Figure 6
MT1-MMP–deficient mice have a defective BM stromal niche with impaired terminal differentiation because of impaired release of HIF-1α–associated factors. (A) Number of colonies in IL-7–containing cultures of MT1-MMP+/+ and MT1-MMP−/− BM cells (n = 3). (B) Coculture of wild-type Lin− BM GFP+ cells on confluent MT1-MMP knockdown or control MS-5 cells with/without KitL. (C-D) PB WBCs (C) and PLT (D) after KitL injections into MT1-MMP+/+ (n ≥ 10) and MT1-MMP−/− mice (n = 3). (E-F) PB WBCs (E) and PLT (F) counts 2 days after initiation of SDF-1 treatment of MT1-MMP+/+ (n ≥ 10) and MT1-MMP−/− mice (n = 2). Errors in bar graphs are SEM; *P < .05, **P < .01.

MT1-MMP–deficient mice have a defective BM stromal niche with impaired terminal differentiation because of impaired release of HIF-1α–associated factors. (A) Number of colonies in IL-7–containing cultures of MT1-MMP+/+ and MT1-MMP−/− BM cells (n = 3). (B) Coculture of wild-type Lin− BM GFP+ cells on confluent MT1-MMP knockdown or control MS-5 cells with/without KitL. (C-D) PB WBCs (C) and PLT (D) after KitL injections into MT1-MMP+/+ (n ≥ 10) and MT1-MMP−/− mice (n = 3). (E-F) PB WBCs (E) and PLT (F) counts 2 days after initiation of SDF-1 treatment of MT1-MMP+/+ (n ≥ 10) and MT1-MMP−/− mice (n = 2). Errors in bar graphs are SEM; *P < .05, **P < .01.

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