A resident histamine-positive, non-mast cell, population found in bone marrow was increased by 25% by ovx.
The chemokine SDF-1, which mediates homing of leukocytes into the bone marrow, was increased by CoPP and reduced by inhibition of HO-1.
As has been shown previously, the number of B lymphocytes in bone marrow was increased after OVX [ 25] and decreased in the arthritic mice [ 26].
Consistent with the increase in mast cells in the skin and gastrointestinal tract (data not shown), the numbers of BMCPs in spleen and MCPs in bone marrow were increased in young (6- to 10- week-old) Plcb3 −/− mice.
Numerous studies have indicated that angiogenesis, a process mediated by endothelial progenitor cells (EPCs) derived from the bone marrow, is increased in many tumors due to elevated levels of angiogenic factors in the peripheral blood.
Studies investigating WT1 as a marker of MRD have clearly demonstrated that its expression is low in normal bone marrow, is increased in AML patients at diagnosis, is decreased after an effective treatment, and becomes elevated again prior to clinical relapse [ 1, 2, 5– 10].
Therefore, at 7 days post injection of either ArtinM or ConA the percentage of mast cells in the bone marrow was dramatically increased.
In vitro, rmRetn could up regulate the CFU number of mice BM and after rmRetn was administered, the cell number of murine bone marrow was significantly increased in vivo after chemotherapy.
However, the frequency of CD8+ T cells positive for activation markers CD56 and CD57 in patients with a skewed TCRVβ repertoire in the bone marrow and peripheral blood, and HLA-DR in patients with a skewed TCRVβ repertoire in the bone marrow, was significantly increased when compared with patients with a polyclonal T-cell repertoire.
Inefficient B cell development in the bone marrow was associated with increased cell death, indicating that ATG5 is important for B cell survival during development.
Apoptosis of HSCs, CMPs, GMPs, and bone marrow neutrophils was increased in STAT5−/− mice, an observation consistent with previous reports that survival of lindimSca-1+ and lindimSca-1neg/lo bone marrow cells is decreased in the absence of STAT5 [26], and that STAT5 may promote the survival of myeloid progenitors through its ability to induce transcription of the bcl-x gene [25].
