Cyclic Compressive Stress Regulates Apoptosis in Rat Osteoblasts: Involvement of PI3K-Akt and JNK MAPK Signaling PathwaysReport as inadecuate




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It is widely accepted that physiological mechanical stimulation suppresses apoptosis and induces synthesis of extracellular matrix by osteoblasts; however, the effect of stress overloading on osteoblasts has not been fully illustrated. In the present study, we investigated the effect of cyclic compressive stress on rat osteoblasts apoptosis, using a novel liquid drop method to generate mechanical stress on osteoblast monolayers. After treatment with different levels of mechanical stress, apoptosis of osteoblasts and activations of mitogen-activated protein kinases MAPKs and PI3-kinase PI3K-Akt signaling pathways were investigated. Osteoblasts apoptosis was observed after treated with specific inhibitors prior to mechanical stimulation. Protein levels of Bax-Bcl-2-caspase-3 signaling were determined using western blot with or without inhibitors of PI3K-Akt and phosphorylation of c-jun N-terminal kinase JNK MAPK. Results showed that mechanical stimulation led to osteoblasts apoptosis in a dose-dependent manner and a remarkable activation of MAPKs and PI3K-Akt signaling pathways. Activation of PI3K-Akt protected against apoptosis, whereas JNK MAPK increased apoptosis via regulation of Bax-Bcl-2-caspase-3 activation. In summary, the PI3K-Akt and JNK MAPK signaling pathways played opposing roles in osteoblasts apoptosis, resulting in inhibition of apoptosis upon small-magnitude stress and increased apoptosis upon large-magnitude stress.



Author: Fanglong Song , Yi Wang , Dawei Jiang, Tianchen Wang, Yinquan Zhang, Hui Ma, Yifan Kang

Source: http://plos.srce.hr/



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