Bone Marrow Stromal Cells of Young and Adult Rats Respond Similarly to Platelet-Released Supernatant and Bone Morphogenetic Protein-6 In Vitro

2006 ◽  
Vol 77 (4) ◽  
pp. 699-706 ◽  
Author(s):  
Silvia Cei ◽  
Barbara Kandler ◽  
Alexander Fügl ◽  
Mario Gabriele ◽  
Jeffrey O. Hollinger ◽  
...  
Nanoscale ◽  
2020 ◽  
Vol 12 (13) ◽  
pp. 7284-7300 ◽  
Author(s):  
Xiangfeng Li ◽  
Minjun Liu ◽  
Fuying Chen ◽  
Yuyi Wang ◽  
Menglu Wang ◽  
...  

Biomimicking the nanostructure of natural bone apatite to enhance the bioactivity of hydroxyapatite (HA) biomaterials is an eternal topic in the bone regeneration field.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3640-3640
Author(s):  
Martin Hildebrandt ◽  
Kurt Bommert ◽  
Kirstin Rautenberg ◽  
Wolf-Dieter Ludwig

Abstract The rare association of pulmonary hypertension and myeloproliferative syndromes (MPS) has been described previously (Garcia-Manero G et al., Am J Hematol1999; 60(2): 130-5, Dingli D et al., Chest2001, 120(3): 801-8), but the mechanisms contributing to this potentially hazardous condition await further elucidation. Bone morphogenetic protein receptors (BMPR) modulate the size of the hematopoetic niche (Zhang J et al., Nature2003, 425(6960): 836-41), with an inhibitory effect on myeloproliferation. In the pulmonary vascular bed, a decreased or deficient expression of BMPR has been shown to result in the proliferation of vascular smooth-muscle cells, asymmetric neointimal hyperplasia in small pulmonary arteries and subsequent pulmonary hypertension (Lane KB et al., Nat Genet2000, 26(1):81-4; Du L et al, N Engl J Med2003, 348(6): 500-9). We hypothesized that, in patients suffering from MPS and pulmonary hypertension, changes in the expression of BMPR and subsequent signalling molecules Angiopoietin-1 (Ang-1) and its receptor, TIE-2, may occur not only in the lung, but also in the bone marrow and correspond with enhanced myeloproliferation in vitro. Bone marrow stromal cells were cultured frompatients with pulmonary hypertension and MPS (n=2),patients with MPS and no evidence of pulmonary hypertension (n=3) andhealthy controls (n=3).The cultured cells were subjected to Western Blot analysis for the expression of BMP receptors BMPR-1A and BMPR-2, Angiopoietin-1 and TIE-2. Furthermore, a modified long-term culture initiating cell (LTC-IC) assay was established using the cultured bone marrow stromal cells as layers for autologous and allogeneic progenitor cell assays. The two patients suffering from both, MPS and pulmonary hypertension, showed a diminished expression of BMPR-1A and an enhanced expression of Ang-1 and TIE-2 in cultured stromal cells when compared to patients with MPS alone and to healthy controls. In one of the two patients, a three- to fourfold increase in the number of long-term culture-initiating cells after seeding of CD34-positive cells and of bone marrow mononuclear cells from healthy donors and from the other patients included was observed in modified LTC-IC assays. Our observations argue in favour of changes in BMP receptor expression and signalling with impact not only on pulmonary hypertension as described before, but also on the emergence of a myeloproliferative state.


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