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Biology subjects

Usami, Y.

Publications and source records attributed to Usami, Y..

4 recordsLinked to original sources

The mechanical force with the physiological movement works as a biological cue in tendon development during the postnatal phase in mice

The musculoskeletal system provides structural stability and coordination to enable movement. Tendons have the essential role of efficiently transmitting force generated from muscle contraction to bone to enable ambulation. In doing so, they resist high external forces. In fact, muscle contraction during embryonic development is required to maintain tendon growth and differentiation. Nonetheless, defining the types and magnitudes of loads that act on tendons during embryonic and early postnatal periods is quite difficult. In this study, we aimed to define the physiologic limb movement and forces experienced during these stages in the murine model. We found that late-stage embryos had limited amniotic space, which attenuated limb movement. In the neonatal phase, physical ability, as measured by rollover function and locomotion, increased. These changes, which likely corresponded to increased forces applied to the tendons, corresponded with the expression of tenogenic markers during the embryo to postnatal phase. In particular, we found that the upregulation of Scx and Tnmd correlated with increased movement during the two weeks after birth. Our results help define the spatiotemporal role of mechanical force, including internal and external factors, in tendon growth and development. HighlightsO_LIAssessed limb movement in amnion. C_LIO_LISpace limitation attenuated limb movement in the late-stage embryos. C_LIO_LIDefined the mechanical force from the limbs physiological environment. C_LIO_LIScx and Tnmd were upregulated synchronically with rollover function and locomotion. C_LIO_LIMechanical forces may work as the cue of tendon development C_LI

developmental biology↗

Characteristic differences in tibial subchondral bone changes in the post-traumatic knee osteoarthritis model

ObjectiveMeniscus degeneration and subchondral bone changes contribute to the development and progression of knee OA. The purpose of this study was to reveal the relationship between medial meniscus degeneration and characteristics of subchondral bone changes in different models DesignWe used the anterior cruciate ligament transection (ACL-T) model, destabilization of the medial meniscus (DMM) model, controlled abnormal tibial translation (CATT) model and a controlled abnormal tibial rotation (CATR) model with different mechanical stresses. We performed histological analysis and micro computed tomography analysis, at 4 and 6 weeks. In addition, we divided the tibial subchondral bone into four compartments and set the regions of interest ResultsMeniscus degeneration was observed in all groups, but there was no significant difference. The ACL-T group showed posterior displacement of the contact area, and the DMM and CATR groups showed lateral deviation of the medial meniscus. The region-specific subchondral bone changes in each model showed that changes in mechanical stress due to ACL and meniscus dysfunction, as well as changes in the contact area, affect the bony structure of the subchondral bone differently in each region. ConclusionsSubchondral bone changes in different models of mechanical stress were different in each region. In particular, changes in the contact area and increased compressive stress due to meniscus dysfunction were suggested to promote bone formation. The results of this study indicate that changes in alignment and contact area in the PTOA model may cause region-specific characteristics of the subchondral bone changes.

pathology↗

Nutrient-regulated dynamics of chondroprogenitors in the postnatal murine growth plate

Longitudinal bone growth relies on endochondral ossification in the cartilaginous growth plate where chondrocytes accumulate and synthesize the matrix scaffold that is replaced by bone. The chondroprogenitors in the resting zone maintain the continuous turnover of chondrocytes in the growth plate. Malnutrition is a leading cause of growth retardation in children; however, after recovery from nutrient deprivation, bone growth is accelerated beyond the normal rate, a phenomenon termed catch-up growth. Though nutritional status is a known regulator of long bone growth, it is largely unknown if and how chondroprogenitor cells respond to deviations in nutrient availability. Here, using fate-mapping analysis in Axin2CreERT2 mice, we showed that dietary restriction increased the number of Axin2+ chondroprogenitors in the resting zone and simultaneously inhibited their differentiation. Once nutrient deficiency was resolved, the accumulated chondroprogenitor cells immediately restarted differentiation and formed chondrocyte columns, contributing to accelerated growth. Furthermore, we showed that nutrient deprivation reduced the level of phosphorylated Akt in the resting zone, and that exogenous IGF-1 canceled this reduction and stimulated differentiation of the pooled chondroprogenitors, decreasing their numbers. Our study of Axin2CreERT2 revealed that nutrient availability regulates the balance between accumulation and differentiation of chondroprogenitors in the growth plate, and further demonstrated that IGF-1 partially mediates this regulation by promoting the committed differentiation of the chondroprogenitor cells.

developmental biology↗

Abnormal Tibia Translation leads Directly the Surface Cartilage Degeneration with Molecular Biological Response using a Novel Non-Invasive ACL ruptured Mice Model

ObjectiveThe ACL-deficient model helps to clarify the mechanism of knee OA; however, the conventional ACL injury model could have included concurrent onset factors such as direct compression stress to cartilage and subchondral bone. In this study, we established a novel Non-invasive ACL-Ruptured mouse model without concurrent injuries and elucidated the relationship between OA progression and joint instability. DesignWe induced the ACL-Rupture non-invasively in twelve-week-old C57BL/6 male mice and evaluated histological, macroscopical, and morphological analysis at 0 days. Next, we created the ACL-R, controlled abnormal tibial translation (CATT), and Sham groups. Then, the joint stability and OA pathophysiology were analyzed at 2, 4, and 8 weeks. ResultsNo intra-articular injuries, except for ACL rupture, were observed in the ACL-R model. ACL-R mice increased anterior tibial displacement compared to the Sham group (p<0.001, 95% CI [-1.509 to -0.966]) and CATT group (p<0.001, 95% CI [-0.841 to -0.298]) at 8 weeks. All mice in the ACL-R group caused cartilage degeneration. The degree of cartilage degeneration in the ACL-R group was higher than in the CATT group (p=0.006) at 8 weeks. The MMP-3-positive cell rate of chondrocytes increased in the ACL-R group than CATT group from 4 weeks (p=0.043; 95% CI [-28.32 to -0.364]) while that of synovial cells increased at 8 weeks (p=0.031; 95% CI [-23.398 to -1.021]). ConclusionWe successfully established a Non-invasive ACL-R model without intra-articular damage. Our model revealed that chondrocytes might react to abnormal mechanical stress prior to synovial cells while the knee OA onset.

molecular biology↗