Hematopoiesis is normally maintained in osteoblast-specific Smad4 gene knockout mice.
- Author:
Yu LAN
1
;
Xiao-Hong TAN
;
Tu-Jun WENG
;
Bing LIU
;
Xiao YANG
Author Information
1. Department of Development and Genetics, Institute of Biotechnology, Academy of Military Medical Sciences, Beijing 100071, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Bone Marrow Cells;
cytology;
Hematopoiesis;
Hematopoietic Stem Cells;
cytology;
physiology;
Mice;
Mice, Knockout;
Osteoblasts;
cytology;
physiology;
Smad4 Protein;
genetics
- From:
Journal of Experimental Hematology
2008;16(1):159-163
- CountryChina
- Language:Chinese
-
Abstract:
It was recently discovered that a subset of osteoblasts functions as a key component of the hematopoietic stem cells (HSC) niche in vivo, controlling HSC self-renewal and multi-lineage differentiation. Disruption of Smad4 gene specifically in osteoblasts leads to a remarkable decrease of osteoblast number and endosteal surface area. In order to elucidate if the osteoblast loss has any effect on hematopoietic activity, the bone marrow (BM) and extramedullary hematopoiesis in the osteoblast-specific Smad4 knockout mice were systematically analyzed, the proportions of mature hematocytes in BM, liver and spleen were detected by flow cytometry, the hematopoietic progenitor number in different stages was measured by colong-forming assay, CFU-S and analysis of LSK cells. The results indicated that the conditional mutant mice demonstrated normal BM hematopoiesis without sign of extramedullary hematopoiesis. Furthermore, the proportion of hematopoietic progenitor cells was normal, while cell number/body weight of the conditional knockout mice increased. It is concluded that hematopoiesis is normally maintained in osteoblast-specific Smad4 knockout mice, and osteoblast loss does not of necessity result in the decrease in BM hematopoiesis.
