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Human mesenchymal stem cells improve myocardial performance in a splenectomized rat model of chronic myocardial infarction.
Type
article
Resource
J Formos Med Assoc.(107):165-74.
Date Issued
2008
Author(s)
徐國基
Liu JF; Wang BW; Hung FH; Chang H; Shyu KG;
Subjects
臨床醫學研究所
期刊論文
Abstract
Background/Purpose: Cellular therapy has been applied to animal studies and clinical trials for acute or
subacute myocardial infarction. Little is known about the effect of cell therapy on chronic myocardial infarction.
The goal of this study was to investigate myocardial performance after human bone marrow-derived
mesenchymal stem cell (hMSCs) transplantation in rats with chronic myocardial infarction.
Methods: The hMSCs were obtained from adult human bone marrow and expanded in vitro. The purity
and characteristics of hMSCs were identified by flow cytometry and immunophenotyping. Splenectomy
in male rats was performed to prevent immune reaction. One week after splenectomy, ligation of the left
anterior descending coronary artery was performed to induce myocardial infarction. Four weeks after ligation
of the coronary artery, culture-expanded hMSCs were injected intramyocardially at the left anterior free
wall. Left ventricular function measured by echocardiography, infarct size and immunohistochemical
stain were performed to evaluate the effect of the therapy.
Results: The engrafted hMSCs were positive for the cardiac marker troponin T. Infarct size (35.4 ± 3.4% vs.
53.3 ± 3.0%, p < 0.001) and fibrotic area (2.6 ± 0.1% vs. 5.9 ± 0.2%, p < 0.001) were significantly smaller in
the hMSC-treated group than in the control group at 28 days after therapy. hMSC transplantation resulted
in smaller left ventricular end-diastolic dimension (6.5 ± 0.1mm vs. 7.9 ± 0.7 mm, p < 0.001) and better
left ventricular ejection fraction (88.7 ± 1.2% vs. 65.8 ± 2.5%, p < 0.001) than in the control group.
Capillary density was markedly increased after hMSC transplantation compared with the control group.
Conclusion: This study demonstrates that intramyocardial transplantation of hMSCs improves cardiac
function after chronic myocardial infarction through enhancement of angiogenesis and myogenesis in the
ischemic myocardium. Transplantation of hMSCs for myocardial regeneration may become the future
therapy for chronic myocardial infarction. [J Formos Med Assoc 2008;107(2):165–174]
subacute myocardial infarction. Little is known about the effect of cell therapy on chronic myocardial infarction.
The goal of this study was to investigate myocardial performance after human bone marrow-derived
mesenchymal stem cell (hMSCs) transplantation in rats with chronic myocardial infarction.
Methods: The hMSCs were obtained from adult human bone marrow and expanded in vitro. The purity
and characteristics of hMSCs were identified by flow cytometry and immunophenotyping. Splenectomy
in male rats was performed to prevent immune reaction. One week after splenectomy, ligation of the left
anterior descending coronary artery was performed to induce myocardial infarction. Four weeks after ligation
of the coronary artery, culture-expanded hMSCs were injected intramyocardially at the left anterior free
wall. Left ventricular function measured by echocardiography, infarct size and immunohistochemical
stain were performed to evaluate the effect of the therapy.
Results: The engrafted hMSCs were positive for the cardiac marker troponin T. Infarct size (35.4 ± 3.4% vs.
53.3 ± 3.0%, p < 0.001) and fibrotic area (2.6 ± 0.1% vs. 5.9 ± 0.2%, p < 0.001) were significantly smaller in
the hMSC-treated group than in the control group at 28 days after therapy. hMSC transplantation resulted
in smaller left ventricular end-diastolic dimension (6.5 ± 0.1mm vs. 7.9 ± 0.7 mm, p < 0.001) and better
left ventricular ejection fraction (88.7 ± 1.2% vs. 65.8 ± 2.5%, p < 0.001) than in the control group.
Capillary density was markedly increased after hMSC transplantation compared with the control group.
Conclusion: This study demonstrates that intramyocardial transplantation of hMSCs improves cardiac
function after chronic myocardial infarction through enhancement of angiogenesis and myogenesis in the
ischemic myocardium. Transplantation of hMSCs for myocardial regeneration may become the future
therapy for chronic myocardial infarction. [J Formos Med Assoc 2008;107(2):165–174]
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