FRIL maintains quiescence of hematopoietic stem cells through regulation of cell cycle related factors.
- Author:
Jin LI
1
;
Xiao-yan XIE
;
Dong-mei WANG
;
Xue-tao PEI
Author Information
- Publication Type:Journal Article
- MeSH: Antigens, CD34; Cell Cycle; drug effects; Cell Cycle Proteins; genetics; metabolism; Cells, Cultured; Fetal Blood; cytology; Hematopoietic Stem Cells; cytology; drug effects; metabolism; Humans; Mannose-Binding Lectins; pharmacology; Plant Lectins; pharmacology; RNA, Messenger; genetics
- From: Chinese Journal of Hematology 2007;28(1):37-40
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the mechanism of Flt3 receptor-interacting lectin (FRIL) maintains quiescence of hematopoietic stem cells (HSCs) in vitro.
METHODSCord blood CD34+ cells were cultured in suspension medium supplemented with or without FRIL and FL. Cells were collected at different time points and the expression of some cell cycle regulators, especially those involved in G0/G1 phase regulation were detected on mRNA and protein level.
RESULTSThe expressions of G0/G1 phase related cyclins or CDKs were undetectable in the newly isolated CD34+ cells, expressions of Cyclin D3, CDK6 and P27 were the lowest in FRIL cultured group after 3d's culture (FRIL group: 483 +/- 63, 553 +/- 39, 0.312 +/- 0.030; FL group: 2437 +/- 52, 3209 +/- 98, 0.787 +/- 0.024; BLANK: 914 +/- 105, 1497 +/- 55, 0.616 +/- 0.029, respectively), but the expression of P53 was the highest in FRIL group (FRIL group: 4.476 +/- 0.159; FL group: 0.581 +/- 0.099, BLANK: 2.167 +/- 0.114). The expression of positive regulators of cell cycle in FRIL group were the same as that of FL group and blank group or lower.
CONCLUSIONFRIL preserves HSCs effectively in vitro through the mechanisms of down-regulation of cyclin D3 and CDK6 and activation of P53. P27 is mostly involved in the differentiation of HSCs.
