Bone regeneration following a fracture progresses through sequential phases similar to endochondral ossification, starting with chemotaxis and proliferation of MPCs [2], [3], [4], [5].
Upon analyzing the 14 types of BMPs, we found that BMP9 is one of the most potent BMPs in inducing osteogenic differentiation of MPCs [19], [24], [25], [26], [27], [28], [29], [30], [31].
We further demonstrated that BMP9 regulates a distinct set of downstream targets that may play a role in regulating BMP-induced osteoblast differentiation of MPCs [19], [26], [27], [28], [29], [31].
P. aeruginosa exhibited similar MPCs (16 128 μg/ml) and MPC/MIC ratios (16 64) for all original strains.
In S. pseudintermedius, the MPCs (16 128 μg/ml) and MPC/MIC ratios (16 128) in low-susceptible strains (S7 S10) with one QRDR mutation were higher than those in high-susceptible strains without QRDR mutations (S1 S6; MPC: 2 8 μg/ml and MPC/MIC: 4 16).
MPCs (5 × 104 cells unless stated otherwise) were added to obtain a final volume of 300 μL.
Briefly, single-cell suspensions of cultured MPCs (2 × 104 cells/well) were plated in serum-free media supplemented with 0, 1, 2, 5 and 10 μg/ml PPS.
In this species, low-susceptible strains with one QRDR mutation (strains E7 E10) had relatively higher MPCs (8 32 μg/ml), compared with high-susceptible strains (0.5 2 μg/ml).
Furthermore, numbers of MPCs (CD34+/Sca-1−/CD45− cells) were significantly increased in mice receiving CCR2−/− BM despite the decreased size of regenerated myofibers.
With regard to the above, previous in vitro studies have documented the complex, bidirectional interactions between macrophages and MPCs (43, 63 63 63 63 63).
