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Interestingly, sepsis is also associated with elevated levels of BSP [ 12, 13].
At 15 h after BMP-2 addition, the levels of Osx RNA were already high but levels of Bsp and Oc RNAs were still very low.
Elevated levels of BSP have been reported in tumors and serum from patients with breast, lung, prostate, or thyroid cancer [ 2].
Immunohistochemistry analysis revealed that elevated levels of BSP in bone lesions were more frequently associated with PCa metastases with respect to pure osteolytic metastases from breast cancer [ 116].
However, among the experimental biomarkers, it should be noted that baseline levels of BSP were moderately associated with duration of bone metastases, and were also associated with failure to complete the study despite the fact that BSP did not reach statistical significance for an association with incidence of on-study SRE.
Real time RT-PCR data noted that MDPC-23 cultured on the COL-I-coated substrates had stimulated mRNA levels of BSP on day 7; surprisingly, the mRNA expression level of DMP-1 was suppressed by P-COL (0.59 ± 0.11 fold) (p < 0.05) and T-COL (0.74 ± 0.25 fold) (p > 0.05) on day 10; this is in agreement with a previous study from Mizuno et al. [ 31].
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The main result of the present study is that, despite very high cytokine concentrations during experimental endotoxemia, no indications were found that acute systemic inflammation results in increased levels of BSPs and deterioration of CFs in humans in vivo.
The level of BSP mRNA was 4.68-fold (p = 2.57 × 10−8) higher in the OC-stimulated 4T1 cells than in the cells without stimulation, and OCN increased by 5.67-fold (p = 3.01 × 10−5) when 4T1 cells were incubated in OC for 28 days.
Confocal imaging of cpTi-treated hMSC cultures revealed patchy groups of cells displaying disorganized cytoskeletal architecture and low levels of extracellular BSP.
At 30 h after BMP-2 addition, RNA levels of Osx, Bsp, and Oc were all high.
Before BMP-2 addition, the RNA levels of Osx, Bsp, and Oc were either undetectable or very low.
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