Home LiteratureArticle Details
PMID: 16926022 Published · ppublish English Journal Article Research Support, N.I.H., Extramural

Evidence for ischemia induced host-derived bone marrow cell mobilization into cardiac allografts.

Journal of molecular and cellular cardiology ·Vol. 41 ·No. 3 ·2006-09-00 ·Pages 478-87

Wang Y, Haider HKh, Ahmad N, Zhang D, Ashraf M

Abstract

Mobilized bone marrow stem cells (BMSC) exhibit high degree of plasticity and participate in the repair process in the event of myocardial damage. In this study, we verified the proportional contribution of recipient BMSC in the repair process and identified their specific surface markers. Wild-type (WT) donor female heart was transplanted into abdominal cavity of male rat (Group I). In some of recipient animals, infarction was created by LAD occlusion (Group II). Two weeks later, transplanted female hearts were harvested for histological analysis of the mobilized cells. C-kit, CD31, Ki67 and Y-chromosome were used as markers to identify mobilized cells in the female hearts. Y-chromosome positive cells were found in the donor female cardiac allografts. Acute myocardial infarction (AMI) of recipient heart induced migration of progenitor cells into the lesions of chronic rejection in the allograft. Donor ventricular mass reduction was more pronounced in Group I. Endothelial progenitor cells induced by AMI from male recipient extensively migrated into the cardiac allograft. SDF-1 mRNA levels significantly increased (peak level at 24 h after AMI) in recipient heart. CXCR4 was strongly expressed in the transplanted hearts around the perivascular area. Spontaneous mobilization of hematopoietic progenitor cells (HPCs) occurred in cardiac allografts after creating recipient heart AMI and was detectable until 2 weeks. These data suggests that CXCR4 overexpression enhances vascularization in the damaged myocardium and SDF-1/CXCR4 axis seems particularly important in progenitor cell chemotaxis, homing, engraftment and retention in damaged myocardium. In addition, BMSC attracted to the site of ischemic injury participate in cardiac repair.

MeSH Terms
Animals Apoptosis Bone Marrow Cells/cytology,metabolism Female Heart Transplantation/methods Hematopoietic Stem Cells/metabolism Ki-67 Antigen/biosynthesis Male Muscle Cells/metabolism Myocardial Infarction/metabolism Myocardial Ischemia/pathology Neovascularization, Pathologic Rats Rats, Inbred F344 Sex Factors
Chemicals
Ki-67 Antigen
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Wang Yigang
Department of Pathology and Laboratory Medicine, University of Cincinnati Medical Center, College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0529, USA.
Haider Husnain Kh
Ahmad Nauman
Zhang Dongsheng
Ashraf Muhammad
Article Info
Journal
Journal of molecular and cellular cardiology
Abbr.
J Mol Cell Cardiol
ISSN
0022-2828
Published
2006-09-00
Epub
2006-00-22
Pages
478-87
Language
English
Region
England
NLM ID
0262322
Subset
IM
Grants
NHLBI NIH HHS · HL-081859-01 · United States
NHLBI NIH HHS · HL080686 · United States
NHLBI NIH HHS · HL70062 · United States
NHLBI NIH HHS · R37-HL-74272 · United States
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]