation myocardial infarction. Methods: We grafted an acellular 3-dimensional (3D) collagen type 1 scaffold (solid porous foam) onto infarcted myocardium in rats. Three weeks after grafting, the scaffold was integrated into the myocardium and retarded cardiac remodeling by reducing left ventricular (LV) dilation. The LV inner and outer diameters, measured at the equator at zero LV pressure, decreased (p < 0.05) from 11,040 ± 212 to 9,144 ± 135 μm, and 13,469 ± 187 to 11,673 ± 104 μm (N = 12), after scaffold transplantation onto infarcted myocardium. The scaffold also shifted the LV pressure-volume curve to the left toward control and induced neo-angiogenesis (700 ± 25 vs 75 ± 11 neo-vessels/cm2, N = 5, p < 0.05). These vessels (75 ± 11%) ranged in diameter from 25 to 100 μm and connected to the native coronary vasculature. Systemic treatment with granulocyte-colony stimulating factor (G-CSF), 50 μg/kg/day for 5 days immediately after myocardial injury, increased (p < 0.05) neo-vascular density from 700 ± 25 to 978 ± 57 neo-vessels/cm2. Conclusions: A 3D collagen type 1 scaffold grafted onto an injured myocardium induced neo-vessel formation and reduced LV remodeling. Treatment with G-CSF further increased the number of vessels in the myocardium, possibly due to mobilization of bone marrow cells.

Original languageEnglish (US)
Pages (from-to)946-954
Number of pages9
JournalJournal of Heart and Lung Transplantation
Volume25
Issue number8
DOIs
StatePublished - Aug 2006

Fingerprint

Myocardium
Collagen
Ventricular Remodeling
Granulocyte Colony-Stimulating Factor
Ventricular Pressure
Collagen Type I
Tissue Engineering
Bone Marrow Cells
Blood Vessels
Dilatation
Transplantation
Wounds and Injuries

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery
  • Transplantation

Cite this

Grafting an Acellular 3-Dimensional Collagen Scaffold Onto a Non-transmural Infarcted Myocardium Induces Neo-angiogenesis and Reduces Cardiac Remodeling. / Gaballa, Mohamed A.; Sunkomat, Julia N E; Thai, Hoang; Morkin, Eugene; Ewy, Gordon; Goldman, Steven.

In: Journal of Heart and Lung Transplantation, Vol. 25, No. 8, 08.2006, p. 946-954.

Research output: Contribution to journalArticle

@article{4d48a290aeec418b9db51eeffe20eaaa,
title = "Grafting an Acellular 3-Dimensional Collagen Scaffold Onto a Non-transmural Infarcted Myocardium Induces Neo-angiogenesis and Reduces Cardiac Remodeling",
abstract = "Background: This study was designed to determine whether tissue engineering could be used to reduce ventricular remodeling in a rat model of non-transmural, non-ST-elevation myocardial infarction. Methods: We grafted an acellular 3-dimensional (3D) collagen type 1 scaffold (solid porous foam) onto infarcted myocardium in rats. Three weeks after grafting, the scaffold was integrated into the myocardium and retarded cardiac remodeling by reducing left ventricular (LV) dilation. The LV inner and outer diameters, measured at the equator at zero LV pressure, decreased (p < 0.05) from 11,040 ± 212 to 9,144 ± 135 μm, and 13,469 ± 187 to 11,673 ± 104 μm (N = 12), after scaffold transplantation onto infarcted myocardium. The scaffold also shifted the LV pressure-volume curve to the left toward control and induced neo-angiogenesis (700 ± 25 vs 75 ± 11 neo-vessels/cm2, N = 5, p < 0.05). These vessels (75 ± 11{\%}) ranged in diameter from 25 to 100 μm and connected to the native coronary vasculature. Systemic treatment with granulocyte-colony stimulating factor (G-CSF), 50 μg/kg/day for 5 days immediately after myocardial injury, increased (p < 0.05) neo-vascular density from 700 ± 25 to 978 ± 57 neo-vessels/cm2. Conclusions: A 3D collagen type 1 scaffold grafted onto an injured myocardium induced neo-vessel formation and reduced LV remodeling. Treatment with G-CSF further increased the number of vessels in the myocardium, possibly due to mobilization of bone marrow cells.",
author = "Gaballa, {Mohamed A.} and Sunkomat, {Julia N E} and Hoang Thai and Eugene Morkin and Gordon Ewy and Steven Goldman",
year = "2006",
month = "8",
doi = "10.1016/j.healun.2006.04.008",
language = "English (US)",
volume = "25",
pages = "946--954",
journal = "Journal of Heart and Lung Transplantation",
issn = "1053-2498",
publisher = "Elsevier USA",
number = "8",

}

TY - JOUR

T1 - Grafting an Acellular 3-Dimensional Collagen Scaffold Onto a Non-transmural Infarcted Myocardium Induces Neo-angiogenesis and Reduces Cardiac Remodeling

AU - Gaballa, Mohamed A.

AU - Sunkomat, Julia N E

AU - Thai, Hoang

AU - Morkin, Eugene

AU - Ewy, Gordon

AU - Goldman, Steven

PY - 2006/8

Y1 - 2006/8

N2 - Background: This study was designed to determine whether tissue engineering could be used to reduce ventricular remodeling in a rat model of non-transmural, non-ST-elevation myocardial infarction. Methods: We grafted an acellular 3-dimensional (3D) collagen type 1 scaffold (solid porous foam) onto infarcted myocardium in rats. Three weeks after grafting, the scaffold was integrated into the myocardium and retarded cardiac remodeling by reducing left ventricular (LV) dilation. The LV inner and outer diameters, measured at the equator at zero LV pressure, decreased (p < 0.05) from 11,040 ± 212 to 9,144 ± 135 μm, and 13,469 ± 187 to 11,673 ± 104 μm (N = 12), after scaffold transplantation onto infarcted myocardium. The scaffold also shifted the LV pressure-volume curve to the left toward control and induced neo-angiogenesis (700 ± 25 vs 75 ± 11 neo-vessels/cm2, N = 5, p < 0.05). These vessels (75 ± 11%) ranged in diameter from 25 to 100 μm and connected to the native coronary vasculature. Systemic treatment with granulocyte-colony stimulating factor (G-CSF), 50 μg/kg/day for 5 days immediately after myocardial injury, increased (p < 0.05) neo-vascular density from 700 ± 25 to 978 ± 57 neo-vessels/cm2. Conclusions: A 3D collagen type 1 scaffold grafted onto an injured myocardium induced neo-vessel formation and reduced LV remodeling. Treatment with G-CSF further increased the number of vessels in the myocardium, possibly due to mobilization of bone marrow cells.

AB - Background: This study was designed to determine whether tissue engineering could be used to reduce ventricular remodeling in a rat model of non-transmural, non-ST-elevation myocardial infarction. Methods: We grafted an acellular 3-dimensional (3D) collagen type 1 scaffold (solid porous foam) onto infarcted myocardium in rats. Three weeks after grafting, the scaffold was integrated into the myocardium and retarded cardiac remodeling by reducing left ventricular (LV) dilation. The LV inner and outer diameters, measured at the equator at zero LV pressure, decreased (p < 0.05) from 11,040 ± 212 to 9,144 ± 135 μm, and 13,469 ± 187 to 11,673 ± 104 μm (N = 12), after scaffold transplantation onto infarcted myocardium. The scaffold also shifted the LV pressure-volume curve to the left toward control and induced neo-angiogenesis (700 ± 25 vs 75 ± 11 neo-vessels/cm2, N = 5, p < 0.05). These vessels (75 ± 11%) ranged in diameter from 25 to 100 μm and connected to the native coronary vasculature. Systemic treatment with granulocyte-colony stimulating factor (G-CSF), 50 μg/kg/day for 5 days immediately after myocardial injury, increased (p < 0.05) neo-vascular density from 700 ± 25 to 978 ± 57 neo-vessels/cm2. Conclusions: A 3D collagen type 1 scaffold grafted onto an injured myocardium induced neo-vessel formation and reduced LV remodeling. Treatment with G-CSF further increased the number of vessels in the myocardium, possibly due to mobilization of bone marrow cells.

UR - http://www.scopus.com/inward/record.url?scp=33746616908&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746616908&partnerID=8YFLogxK

U2 - 10.1016/j.healun.2006.04.008

DO - 10.1016/j.healun.2006.04.008

M3 - Article

C2 - 16890116

AN - SCOPUS:33746616908

VL - 25

SP - 946

EP - 954

JO - Journal of Heart and Lung Transplantation

JF - Journal of Heart and Lung Transplantation

SN - 1053-2498

IS - 8

ER -