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Michihiko Usui

Publications and source records attributed to Michihiko Usui.

5 recordsLinked to original sources
PubMed2006

Expression analysis of LacZ gene placed in the locus of Cnot7 exhibits its activity in osteoblasts in vivo and in mineralized nodules in vitro.

CCR4-NOT complex 7 (Cnot7) was identified as a regulator of gene expression in yeast and evolutionally conserved in mammals. Cnot7 deficient male mice exhibit abnormality in spermatogenesis. As these mice contained construct to express LacZ, we followed the expression patterning in these animals. LacZ was expressed in osteoblasts located in the primary spongiosa in adult mice. Cellular analysis indicated that LacZ is expressed in osteoblasts but not in osteoclasts. In the mineralized nodules formed in the culture of bone marrow cells obtained from Cnot7 +/- mice, LacZ expression was mainly observed in the cells forming mineralized nodules but not in un-mineralized area scattered around the periphery of the nodules. LacZ blue positive cells were gradually depositing minerals along its time course of the in vitro mineralization assay. Cnot7 expression was enhanced by the treatment with BMP. These data suggest that Cnot7 is expressed in osteoblasts and is associated with mineralization.

3T3 Cells↗
PubMed2004

Tob deficiency superenhances osteoblastic activity after ovariectomy to block estrogen deficiency-induced osteoporosis.

Tob (transducer of erbB2) is a member of antiproliferative family proteins and acts as a bone morphogenic protein inhibitor as well as a suppressor of proliferation in T cells, which have been implicated in postmenopausal bone loss. To determine the effect of Tob deficiency on estrogen deficiency-induced bone loss, we analyzed bone metabolism after ovariectomy or sham operation in Tob-deficient mice. Ovariectomy in WT mice decreased trabecular bone volume and bone mineral density (BMD) as expected. In Tob-deficient mice, ovariectomy reduced bone volume and BMD. However, even after ovariectomy, both trabecular bone volume and BMD levels in Tob-deficient bone were comparable to those in sham-operated WT bones. Bone formation parameters (mineral apposition rate and bone formation rate) in the ovariectomized Tob-deficient mice were significantly higher than those in the ovariectomized WT mice. In contrast, the ovariectomy-induced increase in the bone resorption parameters, osteoclast surface, and osteoclast number was similar between Tob-deficient mice and WT mice. Furthermore, in ex vivo nodule formation assay, ovariectomy-induced enhancement of nodule formation was significantly higher in the bone marrow cells from Tob-deficient mice than in the bone marrow cells from ovariectomized WT mice. Both Tob and estrogen signalings converge at bone morphogenic protein activation of alkaline phosphatase and GCCG-reporter gene expression in osteoblasts, revealing interaction between the two signals. These data indicate that Tob deficiency prevents ovariectomy-induced bone loss through the superenhancement of osteoblastic activities in bone and that this results in further augmentation in the bone formation rate and the mineral apposition rate after ovariectomy in vivo.

3T3 Cells↗
PubMed2004

[Osteoporosis from the point of view of dental practice].

When dentists examine a patient with osteoporosis, they should consider the condition of periodontal disease, because both osteoporosis and periodontal disease share the same symptoms such as reduction of the bone volume. Many studies have attempted to define the relationship between these two diseases. Although most studies support a positive association between them, the mechanism of correlation still remains unclear. To establish novel treatment modalities of these diseases, further studies are necessary to elucidate the detailed mechanisms of interaction between them.

Female↗
PubMed2002

Enhancing effect of Tob deficiency on bone formation is specific to bone morphogenetic protein-induced osteogenesis.

Tob is a recently reported novel bone morphogenetic protein (BMP) inhibitor, which originally was identified by West-Western procedure using ErbB2 as a probe and contains a nuclear localization signal. To further characterize the effects of Tob deficiency on BMP-induced new bone (NB) formation, we examined microcomputed tomography (microCT) on the cross-section of the bone induced by daily injection with BMP onto the calvariae of newborn mice. The calvariae of the saline-injected Tob-deficient (TD) mice were similar to those of the saline-injected or untreated wild-type (WT) mice. BMP injection locally produced NB on the calvaria in WT mice as known previously. In contrast to WT mice, BMP injection onto the calvariae of TD mice produced a calcified area in the cross-section of NB, which was more than that produced by BMP in the WT calvariae. In addition, the horizontal width and the vertical height of the NB induced by BMP in TD mice were several-fold more than those in WT mice. The effect of Tob deficiency on bone-forming activity was selective to the response to the injection with BMP because the levels of injury-induced NB formation examined by microCT 10 days after bone marrow ablation in the femora were similar between the TD and WT mice. These data indicate that Tob acts as a novel specific antagonist against bone formation induced by BMP treatment in bone.

Animals↗