Effects of bone marrow-derived endothelial progenitor cell transplantation on vein microenvironment in a rat model of chronic thrombosis.
- Author:
Xiao-qiang LI
1
;
Qing-you MENG
;
Hao-rong WU
Author Information
- Publication Type:Journal Article
- MeSH: Angiopoietin-1; analysis; genetics; Animals; Bone Marrow Cells; cytology; Chemokine CCL2; analysis; genetics; Chronic Disease; Disease Models, Animal; Endothelial Cells; cytology; Fluorescent Antibody Technique; Immunohistochemistry; RNA, Messenger; analysis; Rats; Stem Cell Transplantation; Vascular Endothelial Growth Factor A; analysis; genetics; Venous Thrombosis; therapy
- From: Chinese Medical Journal 2007;120(24):2245-2249
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDEndothelial progenitor cells (EPCs) have been used in both experimental studies and clinical treatments of limb ischemia, as well as in the construction of engineered vascular tissue. The objective of this study was to investigate the effects of transplanted bone marrow-derived EPCs on the vein microenvironment in a rat model of chronic vein thrombosis.
METHODSMononuclear cells were isolated from the bone marrow of immature rats by density gradient centrifugation, cultured, and then transplanted into experimentally induced thrombi into inferior vena cava through the femoral vein. Vascular endothelial growth factor (VEGF), angiopoietin-1 (ANG-1) and monocyte chemotactic protein-1 (MCP-1) mRNA and protein expression levels were measured by real-time quantitative polymerase chain reaction and Western blotting of thrombi and adjacent caval walls 28 days post-transplantation.
RESULTSLevels of VEGF, ANG-1, and MCP-1 mRNA in EPC-transplanted thrombi were 100%, 230.7%, and 212.5% of levels detected in the sham-operated group (P < 0.01), and 99.9%, 215.4%, and 177.8% of levels detected in the experimental control group (P < 0.01). VEGF, ANG-1 and MCP-1 protein levels exhibited a similar trend.
CONCLUSIONSTransplanted bone marrow-derived EPCs appear to alter the vein microenvironment in experimentally induced chronic vein thrombosis by upregulating cytokines associated with thrombic organization and recanalization.
