Hematopoiesis support of mesenchymal stem cells in children with aplastic anemia.
- Author:
Yan WU
1
;
Jie YU
;
Lei ZHANG
;
Qing LUO
;
Jian-Wen XIAO
;
Xiao-Mei LIU
;
Ying XIAN
;
Bi-Tao DAI
;
You-Hua XU
;
Yong-Chun SU
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Anemia, Aplastic; physiopathology; Cell Adhesion; Child; Child, Preschool; Female; Hematopoiesis; Humans; Leukocytes, Mononuclear; physiology; Male; Mesenchymal Stromal Cells; physiology; Stem Cell Factor; physiology
- From: Chinese Journal of Contemporary Pediatrics 2008;10(4):455-459
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEThe abnormality of hemopoietic inductive microenvironment (HIM) is involved in the pathophysiology of aplastic anemia (AA). Mesenchymal stem cells (MSC) are main source of bone marrow stromal cells which constitute the bone marrow HIM. Thus, the bone marrow failure in AA may be related to the function of MSC. The aim of the study was to investigate the hematopoiesis support function of MSC in children with AA in vitro.
METHODSBone marrow samples were collected from 24 children with AA at diagnosis and 19 children with idiopathic thrombocytopenic purpura (ITP), infectious mononucleosis or lymphadenitis (controls). MSCs from bone marrow samples were isolated, cultured and expanded. Morphology, proliferation activity and colony forming unit-fibroblast (CFU-F) were measured. The ability of bone marrow MSC to adhere hemopoietic cells was assayed by MTT. The concentration of stem cell factor (SCF) released from MSC was tested using ELISA. Mononuclear cells (MNC) of bone marrow were plated onto a feeder layer formed by MSC. Cells count and BFU-E, CFU-GM, CFU-GMME productions were measured.
RESULTSThe first and third passage time of MSC in children with AA was longer than that in the controls. The number of CFU-F in children with AA (15.70+/-5.78) was less than that in the controls (21.73+/-5.74) (P<0.05). The concentration of SCF in MSC supernatants in children with AA (30.69+/-16.82 pg/mL) was significantly lower than the controls (50.74+/-14.83 pg/mL) (P<0.01). The total MNC count and the number of BFU-E, CFU-GM and CFU-GMME colonies in the support of MSC in children with AA were significantly lower than those in the controls (P<0.01).
CONCLUSIONSThe hematopoiesis support function of MSC was significantly reduced in children with AA in vitro. The decreased hematopoiesis support function of MSC may be related its decreased proliferation capacity and SCF release activity.