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Jack P Callaghan - One of the best experts on this subject based on the ideXlab platform.
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characterizing the combined effects of Force repetition and posture on injury pathways and micro structural damage in isolated functional spinal units from sub acute failure magnitudes of cyclic Compressive loading
Clinical Biomechanics, 2015Co-Authors: Chad E Gooyers, Mamiko Noguchi, Elliott M Mcmillan, Joe Quadrilatero, Jack P CallaghanAbstract:Abstract Background Previous research suggests that when the magnitude of peak Compressive Force applied during cyclic loading exceeds 30% of a functional spinal unit's estimated ultimate Compressive tolerance, fatigue failure of the cartilaginous endplate or vertebra will occur before intervertebral disc herniation. Methods Three levels of peak Compressive Force, three cycle rates and two dynamic postural conditions were examined using a full-factorial design. Cyclic Compressive Force was applied using a modified material testing apparatus, in accordance with a biofidelic time-varying waveform with synchronous flexion/extension rotation for 5000 cycles. Annulus fibrosus tissue from 36 “survivor” FSUs was excised for histological analysis. Results 80% of specimens survived 5000 cycles of cyclic loading. A marked difference of the magnitude of peak Compressive Force was noted in the Kaplan–Meier survival function of experimental conditions that induced fatigue injury. Overall, in the 40% ultimate Compressive tolerance load condition, the probability of survival was less than 67%. The micro-structural damage detected in excised samples of annulus fibrosus tissue consisted of clefts and fissures within the intra-lamellar matrix, as well as delamination within the inter-lamellar matrix. Interpretation Consistent with previous research, our findings support a threshold of peak Compressive Force of 30% ultimate Compressive tolerance, where cyclic loading above this level will likely result in fatigue injury in less than 5000 cycles of in vitro mechanical loading. However, findings from our histological analyses demonstrate that considerable micro-structural damage occurred in specimens that “survived” the cyclic loading exposure.
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the impact of Compressive Force magnitude on the in vitro neutral zone range and passive stiffness during a flexion extension range of motion test
Cogent engineering, 2015Co-Authors: Mamiko Noguchi, Chad E Gooyers, Michael W R Holmes, Jack P CallaghanAbstract:AbstractThe objective of this work was to examine the influence of Compressive Force magnitude on a functional spinal unit’s (FSU) flexion–extension neutral zone measured during pure moment (PM) tests. Each porcine cervical FSU received four repeats of a PM test with 10, 300, 900 and 1,800 N of Compressive Force, in a randomized order. Increasing the magnitude of compression significantly decreased the neutral zone range (p < 0.001), while increasing passive stiffness (p < 0.001). The flexion limit at 10 N was significantly lower (p < 0.05) than the other loading conditions. Reporting the Compressive Force magnitude is important when posture is a standardized experimental factor considered in the design of in vitro spine biomechanics studies.
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biomedical engineering research article the impact of Compressive Force magnitude on the in vitro neutral zone range and passive stiffness during a flexion extension range of motion test
2015Co-Authors: Mamiko Noguchi, Chad E Gooyers, Michael W R Holmes, Jack P CallaghanAbstract:4, * Abstract: The objective of this work was to examine the influence of Compressive Force magnitude on a functional spinal unit's (FSU) flexion-extension neutral zone measured during pure moment (PM) tests. Each porcine cervical FSU received four repeats of a PM test with 10, 300, 900 and 1,800 N of Compressive Force, in a randomized order. Increasing the magnitude of compression significantly decreased the neutral zone range (p < 0.001), while increasing passive stiffness (p < 0.001). The flexion limit at 10 N was significantly lower (p < 0.05) than the other loading conditions. Reporting the Compressive Force magnitude is important when posture is a standardized experimental factor considered in the design of in vitro spine biomechanics studies. Subjects: Bioscience; Engineering & Technology; Medicine, Dentistry, Nursing & Allied Health
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Compressive Force magnitude and intervertebral joint flexion extension angle influence shear failure Force magnitude in the porcine cervical spine
Journal of Biomechanics, 2012Co-Authors: Samuel J Howarth, Jack P CallaghanAbstract:Abstract Despite the findings that peak anterior shear load is highly correlated with low-back pain reporting, very little research has been conducted to determine how vertebral shear injury potential is influenced. The current study quantified the combined effects of vertebral joint compression and flexion/extension postural deviation from neutral on ultimate shear failure. Ninety-six porcine cervical specimens (48C3–C4, 48C5–C6) were tested. Each specimen was randomly assigned to one of twelve combinations of Compressive Force (15%, 30%, 45%, or 60% of predicted Compressive failure Force) and flexion/extension postural deviation (extended, neutral, or flexed). Vertebral joint shear failure was induced by applying posterior shear displacement of the caudal vertebra at a constant rate of 0.15 mm/s. Throughout shear failure tests, vertebral joint kinematics were measured using an optoelectronic camera and a series of infrared light emitting diodes while shear Force was measured from load cells rigidly interfaced in series with linear actuators that applied the shear displacement. Measurements of shear stiffness, ultimate Force, displacement, and energy stored were made from the Force–displacement data. Compressive Force and postural deviation demonstrated main effects without a statistically significant interaction for any of the measurements. Shear failure Force increased by 11.1% for each 15% increment in Compressive Force ( p p p
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intervertebral disc herniation studies on a porcine model exposed to highly repetitive flexion extension motion with Compressive Force
Clinical Biomechanics, 2001Co-Authors: Jack P Callaghan, Stuart M McgillAbstract:Abstract Objective. To determine whether repeated motion with low magnitude joint Forces, and flexion/extension moments consistently produce herniation in a non-degenerated, controlled porcine spine motion segment. Design. Combined loading (flexion/extension motions and Compressive Forces) was applied to in vitro porcine functional spinal units. Biomechanical and radiographic characteristics were documented. Background. While most studies performed in vitro have examined uniaxial or fixed position loading to older specimens, there have been few studies that have examined whether `healthy' intervertebral discs can be injured by low magnitude repeated combined loading. Methods. Porcine cervical spine motion segments (C3–C4) were mounted in a custom jig which applied axial Compressive loads with pure flexion/extension moments. Dynamic testing was conducted to a maximum of 86 400 bending cycles at a rate of 1 Hz with simultaneous torques, angular rotations, axial deformations recorded for the duration of the test. Results. Herniation (posterior and posterior-lateral regions of the annulus) occurred with relatively modest joint compression but with highly repetitive flexion/extension moments. Increased magnitudes of axial Compressive Force resulted in more frequent and more severe disc injuries. Conclusions. The results support the notion that intervertebral disc herniation may be more linked to repeated flexion extension motions than applied joint compression, at least with younger, non-degenerated specimens. Relevance While intervertebral disc herniations are observed clinically, consistent reproduction of this injury in the laboratory has been elusive. This study was designed to examine the biomechanical response and failure mechanics of spine motion segments to highly repetitive low magnitude complex loading.
Noriyoshi Shimizu - One of the best experts on this subject based on the ideXlab platform.
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Compressive Force stimulates the gene expression of il 17s and their receptors in mc3t3 e1 cells
Connective Tissue Research, 2010Co-Authors: Fan Zhang, Kotoe Mayahara, Narihiro Mitsui, Naoto Suzuki, Noriyoshi Shimizu, Yuki Koyama, Chunling Wang, Chieko Shionome, Rina Sanuki, Masao MaenoAbstract:During orthodontic tooth movement, cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts can alter the process of bone remodeling. Recently, interleukin-17 (IL-17) was found to stimulate osteoclastic resorption through osteoblasts by inducing receptor activator of nuclear factor κB ligand (RANKL) expression. However, the relationship between mechanical stress and IL-17 production by osteoblasts is not clear. Therefore, we examined the effect of Compressive Force on the expressions of IL-17A, IL-17B, IL-17C, IL-17D, IL-17E, IL-17F, and their receptors (IL-17RA, IL-17RB, IL-17RC, IL-17RD, and IL-17RE) using MC3T3-E1 cells as osteoblast-like cells. We also examined the effect of IL-17A on the expression of IL-17Rs, RANKL, macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG). The cells were cultured with or without continuous Compressive Force (1.0 and 2.0 g/cm(2)) for up to 24 hr. The cells were also cultured with or without IL-17A (0.1, 1.0, or 10 ng/ml) for up to 72 hr. The mRNA expressions of IL-17s and their receptors were estimated by real-time polymerase chain reaction. The expression levels of IL-17s and their receptors increased depending on the Compressive Force. The addition of IL-17A increased the expression of IL-17RA, IL-17RB, IL-17RC, IL-17RE, RANKL, and M-CSF, whereas it decreased OPG expression. These results indicate that Compressive Force induces the expression of IL-17s and their receptors in osteoblast-like cells and that IL-17s and their receptors produced in response to Compressive Force may affect osteoclastogenesis through the expression of RANKL, M-CSF, and OPG.
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Compressive Force induces osteoclast differentiation via prostaglandin e2 production in mc3t3 e1 cells
Connective Tissue Research, 2010Co-Authors: Rina Sanuki, Narihiro Mitsui, Naoto Suzuki, Noriyoshi Shimizu, Yuki Koyama, Fan Zhang, Chieko Shionome, Akiko Kuwabara, Masao MaenoAbstract:In orthodontic tooth movement, prostaglandin E(2) (PGE(2)) released from osteoblasts can alter the normal process of bone remodeling. We previously showed that Compressive Force (CF) controls bone formation by stimulating the production of PGE(2) and Ep2 and/or Ep4 receptors in osteoblasts. The present study was undertaken to examine the effect of CF on the production of PGE(2), cyclooxygenase-2 (COX-2), macrophage colony-stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) using osteoblastic MC3T3-E1 cells and to examine the indirect effect of CF on osteoclast differentiation using RAW264.7 cells as osteoclast precursors. MC3T3-E1 cells were cultured with or without continuous CF (1.0 or 3.0 g/cm(2)) for 24 hr, and PGE(2) production was determined using ELISA. The expression of COX-2, M-CSF, RANKL, and OPG genes and proteins was determined using real-time PCR and ELISA, respectively. Osteoclast differentiation was estimated using tartrate-resistant acid phosphatase (TRAP) staining of RAW 264.7 cells cultured for 10 days with conditioned medium from CF-treated MC3T3-E1 cells and soluble RANKL. As CF increased, PGE(2) production and the expression of COX-2, M-CSF, and RANKL increased, whereas OPG expression decreased. The number of TRAP-positive cells increased as CF increased. Celecoxib, a specific inhibitor of COX-2, blocked the stimulatory effect of CF on TRAP staining and the production of PGE(2), M-CSF, RANKL, and OPG. These results suggest that CF induces osteoclast differentiation by increasing M-CSF production and decreasing OPG production via PGE(2) in osteoblasts.
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effect of Compressive Force on the expression of inflammatory cytokines and their receptors in osteoblastic saos 2 cells
Archives of Oral Biology, 2008Co-Authors: Yuki Koyama, Narihiro Mitsui, Naoto Suzuki, Momoko Yanagisawa, Noriyoshi Shimizu, Rina Sanuki, Keitaro Isokawa, Masao MaenoAbstract:Abstract Objective In orthodontic tooth movement, some cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts on the pressure side can alter the normal processes of bone remodelling, resulting in physiological bone resorption. We examined the effect of Compressive Force and interleukin (IL)-1 type I receptor antagonist (IL-1ra) on the expression of inflammatory cytokines that promote osteoclast formation, as well as on their receptors, in osteoblastic Saos-2 cells. Design The cells were cultured in Dulbecco's modified Eagle medium containing 10% fetal bovine serum with or without continuous Compressive Force (0.5–3.0 g/cm2) and/or IL-1ra for up to 24 h. The gene expression levels of the cytokines and their receptors were estimated by determining mRNA levels using real-time PCR; the protein levels were determined using ELISA or immunohistochemical staining. Results The expression of IL-1β, IL-1 receptor, IL-6, IL-6 receptor, IL-8 receptor, IL-11 and tumor necrosis factor-α (TNFα) increased depending on the strength and duration of the Compressive Force, whereas the expression of IL-8, IL-11 receptor and TNFα receptor did not change with the application of Compressive Force. The expression of cytokines and their receptors produced by 3.0 g/cm2 of Compressive Force decreased with the simultaneous addition of IL-1ra and the decrease was remarkable in IL-8 receptor, IL-11 and TNFα. Conclusion These results indicate that mechanical stress induces the production of inflammatory cytokines and their receptors in osteoblasts and the phenomenon is enhanced by the autocrine action of IL-1β, which is increased in amount by mechanical stress.
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effects of Compressive Force on the differentiation of pluripotent mesenchymal cells
Life Sciences, 2007Co-Authors: Momoko Yanagisawa, Narihiro Mitsui, Naoto Suzuki, Kichibee Otsuka, Yuki Koyama, Noriyoshi ShimizuAbstract:The purpose of this study was to determine the effect of mechanical stress on the differentiation of the pluripotent mesenchymal cell line C2C12. C2C12 cells were cultured continuously under Compressive Force (0.25-2.0 g/cm(2)). After mechanical stress loading, the levels of expression of mRNAs and proteins for phenotype-specific markers of osteoblasts (Runx2, Msx2, Dlx5, Osterix, AJ18), chondroblasts (Sox5, Sox9), myoblasts (MyoD), and adipocytes (PPAR gamma) were measured by real-time polymerase chain reaction analysis and Western blot analysis, respectively. The expression of activated p38 mitogen-activated protein kinase (p38 MAPK) was measured by Western blotting and/or ELISA. Loading 0.5 g/cm(2) of Compressive Force significantly increased the expression levels of Runx2, Msx2, Dlx5, Osterix, Sox5, and Sox9. In contrast, the expression levels of AJ18, MyoD, and PPAR gamma were decreased by exposure to 0.5 g/cm(2) of Compressive Force. Loading 0.5 g/cm(2) of Compressive Force also induced the phosphorylation of p38 MAPK. SB203580, which is a specific inhibitor of p38 MAPK, inhibited the Compressive Force-induced phosphorylation of p38 MAPK and partially blocked Compressive Force-induced Runx2 mRNA expression. These results demonstrate that Compressive Force stimulation directs the differentiation pathway of C2C12 cells into the osteoblast and chondroblast lineage via activated phosphorylation of p38 MAPK.
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optimal Compressive Force induces bone formation via increasing bone morphogenetic proteins production and decreasing their antagonists production by saos 2 cells
Life Sciences, 2006Co-Authors: Narihiro Mitsui, Naoto Suzuki, Masao Maeno, Momoko Yanagisawa, Kichibee Otsuka, Yuki Koyama, Noriyoshi ShimizuAbstract:Orthodontic tooth movement induced alveolar bone resorption and formation around the teeth applied mechanical Force. Although mechanical Force can promote bone formation, the molecular mechanism that underlies this phenomenon is not fully understood. The purposes of this study were to determine how mechanical stress affects the osteogenic response of human osteoblastic cells (Saos-2), and also to examine the optimal Compressive Force for osteogenesis in vitro. Saos-2 cells were cultured with or without continuously Compressive Force (0.5-3.0 g/cm2). The expression of bone morphogenetic proteins (BMPs), their antagonists, and transcription factors which involved in osteogenesis were measured using real-time PCR and/or Western blot analysis. Phosphorylation of Smad1 was determined by Western blot. Loading with 1.0 g/cm2 of Compressive Force significantly increased the expression of BMPs, Runx2 and osterix. In contrast, the expression of BMP antagonists and AJ18 was decreased with 1.0 g/cm2 of Compressive Force. Loading with 1.0 g/cm2 of Compressive Force also induced phosphorylation of Smad1. Noggin inhibited the Compressive Force-induced phosphorylation of Smad1 markedly, and also partially blocked Compressive Force-induced Runx2 mRNA expression. Moreover, the conditioned medium from 1.0 g/cm2 of Compressive Force applied cells apparently increased calcium content in mineralized nodules of Saos-2 culture. This study demonstrates that an optimal Compressive Force stimulates in vitro mineralization via increasing BMPs production and decreasing their antagonists production.
Narihiro Mitsui - One of the best experts on this subject based on the ideXlab platform.
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Compressive Force stimulates the gene expression of il 17s and their receptors in mc3t3 e1 cells
Connective Tissue Research, 2010Co-Authors: Fan Zhang, Kotoe Mayahara, Narihiro Mitsui, Naoto Suzuki, Noriyoshi Shimizu, Yuki Koyama, Chunling Wang, Chieko Shionome, Rina Sanuki, Masao MaenoAbstract:During orthodontic tooth movement, cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts can alter the process of bone remodeling. Recently, interleukin-17 (IL-17) was found to stimulate osteoclastic resorption through osteoblasts by inducing receptor activator of nuclear factor κB ligand (RANKL) expression. However, the relationship between mechanical stress and IL-17 production by osteoblasts is not clear. Therefore, we examined the effect of Compressive Force on the expressions of IL-17A, IL-17B, IL-17C, IL-17D, IL-17E, IL-17F, and their receptors (IL-17RA, IL-17RB, IL-17RC, IL-17RD, and IL-17RE) using MC3T3-E1 cells as osteoblast-like cells. We also examined the effect of IL-17A on the expression of IL-17Rs, RANKL, macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG). The cells were cultured with or without continuous Compressive Force (1.0 and 2.0 g/cm(2)) for up to 24 hr. The cells were also cultured with or without IL-17A (0.1, 1.0, or 10 ng/ml) for up to 72 hr. The mRNA expressions of IL-17s and their receptors were estimated by real-time polymerase chain reaction. The expression levels of IL-17s and their receptors increased depending on the Compressive Force. The addition of IL-17A increased the expression of IL-17RA, IL-17RB, IL-17RC, IL-17RE, RANKL, and M-CSF, whereas it decreased OPG expression. These results indicate that Compressive Force induces the expression of IL-17s and their receptors in osteoblast-like cells and that IL-17s and their receptors produced in response to Compressive Force may affect osteoclastogenesis through the expression of RANKL, M-CSF, and OPG.
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Compressive Force induces osteoclast differentiation via prostaglandin e2 production in mc3t3 e1 cells
Connective Tissue Research, 2010Co-Authors: Rina Sanuki, Narihiro Mitsui, Naoto Suzuki, Noriyoshi Shimizu, Yuki Koyama, Fan Zhang, Chieko Shionome, Akiko Kuwabara, Masao MaenoAbstract:In orthodontic tooth movement, prostaglandin E(2) (PGE(2)) released from osteoblasts can alter the normal process of bone remodeling. We previously showed that Compressive Force (CF) controls bone formation by stimulating the production of PGE(2) and Ep2 and/or Ep4 receptors in osteoblasts. The present study was undertaken to examine the effect of CF on the production of PGE(2), cyclooxygenase-2 (COX-2), macrophage colony-stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) using osteoblastic MC3T3-E1 cells and to examine the indirect effect of CF on osteoclast differentiation using RAW264.7 cells as osteoclast precursors. MC3T3-E1 cells were cultured with or without continuous CF (1.0 or 3.0 g/cm(2)) for 24 hr, and PGE(2) production was determined using ELISA. The expression of COX-2, M-CSF, RANKL, and OPG genes and proteins was determined using real-time PCR and ELISA, respectively. Osteoclast differentiation was estimated using tartrate-resistant acid phosphatase (TRAP) staining of RAW 264.7 cells cultured for 10 days with conditioned medium from CF-treated MC3T3-E1 cells and soluble RANKL. As CF increased, PGE(2) production and the expression of COX-2, M-CSF, and RANKL increased, whereas OPG expression decreased. The number of TRAP-positive cells increased as CF increased. Celecoxib, a specific inhibitor of COX-2, blocked the stimulatory effect of CF on TRAP staining and the production of PGE(2), M-CSF, RANKL, and OPG. These results suggest that CF induces osteoclast differentiation by increasing M-CSF production and decreasing OPG production via PGE(2) in osteoblasts.
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effect of Compressive Force on the expression of inflammatory cytokines and their receptors in osteoblastic saos 2 cells
Archives of Oral Biology, 2008Co-Authors: Yuki Koyama, Narihiro Mitsui, Naoto Suzuki, Momoko Yanagisawa, Noriyoshi Shimizu, Rina Sanuki, Keitaro Isokawa, Masao MaenoAbstract:Abstract Objective In orthodontic tooth movement, some cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts on the pressure side can alter the normal processes of bone remodelling, resulting in physiological bone resorption. We examined the effect of Compressive Force and interleukin (IL)-1 type I receptor antagonist (IL-1ra) on the expression of inflammatory cytokines that promote osteoclast formation, as well as on their receptors, in osteoblastic Saos-2 cells. Design The cells were cultured in Dulbecco's modified Eagle medium containing 10% fetal bovine serum with or without continuous Compressive Force (0.5–3.0 g/cm2) and/or IL-1ra for up to 24 h. The gene expression levels of the cytokines and their receptors were estimated by determining mRNA levels using real-time PCR; the protein levels were determined using ELISA or immunohistochemical staining. Results The expression of IL-1β, IL-1 receptor, IL-6, IL-6 receptor, IL-8 receptor, IL-11 and tumor necrosis factor-α (TNFα) increased depending on the strength and duration of the Compressive Force, whereas the expression of IL-8, IL-11 receptor and TNFα receptor did not change with the application of Compressive Force. The expression of cytokines and their receptors produced by 3.0 g/cm2 of Compressive Force decreased with the simultaneous addition of IL-1ra and the decrease was remarkable in IL-8 receptor, IL-11 and TNFα. Conclusion These results indicate that mechanical stress induces the production of inflammatory cytokines and their receptors in osteoblasts and the phenomenon is enhanced by the autocrine action of IL-1β, which is increased in amount by mechanical stress.
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effects of Compressive Force on the differentiation of pluripotent mesenchymal cells
Life Sciences, 2007Co-Authors: Momoko Yanagisawa, Narihiro Mitsui, Naoto Suzuki, Kichibee Otsuka, Yuki Koyama, Noriyoshi ShimizuAbstract:The purpose of this study was to determine the effect of mechanical stress on the differentiation of the pluripotent mesenchymal cell line C2C12. C2C12 cells were cultured continuously under Compressive Force (0.25-2.0 g/cm(2)). After mechanical stress loading, the levels of expression of mRNAs and proteins for phenotype-specific markers of osteoblasts (Runx2, Msx2, Dlx5, Osterix, AJ18), chondroblasts (Sox5, Sox9), myoblasts (MyoD), and adipocytes (PPAR gamma) were measured by real-time polymerase chain reaction analysis and Western blot analysis, respectively. The expression of activated p38 mitogen-activated protein kinase (p38 MAPK) was measured by Western blotting and/or ELISA. Loading 0.5 g/cm(2) of Compressive Force significantly increased the expression levels of Runx2, Msx2, Dlx5, Osterix, Sox5, and Sox9. In contrast, the expression levels of AJ18, MyoD, and PPAR gamma were decreased by exposure to 0.5 g/cm(2) of Compressive Force. Loading 0.5 g/cm(2) of Compressive Force also induced the phosphorylation of p38 MAPK. SB203580, which is a specific inhibitor of p38 MAPK, inhibited the Compressive Force-induced phosphorylation of p38 MAPK and partially blocked Compressive Force-induced Runx2 mRNA expression. These results demonstrate that Compressive Force stimulation directs the differentiation pathway of C2C12 cells into the osteoblast and chondroblast lineage via activated phosphorylation of p38 MAPK.
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optimal Compressive Force induces bone formation via increasing bone morphogenetic proteins production and decreasing their antagonists production by saos 2 cells
Life Sciences, 2006Co-Authors: Narihiro Mitsui, Naoto Suzuki, Masao Maeno, Momoko Yanagisawa, Kichibee Otsuka, Yuki Koyama, Noriyoshi ShimizuAbstract:Orthodontic tooth movement induced alveolar bone resorption and formation around the teeth applied mechanical Force. Although mechanical Force can promote bone formation, the molecular mechanism that underlies this phenomenon is not fully understood. The purposes of this study were to determine how mechanical stress affects the osteogenic response of human osteoblastic cells (Saos-2), and also to examine the optimal Compressive Force for osteogenesis in vitro. Saos-2 cells were cultured with or without continuously Compressive Force (0.5-3.0 g/cm2). The expression of bone morphogenetic proteins (BMPs), their antagonists, and transcription factors which involved in osteogenesis were measured using real-time PCR and/or Western blot analysis. Phosphorylation of Smad1 was determined by Western blot. Loading with 1.0 g/cm2 of Compressive Force significantly increased the expression of BMPs, Runx2 and osterix. In contrast, the expression of BMP antagonists and AJ18 was decreased with 1.0 g/cm2 of Compressive Force. Loading with 1.0 g/cm2 of Compressive Force also induced phosphorylation of Smad1. Noggin inhibited the Compressive Force-induced phosphorylation of Smad1 markedly, and also partially blocked Compressive Force-induced Runx2 mRNA expression. Moreover, the conditioned medium from 1.0 g/cm2 of Compressive Force applied cells apparently increased calcium content in mineralized nodules of Saos-2 culture. This study demonstrates that an optimal Compressive Force stimulates in vitro mineralization via increasing BMPs production and decreasing their antagonists production.
Naoto Suzuki - One of the best experts on this subject based on the ideXlab platform.
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Compressive Force stimulates the gene expression of il 17s and their receptors in mc3t3 e1 cells
Connective Tissue Research, 2010Co-Authors: Fan Zhang, Kotoe Mayahara, Narihiro Mitsui, Naoto Suzuki, Noriyoshi Shimizu, Yuki Koyama, Chunling Wang, Chieko Shionome, Rina Sanuki, Masao MaenoAbstract:During orthodontic tooth movement, cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts can alter the process of bone remodeling. Recently, interleukin-17 (IL-17) was found to stimulate osteoclastic resorption through osteoblasts by inducing receptor activator of nuclear factor κB ligand (RANKL) expression. However, the relationship between mechanical stress and IL-17 production by osteoblasts is not clear. Therefore, we examined the effect of Compressive Force on the expressions of IL-17A, IL-17B, IL-17C, IL-17D, IL-17E, IL-17F, and their receptors (IL-17RA, IL-17RB, IL-17RC, IL-17RD, and IL-17RE) using MC3T3-E1 cells as osteoblast-like cells. We also examined the effect of IL-17A on the expression of IL-17Rs, RANKL, macrophage colony-stimulating factor (M-CSF), and osteoprotegerin (OPG). The cells were cultured with or without continuous Compressive Force (1.0 and 2.0 g/cm(2)) for up to 24 hr. The cells were also cultured with or without IL-17A (0.1, 1.0, or 10 ng/ml) for up to 72 hr. The mRNA expressions of IL-17s and their receptors were estimated by real-time polymerase chain reaction. The expression levels of IL-17s and their receptors increased depending on the Compressive Force. The addition of IL-17A increased the expression of IL-17RA, IL-17RB, IL-17RC, IL-17RE, RANKL, and M-CSF, whereas it decreased OPG expression. These results indicate that Compressive Force induces the expression of IL-17s and their receptors in osteoblast-like cells and that IL-17s and their receptors produced in response to Compressive Force may affect osteoclastogenesis through the expression of RANKL, M-CSF, and OPG.
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Compressive Force induces osteoclast differentiation via prostaglandin e2 production in mc3t3 e1 cells
Connective Tissue Research, 2010Co-Authors: Rina Sanuki, Narihiro Mitsui, Naoto Suzuki, Noriyoshi Shimizu, Yuki Koyama, Fan Zhang, Chieko Shionome, Akiko Kuwabara, Masao MaenoAbstract:In orthodontic tooth movement, prostaglandin E(2) (PGE(2)) released from osteoblasts can alter the normal process of bone remodeling. We previously showed that Compressive Force (CF) controls bone formation by stimulating the production of PGE(2) and Ep2 and/or Ep4 receptors in osteoblasts. The present study was undertaken to examine the effect of CF on the production of PGE(2), cyclooxygenase-2 (COX-2), macrophage colony-stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) using osteoblastic MC3T3-E1 cells and to examine the indirect effect of CF on osteoclast differentiation using RAW264.7 cells as osteoclast precursors. MC3T3-E1 cells were cultured with or without continuous CF (1.0 or 3.0 g/cm(2)) for 24 hr, and PGE(2) production was determined using ELISA. The expression of COX-2, M-CSF, RANKL, and OPG genes and proteins was determined using real-time PCR and ELISA, respectively. Osteoclast differentiation was estimated using tartrate-resistant acid phosphatase (TRAP) staining of RAW 264.7 cells cultured for 10 days with conditioned medium from CF-treated MC3T3-E1 cells and soluble RANKL. As CF increased, PGE(2) production and the expression of COX-2, M-CSF, and RANKL increased, whereas OPG expression decreased. The number of TRAP-positive cells increased as CF increased. Celecoxib, a specific inhibitor of COX-2, blocked the stimulatory effect of CF on TRAP staining and the production of PGE(2), M-CSF, RANKL, and OPG. These results suggest that CF induces osteoclast differentiation by increasing M-CSF production and decreasing OPG production via PGE(2) in osteoblasts.
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effect of Compressive Force on the expression of inflammatory cytokines and their receptors in osteoblastic saos 2 cells
Archives of Oral Biology, 2008Co-Authors: Yuki Koyama, Narihiro Mitsui, Naoto Suzuki, Momoko Yanagisawa, Noriyoshi Shimizu, Rina Sanuki, Keitaro Isokawa, Masao MaenoAbstract:Abstract Objective In orthodontic tooth movement, some cytokines released from periodontal ligament fibroblasts and alveolar bone osteoblasts on the pressure side can alter the normal processes of bone remodelling, resulting in physiological bone resorption. We examined the effect of Compressive Force and interleukin (IL)-1 type I receptor antagonist (IL-1ra) on the expression of inflammatory cytokines that promote osteoclast formation, as well as on their receptors, in osteoblastic Saos-2 cells. Design The cells were cultured in Dulbecco's modified Eagle medium containing 10% fetal bovine serum with or without continuous Compressive Force (0.5–3.0 g/cm2) and/or IL-1ra for up to 24 h. The gene expression levels of the cytokines and their receptors were estimated by determining mRNA levels using real-time PCR; the protein levels were determined using ELISA or immunohistochemical staining. Results The expression of IL-1β, IL-1 receptor, IL-6, IL-6 receptor, IL-8 receptor, IL-11 and tumor necrosis factor-α (TNFα) increased depending on the strength and duration of the Compressive Force, whereas the expression of IL-8, IL-11 receptor and TNFα receptor did not change with the application of Compressive Force. The expression of cytokines and their receptors produced by 3.0 g/cm2 of Compressive Force decreased with the simultaneous addition of IL-1ra and the decrease was remarkable in IL-8 receptor, IL-11 and TNFα. Conclusion These results indicate that mechanical stress induces the production of inflammatory cytokines and their receptors in osteoblasts and the phenomenon is enhanced by the autocrine action of IL-1β, which is increased in amount by mechanical stress.
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effects of Compressive Force on the differentiation of pluripotent mesenchymal cells
Life Sciences, 2007Co-Authors: Momoko Yanagisawa, Narihiro Mitsui, Naoto Suzuki, Kichibee Otsuka, Yuki Koyama, Noriyoshi ShimizuAbstract:The purpose of this study was to determine the effect of mechanical stress on the differentiation of the pluripotent mesenchymal cell line C2C12. C2C12 cells were cultured continuously under Compressive Force (0.25-2.0 g/cm(2)). After mechanical stress loading, the levels of expression of mRNAs and proteins for phenotype-specific markers of osteoblasts (Runx2, Msx2, Dlx5, Osterix, AJ18), chondroblasts (Sox5, Sox9), myoblasts (MyoD), and adipocytes (PPAR gamma) were measured by real-time polymerase chain reaction analysis and Western blot analysis, respectively. The expression of activated p38 mitogen-activated protein kinase (p38 MAPK) was measured by Western blotting and/or ELISA. Loading 0.5 g/cm(2) of Compressive Force significantly increased the expression levels of Runx2, Msx2, Dlx5, Osterix, Sox5, and Sox9. In contrast, the expression levels of AJ18, MyoD, and PPAR gamma were decreased by exposure to 0.5 g/cm(2) of Compressive Force. Loading 0.5 g/cm(2) of Compressive Force also induced the phosphorylation of p38 MAPK. SB203580, which is a specific inhibitor of p38 MAPK, inhibited the Compressive Force-induced phosphorylation of p38 MAPK and partially blocked Compressive Force-induced Runx2 mRNA expression. These results demonstrate that Compressive Force stimulation directs the differentiation pathway of C2C12 cells into the osteoblast and chondroblast lineage via activated phosphorylation of p38 MAPK.
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optimal Compressive Force induces bone formation via increasing bone morphogenetic proteins production and decreasing their antagonists production by saos 2 cells
Life Sciences, 2006Co-Authors: Narihiro Mitsui, Naoto Suzuki, Masao Maeno, Momoko Yanagisawa, Kichibee Otsuka, Yuki Koyama, Noriyoshi ShimizuAbstract:Orthodontic tooth movement induced alveolar bone resorption and formation around the teeth applied mechanical Force. Although mechanical Force can promote bone formation, the molecular mechanism that underlies this phenomenon is not fully understood. The purposes of this study were to determine how mechanical stress affects the osteogenic response of human osteoblastic cells (Saos-2), and also to examine the optimal Compressive Force for osteogenesis in vitro. Saos-2 cells were cultured with or without continuously Compressive Force (0.5-3.0 g/cm2). The expression of bone morphogenetic proteins (BMPs), their antagonists, and transcription factors which involved in osteogenesis were measured using real-time PCR and/or Western blot analysis. Phosphorylation of Smad1 was determined by Western blot. Loading with 1.0 g/cm2 of Compressive Force significantly increased the expression of BMPs, Runx2 and osterix. In contrast, the expression of BMP antagonists and AJ18 was decreased with 1.0 g/cm2 of Compressive Force. Loading with 1.0 g/cm2 of Compressive Force also induced phosphorylation of Smad1. Noggin inhibited the Compressive Force-induced phosphorylation of Smad1 markedly, and also partially blocked Compressive Force-induced Runx2 mRNA expression. Moreover, the conditioned medium from 1.0 g/cm2 of Compressive Force applied cells apparently increased calcium content in mineralized nodules of Saos-2 culture. This study demonstrates that an optimal Compressive Force stimulates in vitro mineralization via increasing BMPs production and decreasing their antagonists production.
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crosslinking actin networks produces Compressive Force
Cytoskeleton, 2019Co-Authors: Julien BerroAbstract:Actin has been shown to be essential for clathrin-mediated endocytosis in yeast. However, actin polymerization alone is likely insufficient to produce enough Force to deform the membrane against the huge turgor pressure of yeast cells. In this paper, we used Brownian dynamics simulations to demonstrate that crosslinking of a meshwork of nonpolymerizing actin filaments is able to produce Compressive Forces. We show that the Force can be up to several thousand pico-Newtons if the crosslinker has a high stiffness. The Force decays over time as a result of crosslinker turnover, and is a result of converting chemical binding energy into elastic energy.
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crosslinking actin networks produces Compressive Force
bioRxiv, 2019Co-Authors: Julien BerroAbstract:Abstract Actin has been shown to be essential for clathrin-mediated endocytosis in yeast. However, actin polymerization alone is likely insufficient to produce enough Force to deform the membrane against the huge turgor pressure of yeast cells. In this paper, we used Brownian dynamics simulations to demonstrate that crosslinking of a meshwork of non-polymerizing actin filaments is able to produce Compressive Forces. We show that the Force can be up to thousands of piconewtons if the crosslinker has a high stiffness. The Force decays over time as a result of crosslinker turnover, and is a result of converting chemical binding energy into elastic energy.