The effect of mechanical stretch stress on the differentiation and apoptosis of human growth plate chondrocytes

Sun, Keming; Liu, Fangna; Wang, Junjian; Guo, Zhanhao; Ji, Zejuan; Yao, Manye

doi:10.1007/s11626-016-0090-5

Cited by 13 publications

(14 citation statements)

References 26 publications

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“…Second, it was shown that cyclic mechanical stretch can increase the opening of the MPTP, thereby increasing mitochondrial permeability. Furthermore, it was found that lY294002, a Pi3K/akt overloading mechanical stretch may cause injury or apoptosis in skeletal muscle (11). Several studies have shown that excessive stretch can seriously damage the structure and physiological function of cells (9).…”

Section: Discussionmentioning

confidence: 99%

“…research has suggested that skeletal muscle proliferation, differentiation, migration and apoptosis occur as a result of significant levels of mechanical stretch (7). Mechanical stretching of skeletal muscle initiates a series of cellular responses that can cause stem or progenitor cells to enter the cell cycle, divide, differentiate and fuse with other cells to repair damaged areas (8,9), or alternatively to undergo apoptosis (10,11). Previous studies have focused on the response of cell proliferation and differentiation to adaptive mechanical stretching of muscle cells (12,13).…”

Section: Introductionmentioning

confidence: 99%

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Phosphorylated GSK‑3β protects stress‑induced apoptosis of myoblasts via the PI3K/Akt signaling pathway

et al. 2020

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Facial jaw muscle is involved in the occurrence, development, treatment and maintenance of maxillofacial deformities. The structure and function of this tissue can be altered by changes in external stimuli, and orthodontists can regulate its reconstruction using orthopedic forces. The Pi3K/akt signaling pathway is most well-known for its biological functions in cell proliferation, survival and apoptosis. in the present study, the effects of the Pi3K/akt signaling pathway in cyclic stretch-induced myoblast apoptosis were investigated. For this purpose, l6 rat myoblasts were cultured under mechanical stimulation and treated with the Pi3K kinase inhibitor, lY294002, to elucidate the role of the Pi3K/akt signaling pathway. cells were stained with Hoechst 33258 to visualize morphological changes and apoptosis of myoblasts, and western blotting was performed to detect expression of akt, phosphorylated (p)-akt (Ser473), glycogen synthase kinase 3β (GSK-3β) and p-GSK-3β (Ser9). after addition of Pi3K inhibitor, the expression of total akt and GSK-3β did not significantly differ among groups; however, the levels of p-Akt and p-GSK-3β were lower in inhibitor-treated groups than in those treated with loading stress alone. in addition, the rate of apoptosis in myoblasts subjected to cyclic stretch increased in a time-dependent manner, peaking at 24 h. collectively, it was also demonstrated that the Pi3K/akt/GSK-3β pathway plays an important role in stretch-induced myoblast apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Phosphorylated GSK‑3β protects stress‑induced apoptosis of myoblasts via the PI3K/Akt signaling pathway

et al. 2020

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“…Several in vitro impact models have been developed to study the molecular changes associated to trauma-induced OA: In vitro impact models using instrumented drop tower [239], shear stress [240], or compression [128]. Mechanical stresses applied to human cartilage explants [241] or to cartilaginous endplate chondrocytes [242] or to human growth plate chondrocytes [243] result in chondrocytes apoptosis in vivo and in vitro [242] with the associated loss of glycosaminoglycans, aggrecan, and type II collagen [241,244]. In contrast, hydrostatic pressure was reported to increase matrix macromolecule expression [244].…”

Section: Cell Death Regulators In Chondrocytesmentioning

confidence: 99%

“…In contrast, hydrostatic pressure was reported to increase matrix macromolecule expression [244]. Moreover, it is also important to consider the intensity of the stress applied, which can induce either cell proliferation or promote cell death [243]. …”

Section: Cell Death Regulators In Chondrocytesmentioning

confidence: 99%

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

Charlier

Relić

Deroyer

et al. 2016

IJMS

257

220

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Osteoarthritis (OA) is a joint pathology characterized by progressive cartilage degradation. Medical care is mainly based on alleviating pain symptoms. Compelling studies report the presence of empty lacunae and hypocellularity in cartilage with aging and OA progression, suggesting that chondrocyte cell death occurs and participates to OA development. However, the relative contribution of apoptosis per se in OA pathogenesis appears complex to evaluate. Indeed, depending on technical approaches, OA stages, cartilage layers, animal models, as well as in vivo or in vitro experiments, the percentage of apoptosis and cell death types can vary. Apoptosis, chondroptosis, necrosis, and autophagic cell death are described in this review. The question of cell death causality in OA progression is also addressed, as well as the molecular pathways leading to cell death in response to the following inducers: Fas, Interleukin-1β (IL-1β), Tumor Necrosis factor-α (TNF-α), leptin, nitric oxide (NO) donors, and mechanical stresses. Furthermore, the protective role of autophagy in chondrocytes is highlighted, as well as its decline during OA progression, enhancing chondrocyte cell death; the transition being mainly controlled by HIF-1α/HIF-2α imbalance. Finally, we have considered whether interfering in chondrocyte apoptosis or promoting autophagy could constitute therapeutic strategies to impede OA progression.

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“…25 Beyond growth rate, cell-level alterations such as apoptosis regulation, collagen synthesis, and chondrocyte viability have also varied depending on the mechanical loading parameters described above. [26][27][28] Each parameter plays a role in both the macro-scale growth outcome as well as bone and growth plate tissue health.…”

Section: Introductionmentioning

confidence: 99%

Part 1. Review and meta‐analysis of studies on modulation of longitudinal bone growth and growth plate activity: A macro‐scale perspective

D'Andrea

Alfraihat

Singh

et al. 2021

Journal Orthopaedic Research

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Growth modulation is an emerging method for treatment of angular skeletal deformities such as adolescent idiopathic scoliosis (AIS). The Hueter-Volkmann law, by which growth is stimulated in tension and inhibited in compression, is widely understood, and applied in current growth-modulating interventions such as anterior vertebral body tethering (AVBT) for AIS. However, without quantification of the growth rate effects of tension or compression, the possibility of under-or overcorrection exists. A definitive mechanical growth modulation relationship relating to treatment of such skeletal deformities is yet to exist, and the mechanisms by which growth rate is regulated and altered are not fully defined. Review of current literature demonstrates that longitudinal (i.e., lengthwise) growth rate in multiple animal models depend on load magnitude, anatomical location, and species. Additionally, alterations in growth plate morphology and viability vary by loading parameters such as magnitude, frequency, and whether the load was applied persistently or intermittently. The aggregate findings of the reviewed studies will assist in work towards increasingly precise and clinically successful growth modulation methods. Part 1 of this review focuses on the effects of mechanical loading, species, age, and anatomical location on the macro-scale alterations in longitudinal bone growth, as well as factors that affect growth plate material properties. Part 2 considers the effects on micro-scale alterations in growth plate morphology such as zone heights and proportions, chondrocyte viability, and related gene and protein expression.

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The effect of mechanical stretch stress on the differentiation and apoptosis of human growth plate chondrocytes

Cited by 13 publications

References 26 publications

Phosphorylated GSK‑3β protects stress‑induced apoptosis of myoblasts via the PI3K/Akt signaling pathway

Phosphorylated GSK‑3β protects stress‑induced apoptosis of myoblasts via the PI3K/Akt signaling pathway

Insights on Molecular Mechanisms of Chondrocytes Death in Osteoarthritis

Part 1. Review and meta‐analysis of studies on modulation of longitudinal bone growth and growth plate activity: A macro‐scale perspective

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