The Experts below are selected from a list of 195633 Experts worldwide ranked by ideXlab platform
Xizheng Zhang - One of the best experts on this subject based on the ideXlab platform.
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Mechanical Strain promotes osteoblastic differentiation through integrin-β1-mediated β-catenin signaling
International journal of molecular medicine, 2016Co-Authors: Yuxian Yan, Yong Guo, Xizheng Zhang, Yuanwei Gong, Haoyang Sun, Zhixiong Yan, Yang WangAbstract:As integrins are mechanoresponsive, there exists an intimate relationship between integrins and Mechanical Strain. Integrin-1 mediates the impact of Mechanical Strain on bone. Mechanical Strain induces bone formation through the activation of -catenin pathways, which suggests that integrin-1 mediates -catenin signaling in osteoblasts in response to Mechanical Strain. In the present study, we examined the role of integrin-1 in Wnt/-catenin signal transduction in Mechanically Strained osteoblasts. MC3T3-E1 osteoblastic cells were transfected with integrin-1 small interfering RNA (si-Itg1), and exposed to Mechanical tensile Strain of 2,500 microStrain (mu epsilon) using a four-point bending device. The Mechanical Strain enhanced the mRNA expression of integrin-1, the protein levels of phosphorylated (p-) glycogen synthase kinase-3 (GSK-3) and -catenin, simultaneously increased the mRNA levels of runt-related transcriptional factor 2 (Runx2) and osteocalcin (OCN), the protein levels of bone morphogenetic protein (BMP)-2 and -4 and enhanced the alkaline phosphatase (ALP) activity of the ME3T3-E1 cells. The elevations were inhibited by si-Itg1. Additionally, the Mechanical Strain induced the nuclear translocation of -catenin into the nucleus, which was also inhibited by si-Itg1. These findings indicated that Mechanical Strain promoted osteoblastic differentiation through integrin-1-mediated -catenin signaling.
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A comparative study of Mechanical Strain, icariin and combination stimulations on improving osteoinductive potential via NF-kappaB activation in osteoblast-like cells
Biomedical engineering online, 2015Co-Authors: Qiang-song Wang, Xinchang Zhang, Jing-gong Sun, Su Weihua, Yong Guo, Xizheng ZhangAbstract:The combination of drugs and exercise was the effective treatment in bone injure and rebuilding in clinic. As Mechanical Strain has potential in inducing the differentiation of osteoblasts in our previous study, the further research to investigate the combination of Mechanical Strain and icariin stimulation on inducing osteoblast proliferation, differentiation and the possible mechanism in MC3T3-E1 cell line. A whole cell enzyme-linked immunosorbent assay that detects the bromodeoxyuridine incorporation during DNA synthesis was applied to evaluate the proliferation. The mRNA expression of alkaline phosphatase (ALP), osteocalcin (OCN), type I collagen (Col I), bone morphogenetic protein-2 (BMP-2) and BMP-4 was detected by real-time reverse-transcription polymerase chain reaction. The activity of ALP was analyzed by ELISA and the protein expression of OCN, Col I and BMP-2 was assessed by western blot. Moreover, the activity of nuclear transcription factor kappa-B (NF-κB) signaling pathway was investigated with the expression of inhibitor of κB (IκB) α, phosphorylation of IκB-α (P-IκB-α), p65, P-p65 by western blot. We observed that compared to single Mechanical Strain or icariin stimulation, the mRNA and protein expressions of ALP (P < 0.05 or P < 0.01), OCN (P < 0.01) and Col I (P < 0.05 or P < 0.01) were increased significantly by the combination of Mechanical Strain and icariin stimulation. Moreover, the combination of Mechanical Strain and icariin stimulation could up-regulate the expression of BMP-2 (P < 0.01) and BMP-4 compared to single Mechanical Strain or icariin stimulation. The combination of Mechanical Strain and icariin stimulation could activate NF-κB signaling pathway by increasing the expression of IκB α, P-IκB-α, p65, P-p65 (P < 0.01). The combination of Mechanical Strain and icariin stimulation could activate the NF-κB pathway to improve the proliferation, differentiation of osteoblast-like cells.
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Mechanical Strain affects some microRNA profiles in pre-oeteoblasts.
Cellular & molecular biology letters, 2015Co-Authors: Yang Wang, Yong Guo, Xianqiong Zou, Yongming Liu, Qiangcheng Zeng, Xizheng ZhangAbstract:MicroRNAs (miRNAs) are important regulators of cell proliferation, differentiation and function. Mechanical Strain is an essential factor for osteoblast proliferation and differentiation. A previous study revealed that a physiological Mechanical tensile Strain of 2500 microStrain (με) at 0.5 Hz applied once a day for 1 h over 3 consecutive days promoted osteoblast differentiation. However, the mechanoresponsive miRNAs of these osteoblasts were not identified. In this study, we applied the same Mechanical tensile Strain to in vitro cultivated mouse MC3T3-E1 pre-osteoblasts and identified the mechanoresponsive miRNAs. Using miRNA microarray and qRT-PCR assays, the expression patterns of miRNAs were evaluated and 5 of them were found to be significantly different between the Mechanical loading group and the control group: miR-3077-5p, 3090-5p and 3103-5p were significantly upregulated and miR-466i-3p and 466h-3p were downregulated. Bioinformatics analysis revealed possible target genes for these differentially expressed miRNAs. Some target genes correlated with osteoblast differentiation. These findings indicated that the Mechanical Strain changed the expression levels of these miRNAs. This might be a potential regulator of osteoblast differentiation and responses to Mechanical Strain.
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Mechanical Strain Influences Preosteoclasts Apoptosis through Mitochondrial Pathway
2013Co-Authors: Qingxin Hao, Xinchang Zhang, Guo Yong, Li Ruixin, Wu Jimin, Zongmin Wan, Jing Guan, Chunqiu Zhang, Xizheng ZhangAbstract:Background: Osteoclasts, the key differentiated cells mainly responsible for bone resorption, are sensitive to Mechanical Strain. However, the effect of Mechanical Strain on osteoclasts apoptosis is poorly understood. Objectives: To investigate the effects of Mechanical Strain on pre-osteoclast apoptosis in vitro. Methods: After treatment with osteoclast-inductive medium, the pre-osteoclastic RAW264.7 cells were subjected to Mechanical Strains of physiological 2500 micro Strain (μs) and pathologic 5000 μs respectively. Then the apoptosis was detected with Annexin V-FITC/PI binding assay and colorimetric assay of caspase-3 activity, mitochondrial membrane potential (Δψm) was assayed with flow cytometry, and apoptotic proteins were detected with western blots. Results: The Mechanical Strain of 2500 μs decreased pre-osteoclast apoptosis ratio, caspase-3 activity, elevated Δψm and the level of Bcl-2, down-regulated the level of caspase-3 and cytochrome C in cytoplasm. The pre-osteoclasts subjected to 5000 μs Strain showed no evident difference compared to unStrained group. Additionally, pretreatment with cyclosporine A, an inhibitor of mitochondrial permeability transition pore (mPTP), elevated Δψm and lowered Mechanical Strain of 2500 μs reduced apoptosis ratio. Conclusion: Physiological Mechanical Strain of 2500 μs inhibited pre-osteoclast apoptosis, and the 5000 μs Strain had no significant effects on apoptosis. The physiological Strain influenced pre-osteoclast apoptosis through mPTP/ cytochrome C of the mitochondrial pathway.
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Differential effects of Mechanical Strain on osteoclastogenesis and osteoclast-related gene expression in RAW264.7 cells.
Molecular medicine reports, 2012Co-Authors: Chun Guo, Yong Guo, Yuxian Yan, Mei Song, Xizheng ZhangAbstract:Mechanical Strain plays a critical role in the formation, proliferation and maturation of bone cells. However, little is known about the direct effects of different magnitudes of Mechanical Strain on osteoclast differentiation. The aim of the present study was to investigate how the fusion and activation of osteoclasts can be regulated by Mechanical Strain magnitude using the RAW264.7 mouse monocyte/macrophage cell line as an osteoclast precursor. Mechanical Strain (substrate stretching) was applied via a 4-point bending system when RAW cells were treated with macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB (RANK) ligand (RANKL) for an indicated period of time. The numbers of tartrate-resistant acid phosphatase-positive (TRAP+) and apoptotic cells were counted. The expression of TRAP, matrix metalloproteinase-9 (MMP-9), RANK, cathepsin K and carbonic anhydrase II (CAII) was measured by semi-quantitative RT-PCR, and immunocytochemistry staining for RANK was performed. We found that the number of nuclei per osteoclast derived from RAW cells decreased under low magnitude Mechanical Strain and increased under high magnitude Strain within physiological load with an enhanced fusion of TRAP+ osteoclasts, compared to the control with no Mechanical Strain. The expression of RANK mRNA was downregulated by low magnitude Strain and beyond physiological load, while it was upregulated by high magnitude Strain within physiological load, correlating with the increased expression of RANK examined by immunocytochemistry, suggesting the Mechanical regulation of RANK expression. There was also an increase in the expression of MMP-9 mRNA in the groups subjected to a Mechanical Strain of 2,000 and 2,500 µe. No significant differences were detected in the expression of TRAP mRNA, cathepsin K and CAII under Mechanical Strain compared to the control under no Strain (0 µe). These findings indicate that low-magnitude Strain suppresses osteoclast fusion and activation, while high-magnitude Strain within physiological load promotes osteoclast fusion and activation related to a Mechanical magnitude-dependent response of RANK expression. These data, therefore, provide a deeper understanding of how different magnitudes of Mechanical Strains exert their effects on osteoclastogenesis.
Ariel Amir - One of the best experts on this subject based on the ideXlab platform.
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Mechanical Strain sensing implicated in cell shape recovery in escherichia coli
Nature microbiology, 2017Co-Authors: Felix Wong, Gizem Ozbaykal, Jayson Paulose, Sven Van Teeffelen, Lars D. Renner, Douglas B. Weibel, Ariel AmirAbstract:Cell straightening in Escherichia coli is consistent with a Mechanical Strain–sensing mode of growth.
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Mechanical Strain sensing implicated in cell shape recovery in Escherichia coli.
Nature microbiology, 2017Co-Authors: Felix Wong, Gizem Ozbaykal, Jayson Paulose, Lars D. Renner, Douglas B. Weibel, Sven Van Teeffelen, Ariel AmirAbstract:The shapes of most bacteria are imparted by the structures of their peptidoglycan cell walls, which are determined by many dynamic processes that can be described on various length scales ranging from short-range glycan insertions to cellular-scale elasticity1-11. Understanding the mechanisms that maintain stable, rod-like morphologies in certain bacteria has proved to be challenging due to an incomplete understanding of the feedback between growth and the elastic and geometric properties of the cell wall3,4,12-14. Here, we probe the effects of Mechanical Strain on cell shape by modelling the Mechanical Strains caused by bending and differential growth of the cell wall. We show that the spatial coupling of growth to regions of high Mechanical Strain can explain the plastic response of cells to bending4 and quantitatively predict the rate at which bent cells straighten. By growing filamentous Escherichia coli cells in doughnut-shaped microchambers, we find that the cells recovered their straight, native rod-shaped morphologies when released from captivity at a rate consistent with the theoretical prediction. We then measure the localization of MreB, an actin homologue crucial to cell wall synthesis, inside confinement and during the straightening process, and find that it cannot explain the plastic response to bending or the observed straightening rate. Our results implicate Mechanical Strain sensing, implemented by components of the elongasome yet to be fully characterized, as an important component of robust shape regulation in E. coli.
Miriam B. Goodman - One of the best experts on this subject based on the ideXlab platform.
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Touch-induced Mechanical Strain in somatosensory neurons is independent of extracellular matrix mutations in Caenorhabditis elegans.
Molecular biology of the cell, 2020Co-Authors: Adam L. Nekimken, Beth L Pruitt, Miriam B. GoodmanAbstract:Cutaneous mechanosensory neurons are activated by Mechanical loads applied to the skin, and these stimuli are proposed to generate Mechanical Strain within sensory neurons. Using a microfluidic device to deliver controlled stimuli to intact animals and large, immobile, and fluorescent protein-tagged mitochondria as fiducial markers in the touch receptor neurons (TRNs), we visualized and measured touch-induced Mechanical Strain in C. elegans worms. At steady-state, touch stimuli sufficient to activate TRNs induce an average Strain of 3.1% at the center of the actuator and this Strain decays to near zero at the edges of the actuator. We also measured Strain in animals carrying mutations affecting links between the extracellular matrix (ECM) and the TRNs but could not detect any differences in touch-induced Mechanical Strain between wild-type and mutant animals. Collectively, these results demonstrate that touching the skin induces local Mechanical Strain in intact animals and suggest that a fully intact ECM is not essential for transmitting Mechanical Strain from the skin to cutaneous mechanosensory neurons.
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Touch-induced Mechanical Strain in Somatosensory Neurons is Independent of Extracellular Matrix Mutations in C. elegans
2019Co-Authors: Adam L. Nekimken, Beth L Pruitt, Miriam B. GoodmanAbstract:Abstract Cutaneous mechanosensory neurons are activated by Mechanical loads applied to the skin, and these stimuli are proposed to generate Mechanical Strain within sensory neurons. Using a microfluidic device to deliver controlled stimuli to intact animals and large, immobile, and fluorescent protein-tagged mitochondria as fiducial markers in the touch receptor neurons (TRNs), we visualized and measured touch-induced Mechanical Strain in C. elegans worms. At steady-state, touch stimuli sufficient to activate TRNs induce an average Strain of 3.1% at the center of the actuator and this Strain decays to near zero at the edges of the actuator. We also measured Strain in animals carrying mutations affecting links between the extracellular matrix (ECM) and the TRNs but could not detect any differences in touch-induced Mechanical Strain between wild-type and mutant animals. Collectively, these results demonstrate that touching the skin induces local Mechanical Strain in intact animals and suggest that a fully intact ECM is not essential for transmitting Mechanical Strain from the skin to cutaneous mechanosensory neurons.
Yuxian Yan - One of the best experts on this subject based on the ideXlab platform.
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Mechanical Strain promotes osteoblastic differentiation through integrin-β1-mediated β-catenin signaling
International journal of molecular medicine, 2016Co-Authors: Yuxian Yan, Yong Guo, Xizheng Zhang, Yuanwei Gong, Haoyang Sun, Zhixiong Yan, Yang WangAbstract:As integrins are mechanoresponsive, there exists an intimate relationship between integrins and Mechanical Strain. Integrin-1 mediates the impact of Mechanical Strain on bone. Mechanical Strain induces bone formation through the activation of -catenin pathways, which suggests that integrin-1 mediates -catenin signaling in osteoblasts in response to Mechanical Strain. In the present study, we examined the role of integrin-1 in Wnt/-catenin signal transduction in Mechanically Strained osteoblasts. MC3T3-E1 osteoblastic cells were transfected with integrin-1 small interfering RNA (si-Itg1), and exposed to Mechanical tensile Strain of 2,500 microStrain (mu epsilon) using a four-point bending device. The Mechanical Strain enhanced the mRNA expression of integrin-1, the protein levels of phosphorylated (p-) glycogen synthase kinase-3 (GSK-3) and -catenin, simultaneously increased the mRNA levels of runt-related transcriptional factor 2 (Runx2) and osteocalcin (OCN), the protein levels of bone morphogenetic protein (BMP)-2 and -4 and enhanced the alkaline phosphatase (ALP) activity of the ME3T3-E1 cells. The elevations were inhibited by si-Itg1. Additionally, the Mechanical Strain induced the nuclear translocation of -catenin into the nucleus, which was also inhibited by si-Itg1. These findings indicated that Mechanical Strain promoted osteoblastic differentiation through integrin-1-mediated -catenin signaling.
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Differential effects of Mechanical Strain on osteoclastogenesis and osteoclast-related gene expression in RAW264.7 cells.
Molecular medicine reports, 2012Co-Authors: Chun Guo, Yong Guo, Yuxian Yan, Mei Song, Xizheng ZhangAbstract:Mechanical Strain plays a critical role in the formation, proliferation and maturation of bone cells. However, little is known about the direct effects of different magnitudes of Mechanical Strain on osteoclast differentiation. The aim of the present study was to investigate how the fusion and activation of osteoclasts can be regulated by Mechanical Strain magnitude using the RAW264.7 mouse monocyte/macrophage cell line as an osteoclast precursor. Mechanical Strain (substrate stretching) was applied via a 4-point bending system when RAW cells were treated with macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB (RANK) ligand (RANKL) for an indicated period of time. The numbers of tartrate-resistant acid phosphatase-positive (TRAP+) and apoptotic cells were counted. The expression of TRAP, matrix metalloproteinase-9 (MMP-9), RANK, cathepsin K and carbonic anhydrase II (CAII) was measured by semi-quantitative RT-PCR, and immunocytochemistry staining for RANK was performed. We found that the number of nuclei per osteoclast derived from RAW cells decreased under low magnitude Mechanical Strain and increased under high magnitude Strain within physiological load with an enhanced fusion of TRAP+ osteoclasts, compared to the control with no Mechanical Strain. The expression of RANK mRNA was downregulated by low magnitude Strain and beyond physiological load, while it was upregulated by high magnitude Strain within physiological load, correlating with the increased expression of RANK examined by immunocytochemistry, suggesting the Mechanical regulation of RANK expression. There was also an increase in the expression of MMP-9 mRNA in the groups subjected to a Mechanical Strain of 2,000 and 2,500 µe. No significant differences were detected in the expression of TRAP mRNA, cathepsin K and CAII under Mechanical Strain compared to the control under no Strain (0 µe). These findings indicate that low-magnitude Strain suppresses osteoclast fusion and activation, while high-magnitude Strain within physiological load promotes osteoclast fusion and activation related to a Mechanical magnitude-dependent response of RANK expression. These data, therefore, provide a deeper understanding of how different magnitudes of Mechanical Strains exert their effects on osteoclastogenesis.
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Mechanical Strain regulates osteoblast proliferation through integrin mediated erk activation
PLOS ONE, 2012Co-Authors: Yuxian Yan, Yong Guo, Yuanwei Gong, Chun Guo, Yan Zhuang, Yuan Zhang, Xizheng ZhangAbstract:Mechanical Strain plays a critical role in the proliferation, differentiation and maturation of bone cells. As Mechanical receptor cells, osteoblasts perceive and respond to stress force, such as those associated with compression, Strain and shear stress. However, the underlying molecular mechanisms of this process remain unclear. Using a four-point bending device, mouse MC3T3-E1 cells was exposed to Mechanical tensile Strain. Cell proliferation was determined to be most efficient when stimulated once a day by Mechanical Strain at a frequency of 0.5 Hz and intensities of 2500 µe with once a day, and a periodicity of 1 h/day for 3 days. The applied Mechanical Strain resulted in the altered expression of 1992 genes, 41 of which are involved in the mitogen-activated protein kinase (MAPK) signaling pathway. Activation of ERK by Mechanical Strain promoted cell proliferation and inactivation of ERK by PD98059 suppressed proliferation, confirming that ERK plays an important role in the response to Mechanical Strain. Furthermore, the membrane-associated receptors integrin β1 and integrin β5 were determined to regulate ERK activity and the proliferation of Mechanical Strain-treated MC3T3-E1 cells in opposite ways. The knockdown of integrin β1 led to the inhibition of ERK activity and cell proliferation, whereas the knockdown of integrin β5 led to the enhancement of both processes. This study proposes a novel mechanism by which Mechanical Strain regulates bone growth and remodeling.
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Mechanical Strain Regulates Osteoblast Proliferation through Integrin-Mediated ERK Activation
PloS one, 2012Co-Authors: Yuxian Yan, Yong Guo, Yuanwei Gong, Chun Guo, Yan Zhuang, Yuan Zhang, Xizheng ZhangAbstract:Mechanical Strain plays a critical role in the proliferation, differentiation and maturation of bone cells. As Mechanical receptor cells, osteoblasts perceive and respond to stress force, such as those associated with compression, Strain and shear stress. However, the underlying molecular mechanisms of this process remain unclear. Using a four-point bending device, mouse MC3T3-E1 cells was exposed to Mechanical tensile Strain. Cell proliferation was determined to be most efficient when stimulated once a day by Mechanical Strain at a frequency of 0.5 Hz and intensities of 2500 µε with once a day, and a periodicity of 1 h/day for 3 days. The applied Mechanical Strain resulted in the altered expression of 1992 genes, 41 of which are involved in the mitogen-activated protein kinase (MAPK) signaling pathway. Activation of ERK by Mechanical Strain promoted cell proliferation and inactivation of ERK by PD98059 suppressed proliferation, confirming that ERK plays an important role in the response to Mechanical Strain. Furthermore, the membrane-associated receptors integrin β1 and integrin β5 were determined to regulate ERK activity and the proliferation of Mechanical Strain-treated MC3T3-E1 cells in opposite ways. The knockdown of integrin β1 led to the inhibition of ERK activity and cell proliferation, whereas the knockdown of integrin β5 led to the enhancement of both processes. This study proposes a novel mechanism by which Mechanical Strain regulates bone growth and remodeling.
Lars D. Renner - One of the best experts on this subject based on the ideXlab platform.
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Mechanical Strain sensing implicated in cell shape recovery in escherichia coli
Nature microbiology, 2017Co-Authors: Felix Wong, Gizem Ozbaykal, Jayson Paulose, Sven Van Teeffelen, Lars D. Renner, Douglas B. Weibel, Ariel AmirAbstract:Cell straightening in Escherichia coli is consistent with a Mechanical Strain–sensing mode of growth.
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Mechanical Strain sensing implicated in cell shape recovery in Escherichia coli.
Nature microbiology, 2017Co-Authors: Felix Wong, Gizem Ozbaykal, Jayson Paulose, Lars D. Renner, Douglas B. Weibel, Sven Van Teeffelen, Ariel AmirAbstract:The shapes of most bacteria are imparted by the structures of their peptidoglycan cell walls, which are determined by many dynamic processes that can be described on various length scales ranging from short-range glycan insertions to cellular-scale elasticity1-11. Understanding the mechanisms that maintain stable, rod-like morphologies in certain bacteria has proved to be challenging due to an incomplete understanding of the feedback between growth and the elastic and geometric properties of the cell wall3,4,12-14. Here, we probe the effects of Mechanical Strain on cell shape by modelling the Mechanical Strains caused by bending and differential growth of the cell wall. We show that the spatial coupling of growth to regions of high Mechanical Strain can explain the plastic response of cells to bending4 and quantitatively predict the rate at which bent cells straighten. By growing filamentous Escherichia coli cells in doughnut-shaped microchambers, we find that the cells recovered their straight, native rod-shaped morphologies when released from captivity at a rate consistent with the theoretical prediction. We then measure the localization of MreB, an actin homologue crucial to cell wall synthesis, inside confinement and during the straightening process, and find that it cannot explain the plastic response to bending or the observed straightening rate. Our results implicate Mechanical Strain sensing, implemented by components of the elongasome yet to be fully characterized, as an important component of robust shape regulation in E. coli.