Viable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction

Jordan Lancaster, Elizabeth Juneman, Tracy Hagerty, Rose Do, Michael Hicks, Kate Meltzer, Paul Standley, Mohamed Gaballa, Robert S Kellar, Steven Goldman, Hoang Thai

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: This study examines a viable biodegradable three-dimensional fibroblast construct (3DFC) in a model of chronic heart failure. The viable fibroblasts, cultured on a vicryl mesh, secrete growth factors that stimulate angiogenesis. Methods: We ligated the left coronary artery of male Sprague-Dawley rats, implanted the 3DFC 3 weeks after myocardial infarction and obtained end point data 3 weeks later, that is, 6 weeks after myocardial infarction. Results: Implanting the 3DFC increases (p<0.05) myocardial blood flow twofold, microvessel formation (0.02±0.01 vs. 0.07±0.03 vessels/μm2), and ventricular wall thickness (0.53±0.02 to 1.02±0.17mm). The 3DFC shifts the passive pressure volume loop toward the pressure axis but does not alter left ventricular (LV) ejection fraction, systolic displacement, LV end-diastolic pressure/dimension, or LV cavity area. The 3DFC stimulates selected cytokine activation with a decrease in the proinflammatory cascade and increased total protein content stimulated by strained 3DFC in vitro. Conclusion: The 3DFC functions as a cell delivery device providing matrix support for resident cell survival and integration into the heart. The imbedded fibroblasts of the 3DFC release a complex blend of cardioactive cytokines promoting increases in microvessel density and anterior wall blood flow but does not improve ejection fraction or alter LV remodeling.

Original languageEnglish (US)
Pages (from-to)3065-3073
Number of pages9
JournalTissue Engineering - Part A
Volume16
Issue number10
DOIs
StatePublished - Oct 1 2010
Externally publishedYes

Fingerprint

Fibroblasts
Blood
Heart Failure
Myocardial Infarction
Microvessels
Cytokines
Pressure
Polyglactin 910
Ventricular Remodeling
Stroke Volume
Sprague Dawley Rats
Rats
Cell Survival
Intercellular Signaling Peptides and Proteins
Coronary Vessels
Chemical activation
Cells
Blood Pressure
Proteins
Equipment and Supplies

ASJC Scopus subject areas

  • Bioengineering
  • Biochemistry
  • Biomedical Engineering
  • Biomaterials
  • Medicine(all)

Cite this

Viable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction. / Lancaster, Jordan; Juneman, Elizabeth; Hagerty, Tracy; Do, Rose; Hicks, Michael; Meltzer, Kate; Standley, Paul; Gaballa, Mohamed; Kellar, Robert S; Goldman, Steven; Thai, Hoang.

In: Tissue Engineering - Part A, Vol. 16, No. 10, 01.10.2010, p. 3065-3073.

Research output: Contribution to journalArticle

Lancaster, J, Juneman, E, Hagerty, T, Do, R, Hicks, M, Meltzer, K, Standley, P, Gaballa, M, Kellar, RS, Goldman, S & Thai, H 2010, 'Viable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction', Tissue Engineering - Part A, vol. 16, no. 10, pp. 3065-3073. https://doi.org/10.1089/ten.tea.2009.0589
Lancaster, Jordan ; Juneman, Elizabeth ; Hagerty, Tracy ; Do, Rose ; Hicks, Michael ; Meltzer, Kate ; Standley, Paul ; Gaballa, Mohamed ; Kellar, Robert S ; Goldman, Steven ; Thai, Hoang. / Viable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction. In: Tissue Engineering - Part A. 2010 ; Vol. 16, No. 10. pp. 3065-3073.
@article{5a8acd9cef5342cb9431966aad0d06dc,
title = "Viable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction",
abstract = "Background: This study examines a viable biodegradable three-dimensional fibroblast construct (3DFC) in a model of chronic heart failure. The viable fibroblasts, cultured on a vicryl mesh, secrete growth factors that stimulate angiogenesis. Methods: We ligated the left coronary artery of male Sprague-Dawley rats, implanted the 3DFC 3 weeks after myocardial infarction and obtained end point data 3 weeks later, that is, 6 weeks after myocardial infarction. Results: Implanting the 3DFC increases (p<0.05) myocardial blood flow twofold, microvessel formation (0.02±0.01 vs. 0.07±0.03 vessels/μm2), and ventricular wall thickness (0.53±0.02 to 1.02±0.17mm). The 3DFC shifts the passive pressure volume loop toward the pressure axis but does not alter left ventricular (LV) ejection fraction, systolic displacement, LV end-diastolic pressure/dimension, or LV cavity area. The 3DFC stimulates selected cytokine activation with a decrease in the proinflammatory cascade and increased total protein content stimulated by strained 3DFC in vitro. Conclusion: The 3DFC functions as a cell delivery device providing matrix support for resident cell survival and integration into the heart. The imbedded fibroblasts of the 3DFC release a complex blend of cardioactive cytokines promoting increases in microvessel density and anterior wall blood flow but does not improve ejection fraction or alter LV remodeling.",
author = "Jordan Lancaster and Elizabeth Juneman and Tracy Hagerty and Rose Do and Michael Hicks and Kate Meltzer and Paul Standley and Mohamed Gaballa and Kellar, {Robert S} and Steven Goldman and Hoang Thai",
year = "2010",
month = "10",
day = "1",
doi = "10.1089/ten.tea.2009.0589",
language = "English (US)",
volume = "16",
pages = "3065--3073",
journal = "Tissue Engineering - Part A.",
issn = "1937-3341",
publisher = "Mary Ann Liebert Inc.",
number = "10",

}

TY - JOUR

T1 - Viable fibroblast matrix patch induces angiogenesis and increases myocardial blood flow in heart failure after myocardial infarction

AU - Lancaster, Jordan

AU - Juneman, Elizabeth

AU - Hagerty, Tracy

AU - Do, Rose

AU - Hicks, Michael

AU - Meltzer, Kate

AU - Standley, Paul

AU - Gaballa, Mohamed

AU - Kellar, Robert S

AU - Goldman, Steven

AU - Thai, Hoang

PY - 2010/10/1

Y1 - 2010/10/1

N2 - Background: This study examines a viable biodegradable three-dimensional fibroblast construct (3DFC) in a model of chronic heart failure. The viable fibroblasts, cultured on a vicryl mesh, secrete growth factors that stimulate angiogenesis. Methods: We ligated the left coronary artery of male Sprague-Dawley rats, implanted the 3DFC 3 weeks after myocardial infarction and obtained end point data 3 weeks later, that is, 6 weeks after myocardial infarction. Results: Implanting the 3DFC increases (p<0.05) myocardial blood flow twofold, microvessel formation (0.02±0.01 vs. 0.07±0.03 vessels/μm2), and ventricular wall thickness (0.53±0.02 to 1.02±0.17mm). The 3DFC shifts the passive pressure volume loop toward the pressure axis but does not alter left ventricular (LV) ejection fraction, systolic displacement, LV end-diastolic pressure/dimension, or LV cavity area. The 3DFC stimulates selected cytokine activation with a decrease in the proinflammatory cascade and increased total protein content stimulated by strained 3DFC in vitro. Conclusion: The 3DFC functions as a cell delivery device providing matrix support for resident cell survival and integration into the heart. The imbedded fibroblasts of the 3DFC release a complex blend of cardioactive cytokines promoting increases in microvessel density and anterior wall blood flow but does not improve ejection fraction or alter LV remodeling.

AB - Background: This study examines a viable biodegradable three-dimensional fibroblast construct (3DFC) in a model of chronic heart failure. The viable fibroblasts, cultured on a vicryl mesh, secrete growth factors that stimulate angiogenesis. Methods: We ligated the left coronary artery of male Sprague-Dawley rats, implanted the 3DFC 3 weeks after myocardial infarction and obtained end point data 3 weeks later, that is, 6 weeks after myocardial infarction. Results: Implanting the 3DFC increases (p<0.05) myocardial blood flow twofold, microvessel formation (0.02±0.01 vs. 0.07±0.03 vessels/μm2), and ventricular wall thickness (0.53±0.02 to 1.02±0.17mm). The 3DFC shifts the passive pressure volume loop toward the pressure axis but does not alter left ventricular (LV) ejection fraction, systolic displacement, LV end-diastolic pressure/dimension, or LV cavity area. The 3DFC stimulates selected cytokine activation with a decrease in the proinflammatory cascade and increased total protein content stimulated by strained 3DFC in vitro. Conclusion: The 3DFC functions as a cell delivery device providing matrix support for resident cell survival and integration into the heart. The imbedded fibroblasts of the 3DFC release a complex blend of cardioactive cytokines promoting increases in microvessel density and anterior wall blood flow but does not improve ejection fraction or alter LV remodeling.

UR - http://www.scopus.com/inward/record.url?scp=77957661765&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957661765&partnerID=8YFLogxK

U2 - 10.1089/ten.tea.2009.0589

DO - 10.1089/ten.tea.2009.0589

M3 - Article

VL - 16

SP - 3065

EP - 3073

JO - Tissue Engineering - Part A.

JF - Tissue Engineering - Part A.

SN - 1937-3341

IS - 10

ER -